Author: "Erik H, Serné" - Searchworks@Jio Institute Digital Library Search Results

135 results on '"Erik H, Serné"'

101. Premature aging of the microcirculation in patients with advanced chronic kidney disease

Author: Geert-Jan Tangelder, Oanh H. D. Thang, Erik H. Serné, Menso J. Nubé, Muriel P.C. Grooteman, Yvo M. Smulders, Piet M. ter Wee, Nephrology, Internal medicine, Physiology, and ICaR - Circulation and metabolism
Subjects: Premature aging, medicine.medical_specialty, Aging, Vasodilation, Disease, urologic and male genital diseases, lcsh:RC870-923, Microcirculation, Internal medicine, Chronic kidney disease, medicine, In patient, Original Paper, business.industry, Endothelial function, Iontophoresis, Control subjects, medicine.disease, lcsh:Diseases of the genitourinary system. Urology, Endocrinology, Nephrology, Cardiology, Sodium nitroprusside, business, medicine.drug, Kidney disease
Abstract: Background: Increasing age and advanced chronic kidney disease (CKD) are both associated with an attenuated vasodilator response of the skin microcirculation. In the present study, we investigated the effect of aging on microvascular reactivity in patients with advanced CKD. Methods: Acetylcholine (ACh)-mediated endothelium-dependent vasodilation and sodium nitroprusside (SNP)-mediated endothelium-independent vasodilation were assessed by iontophoresis combined with laser Doppler flowmetry. Microvascular function was compared between 52 patients with advanced CKD (stage 4–5: n = 16; end-stage renal disease: n = 36) and 33 healthy control subjects. As aging has an important effect on microvascular function, both control subjects and CKD patients were divided in subgroups younger and older than 45 years. Linear regression analysis was applied to assess potential associations between microvascular function and various demographic and clinical parameters. Results: There were three main findings. (1) In young patients with advanced CKD, both ACh- and SNP-mediated vasodilations were impaired if compared to young healthy controls (p = 0.04 and p = 0.056, respectively). (2) In young patients with advanced CKD, microvascular function was similar to old healthy controls and elderly patients with advanced CKD. (3) Whereas age was inversely associated with microvascular function in healthy controls (log ACh-mediated vasodilation R = –0.41; p = 0.02 and log SNP-mediated vasodilation R = –0.38; p = 0.03), no such relation was found in patients with advanced CKD. Conclusions: Our results are consistent with premature aging of the microvascular vasodilatory capacity in patients with advanced CKD.
Published: 2012
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102. Comment on: A multicentre study on the reliability of qualitative and quantitative nailfold videocapillaroscopy assessment: reply

Author: Erik H. Serné, Anton Vonk Noordegraaf, Tonia L. Moore, Chris Roberts, Joanne Manning, Roger Hesselstrand, Ariane L. Herrick, Agneta Scheja, Herman M. A. Hofstee, Alexandre E. Voskuyl, Marie Wildt, Internal medicine, Pulmonary medicine, Rheumatology, ICaR - Circulation and metabolism, and CCA - Innovative therapy
Subjects: medicine.medical_specialty, Rheumatology, business.industry, medicine, Physical therapy, Nailfold videocapillaroscopy, Pharmacology (medical), business, Reliability (statistics), Surgery
Published: 2012
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103. Meal-related increases in microvascular vasomotion are impaired in obese individuals: a potential mechanism in the pathogenesis of obesity-related insulin resistance

Author: Amy M, Jonk, Alfons J, Houben, Nicolaas C, Schaper, Peter W, de Leeuw, Erik H, Serné, Yvo M, Smulders, and Coen D, Stehouwer
Subjects: Blood Glucose, Male, Glucose, Microvessels, Laser-Doppler Flowmetry, Humans, Insulin, Female, Obesity, Insulin Resistance, Obesity/Lipids
Published: 2011

104. Obesity is associated with impaired endothelial function in the postprandial state

Author: Nicolaas C. Schaper, Alfons J.H.M. Houben, Erik H. Serné, Yvo M. Smulders, A.M. Jonk, Coen D.A. Stehouwer, Peter W. de Leeuw, Internal medicine, ICaR - Ischemia and repair, Interne Geneeskunde, RS: NUTRIM - R1 - Metabolic Syndrome, and RS: CARIM School for Cardiovascular Diseases
Subjects: Blood Glucose, Male, Vasodilator Agents, medicine.medical_treatment, Glucose uptake, Blood Pressure, Vasodilation, HUMAN FOREARM MUSCLE, MIXED MEAL, Biochemistry, Microscopic Angioscopy, Heart Rate, Laser-Doppler Flowmetry, POTENTIAL MECHANISM, Hyperinsulinemia, Insulin, Netherlands, Skin, METABOLIC SYNDROME, INSULIN-RESISTANCE, Iontophoresis, Postprandial Period, Postprandial, Female, Cardiology and Cardiovascular Medicine, Blood Flow Velocity, Adult, medicine.medical_specialty, INDUCED CAPILLARY RECRUITMENT, Microcirculation, Beverages, Young Adult, Insulin resistance, MICROVASCULAR RECRUITMENT, Internal medicine, medicine, Humans, Obesity, NITRIC-OXIDE, business.industry, Cell Biology, RAT SKELETAL-MUSCLE, medicine.disease, Capillaries, Endocrinology, Regional Blood Flow, Endothelium, Vascular, Metabolic syndrome, business, MUSCLE GLUCOSE-UPTAKE
Abstract: Adequate microvascular perfusion is essential for the regulation of tissue metabolism. Therefore, defects in microvascular function may play a role in obesity-associated insulin resistance. Steady-state hyperinsulinemia during a euglycemic hyperinsulinemic clamp stimulates endothelium-dependent vasodilation and capillary recruitment, which contribute to increased glucose uptake. These phenomena have been shown to be blunted in obesity. If insulin's effects on microcirculatory function indeed play a physiological role in regulating insulin-mediated glucose uptake, such effects should be demonstrable not only during steady-state hyperinsulinemia, but also after meal ingestion. We investigated whether similar responses occur after ingestion of a glucose load or a mixed meal. We examined the effects of a glucose drink, a mixed meal drink, or a control drink (water) on skin capillary density (i.e. baseline capillary density, hyperemic capillary recruitment, and density during venous congestion, using capillaroscopy) and skin endothelium-(in)dependent vasodilation (using laser-Doppler flowmetry with iontophoresis of acetylcholine and sodium nitroprusside) in 20 lean and 19 obese individuals. In lean individuals, neither the glucose nor the mixed meal drink induced a significant effect on capillary density or endothelium-(in)dependent vasodilation. Possibly this is related to the modest plasma insulin levels as compared to the insulin clamp. In obese individuals, the mixed meal drink, compared to the control drink, decreased baseline skin perfusion (P
Published: 2011
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105. Microvascular function is preserved in newly diagnosed rheumatoid arthritis and low systemic inflammatory activity

Author: Izhar C. van Eijk, Ben A. C. Dijkmans, Erik H. Serné, Michael T. Nurmohamed, Yvo M. Smulders, Rheumatology, Internal medicine, CCA - Innovative therapy, and ICaR - Ischemia and repair
Subjects: Male, Nitroprusside, medicine.medical_specialty, Time Factors, Vasodilator Agents, Arthritis, Inflammation, Systemic inflammation, Gastroenterology, Microcirculation, Arthritis, Rheumatoid, Rheumatology, Internal medicine, Medicine, Humans, Rheumatoid arthritis, Skin, Microscopy, Video, biology, business.industry, Brief Report, C-reactive protein, General Medicine, Iontophoresis, Middle Aged, Vascular function, medicine.disease, Cardiovascular disease, Acetylcholine, Vasodilation, C-Reactive Protein, Immunology, biology.protein, Female, Sodium nitroprusside, medicine.symptom, business, Blood Flow Velocity, medicine.drug
Abstract: Rheumatoid arthritis (RA) is associated with increased cardiovascular morbidity and mortality. Microvascular function has been linked to several risk factors for cardiovascular disease and may be affected in RA. It is, however, presently unknown at what point in the disease course the abnormalities in microvascular function occur. We determined whether microvascular function is already disturbed in early disease-modifying antirheumatic drugs (DMARD)-naive RA patients with low systemic inflammation. Fifteen consecutive RA patients with a median symptom duration of 5 months, a C-reactive protein level of ≤20 mg/l and without a history of cardiovascular disease, and age 15 and sex-matched healthy controls were recruited. Endothelium-dependent and endothelium-independent vasodilatation in skin was evaluated with laser Doppler fluxmetry after iontophoresis of acetylcholine and sodium nitroprusside, respectively. Videomicroscopy was used to measure recruitment of skin capillaries after arterial occlusion. CRP and ESR levels were mildly, but significantly elevated in patients compared to controls. No differences in both endothelium-dependent vasodilatation and capillary recruitment were observed between groups [709% (95% CI, 457–961%) vs 797% (95% CI, 556–1,037%), P = 0.59 and 37% (95% CI, 26–47%) vs 41% (95% CI, 31–50%), P = 0.59, respectively]. Skin microvascular function is preserved in early, DMARD-naive RA patients with moderately active RA but low systemic inflammatory activity. Both the extent of the systemic inflammation and disease duration, therefore, may be important determinants of microvascular dysfunction and subsequent increased risk for cardiovascular disease.
Published: 2011
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106. Angiotensin II Enhances Insulin-Stimulated Whole-Body Glucose Disposal but Impairs Insulin-Induced Capillary Recruitment in Healthy Volunteers

Author: Peter W. de Leeuw, Erik H. Serné, Alfons J.H.M. Houben, A.M. Jonk, Coen D.A. Stehouwer, Yvo M. Smulders, Nicolaas C. Schaper, Internal medicine, EMGO - Lifestyle, overweight and diabetes, ICaR - Ischemia and repair, Interne Geneeskunde, RS: NUTRIM - R1 - Metabolic Syndrome, and RS: CARIM School for Cardiovascular Diseases
Subjects: Adult, Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Glucose uptake, medicine.medical_treatment, Clinical Biochemistry, TYPE-2 DIABETES-MELLITUS, Blood Pressure, ALDOSTERONE SYSTEM, Essential hypertension, Biochemistry, Microscopic Angioscopy, Endocrinology, Heart Rate, Internal medicine, Hyperinsulinism, Hyperinsulinemia, medicine, Humans, Insulin, CONVERTING ENZYME-INHIBITION, ESSENTIAL-HYPERTENSION, OXIDATIVE STRESS, Reactive hyperemia, REACTIVE HYPEREMIA, biology, Angiotensin II, Biochemistry (medical), PHYSIOLOGICAL HYPERINSULINEMIA, VASCULAR ACTIONS, Middle Aged, medicine.disease, Capillaries, Insulin receptor, Glucose, Basal (medicine), NORMOTENSIVE SUBJECTS, biology.protein, Glucose Clamp Technique, MICROVASCULAR FUNCTION, Female, Insulin Resistance, hormones, hormone substitutes, and hormone antagonists
Abstract: Context: Angiotensin II (AngII) increases insulin-mediated glucose uptake in healthy individuals. The underlying mechanisms are undefined. AngII may increase glucose uptake through a direct effect on muscle cell insulin signaling or through increasing insulin delivery to muscle cells through effects on the microvasculature. Objective: Our objective was to determine whether AngII increases insulin-mediated glucose uptake through effects on insulin-induced capillary recruitment. Design: We examined the effects of AngII on hyperinsulinemia-induced capillary density by measuring skin capillary density, capillary recruitment, and capillary density during venous congestion in 18 healthy subjects in the basal state, during systemic hyperinsulinemia, and during hyperinsulinemia with coinfusion of AngII or phenylephrine (pressor control). In addition, whole-body glucose uptake and blood pressure were measured. Results: Capillaroscopy data of 13 subjects were available for analysis. Compared with the basal state, hyperinsulinemia increased baseline capillary density (51.5 +/- 9.0 vs. 55.2 +/- 10.8 n/mm(2), P < 0.01), capillary recruitment (67.8 +/- 6.8 vs. 70.6 +/- 7.5 n/mm(2), P < 0.05), and capillary density during venous congestion (78.5 +/- 12.0 vs. 80.3 +/- 12.0 n/mm(2), P < 0.01). Infusion of AngII, but not phenylephrine, reduced insulin-induced capillary recruitment (69.3 +/- 8.6 vs. 65.2 +/- 8.0 n/mm(2), P < 0.05) and capillary density during venous congestion (79.7 +/- 15.3 vs. 73.9 +/- 12.1, P < 0.05) while enhancing glucose uptake [2.40 +/- 0.7 vs. 2.68 +/- 0.6 (mg/kg . min per pmol/l) x 100, P < 0.01)] (n = 18). Conclusion: AngII increases insulin-mediated glucose uptake in healthy individuals. This increase was probably not related to increases in microvascular perfusion because infusion of AngII during hyperinsulinemia reduced insulin-mediated skin capillary recruitment. Additional studies are needed to investigate whether AngII directly affects insulin delivery through increasing insulin transport across the microvasculature.
Published: 2010
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107. Sunitinib-induced reduction in skin microvascular density is a reversible phenomenon

Author: Erik H. Serné, A.A.M. Van der Veldt, M. P. de Boer, Nienke J. Wijnstok, Epie Boven, A.J.M. van den Eertwegh, N. A. Lankheet, Internal medicine, Medical oncology, CCA - Innovative therapy, and ICaR - Ischemia and repair
Subjects: Oncology, medicine.medical_specialty, Indoles, Palliative care, medicine.medical_treatment, Angiogenesis Inhibitors, Text mining, Internal medicine, Sunitinib, Carcinoma, medicine, Humans, Pyrroles, Carcinoma, Renal Cell, Reduction (orthopedic surgery), Skin, business.industry, Palliative Care, Microvascular Density, Hematology, medicine.disease, Kidney Neoplasms, Capillaries, Hypertension, business, medicine.drug
Published: 2010
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108. [Raynaud's phenomenon; diagnosis and treatment]

Author: Herman M A, Hofstee, Alexandre E, Voskuyl, Erik H, Serné, and Yvo M, Smulders
Subjects: Antibodies, Antinuclear, Humans, Raynaud Disease, Calcium Channel Blockers, Microscopic Angioscopy
Abstract: Primary Raynaud's phenomenon (RP) is a relatively common disorder. Most patients with primary RP have only mild symptoms and do not develop complications. Distinguishing primary from secondary RP is important with respect to complications, and for prognosis and treatment. Secondary RP mainly manifests as part of systemic connective tissue disease. About 13% of patients diagnosed initially as having primary RP develop a systemic disorder within the following few years. Both auto-immune serology including antinuclear antibodies (ANA), and capillaroscopy are important diagnostic tools if one suspects the existence or development of a systemic disorder. Calcium antagonists are the cornerstone of RP pharmacotherapy.
Published: 2009

109. Commentary on viewpoint: the human cutaneous circulation as a model of generalized microvascular function

Author: Erik H. Serné, Renate T. de Jongh, Richard G. IJzerman, Internal medicine, and ICaR - Ischemia and repair
Subjects: medicine.medical_specialty, Physiology, business.industry, Cardiovascular risk factors, medicine.disease, Coronary circulation, medicine.anatomical_structure, Insulin resistance, Physiology (medical), Internal medicine, medicine, Cardiology, Circulation (currency), business, Function (biology)
Abstract: to the editor: Microvascular dysfunction may be one potential factor explaining the clustering of cardiovascular risk factors including hypertension and insulin resistance ([5][1]). Whereas assessment of microvascular function of muscle, kidneys, and coronary circulation would be most relevant from
Published: 2008
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110. Protein kinase C theta activation induces insulin-mediated constriction of muscle resistance arteries

Author: Coen D.A. Stehouwer, Wineke Bakker, Yvo M. Smulders, Etto C. Eringa, Victor W.M. van Hinsbergh, Pieter Sipkema, Erik H. Serné, Interne Geneeskunde, RS: NUTRIM - R1 - Metabolic Syndrome, RS: CARIM School for Cardiovascular Diseases, Physiology, Internal medicine, and ICaR - Ischemia and repair
Subjects: medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Palmitic Acid, Vasodilation, Biology, Nitric Oxide, Mice, Insulin resistance, Internal medicine, Internal Medicine, medicine, Animals, Humans, Insulin, Muscle, Skeletal, Protein kinase B, Protein Kinase C, Protein kinase C, Mitogen-Activated Protein Kinase 6, Mice, Knockout, Mitogen-Activated Protein Kinase 3, Endothelin-1, Arteries, medicine.disease, Isoenzymes, Insulin receptor, Endocrinology, Protein Kinase C-theta, Vasoconstriction, biology.protein, medicine.symptom, Proto-Oncogene Proteins c-akt, Myograph
Abstract: OBJECTIVE—Protein kinase C (PKC) θ activation is associated with insulin resistance and obesity, but the underlying mechanisms have not been fully elucidated. Impairment of insulin-mediated vasoreactivity in muscle contributes to insulin resistance, but it is unknown whether PKCθ is involved. In this study, we investigated whether PKCθ activation impairs insulin-mediated vasoreactivity and insulin signaling in muscle resistance arteries. RESEARCH DESIGN AND METHODS—Vasoreactivity of isolated resistance arteries of mouse gracilis muscles to insulin (0.02–20 nmol/l) was studied in a pressure myograph with or without PKCθ activation by palmitic acid (PA) (100 μmol/l). RESULTS—In the absence of PKCθ activation, insulin did not alter arterial diameter, which was caused by a balance of nitric oxide–dependent vasodilator and endothelin-dependent vasoconstrictor effects. Using three-dimensional microscopy and Western blotting of muscle resistance arteries, we found that PKCθ is abundantly expressed in endothelium of muscle resistance arteries of both mice and humans and is activated by pathophysiological levels of PA, as indicated by phosphorylation at Thr538 in mouse resistance arteries. In the presence of PA, insulin induced vasoconstriction (21 ± 6% at 2 nmol/l insulin), which was abolished by pharmacological or genetic inactivation of PKCθ. Analysis of intracellular signaling in muscle resistance arteries showed that PKCθ activation reduced insulin-mediated Akt phosphorylation (Ser473) and increased extracellular signal–related kinase (ERK) 1/2 phosphorylation. Inhibition of PKCθ restored insulin-mediated vasoreactivity and insulin-mediated activation of Akt and ERK1/2 in the presence of PA. CONCLUSIONS—PKCθ activation induces insulin-mediated vasoconstriction by inhibition of Akt and stimulation of ERK1/2 in muscle resistance arteries. This provides a new mechanism linking PKCθ activation to insulin resistance.
Published: 2008
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111. Microvascular function: a potential link between salt sensitivity, insulin resistance and hypertension

Author: Erik H. Serné, Coen D.A. Stehouwer, Richard G. IJzerman, Renate T. de Jongh, Internal medicine, ACS - Diabetes & metabolism, and AGEM - Endocrinology, metabolism and nutrition
Subjects: Adult, Male, medicine.medical_specialty, Mean arterial pressure, Ambulatory blood pressure, Physiology, medicine.medical_treatment, Vasodilation, Hyperaemia, Insulin resistance, Internal medicine, Internal Medicine, medicine, Humans, Sodium Chloride, Dietary, business.industry, Insulin, Middle Aged, medicine.disease, Endocrinology, Blood pressure, Case-Control Studies, Hypertension, Blood Vessels, Female, Sodium nitroprusside, medicine.symptom, Insulin Resistance, Cardiology and Cardiovascular Medicine, business, medicine.drug
Abstract: OBJECTIVE: Generalized microvascular dysfunction may contribute to the development of salt sensitivity, insulin resistance and hypertension, and may thus link these cardiovascular risk factors. To test this hypothesis, we examined skin microvascular function, salt sensitivity, insulin sensitivity and blood pressure in 27 normotensive and 26 hypertensive individuals. METHODS: Capillary density was examined by videomicroscopy during venous congestion and postocclusive reactive hyperaemia. Endothelium-(in)dependent vasodilation was assessed by iontophoresis of acetylcholine and sodium nitroprusside and by laser Doppler flowmetry. Salt sensitivity was determined as the difference in mean arterial pressure (MAP) between a 1-week high-salt diet (∼235 mmol NaCl/day) versus low-salt diet (∼55 mmol NaCl/day). Insulin sensitivity was measured with the hyperinsulinaemic, euglycaemic clamp, and blood pressure was assessed by 24-h ambulatory blood pressure monitoring. RESULTS: Salt sensitivity of blood pressure was inversely associated with postocclusive capillary recruitment and endothelium-dependent vasodilation (r = -0.67, P < 0.001 and r = -0.60, P < 0.01, respectively), but not with capillary density during venous congestion or endothelium-independent vasodilation. Salt sensitivity was negatively associated with insulin sensitivity (r = -0.55, P < 0.001) and positively with MAP (r = 0.58, P < 0.001). Multiple regression analyses suggested that associations between salt sensitivity and both insulin sensitivity and MAP were dependent on microvascular function. CONCLUSION: Our results suggest a close inverse association between skin microvascular function and salt sensitivity and a role for generalized microvascular defects as a link between salt sensitivity, insulin resistance and hypertension.
Published: 2007
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112. Regulation of vascular function and insulin sensitivity by adipose tissue: focus on perivascular adipose tissue

Author: Yvo M. Smulders, John S Yudkin, Wineke Bakker, Erik H. Serné, Coen D.A. Stehouwer, and Etto C. Eringa
Subjects: medicine.medical_specialty, Pathology, Physiology, Adipokine, Adipose tissue, Vasodilation, Inflammation, Pathogenesis, Insulin resistance, Physiology (medical), Internal medicine, medicine, Humans, Obesity, Molecular Biology, business.industry, Microcirculation, medicine.disease, Endocrinology, Adipose Tissue, Endothelium, Vascular, medicine.symptom, Insulin Resistance, Cardiology and Cardiovascular Medicine, business, Vasoconstriction
Abstract: Obesity is associated with insulin resistance, hypertension and cardiovascular disease, but the mechanisms underlying these associations are incompletely understood. Microvascular dysfunction may play an important role in the pathogenesis of both insulin resistance and hypertension in obesity. Adipose tissue-derived substances (adipokines) and especially inflammatory products of adipose tissue control insulin sensitivity and vascular function. Recently, adipose tissue associated with the arterial tree, called perivascular adipose tissue (PAT) has been shown to produce a variety of adipokines and to trigger vascular inflammation. This review summarizes the mechanisms linking adipose tissue to (micro)vascular function, inflammation and insulin resistance with a special focus on the role of PAT in the regulation of vascular tone, endothelial function, inflammation and insulin sensitivity.
Published: 2007
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113. Urinary cortisol is inversely associated with capillary recruitment in women: A potential explanation for the cortisol-blood pressure relationship

Author: Mirjam M. van Weissenbruch, Henriette A. Delemarre-van de Waal, Richard G. IJzerman, Jasper J. Voordouw, Coen D.A. Stehouwer, Renate T. de Jongh, Erik H. Serné, Internal medicine, ACS - Diabetes & metabolism, AGEM - Endocrinology, metabolism and nutrition, and Pediatric surgery
Subjects: Adult, Male, Nitroprusside, medicine.medical_specialty, Hydrocortisone, Vasodilator Agents, medicine.medical_treatment, Urinary system, Blood Pressure, Vasodilation, Excretion, Sex Factors, Insulin resistance, Internal medicine, medicine, Humans, Ligation, Skin, Microscopy, Video, business.industry, Insulin, General Medicine, Blood Pressure Monitoring, Ambulatory, Iontophoresis, Middle Aged, medicine.disease, Acetylcholine, Capillaries, Endocrinology, Blood pressure, Regression Analysis, Female, Insulin Resistance, business, Biomarkers, Glucocorticoid, medicine.drug
Abstract: The relationships of cortisol with elevated blood pressure and insulin resistance are likely to be the result of a complex interplay of different mechanisms. We hypothesize that cortisol is associated with impaired microvascular function and that this contributes to cortisol-associated high blood pressure and insulin resistance. We examined 24 h urinary free cortisol excretion in 56 healthy adults (26 women). Blood pressure was assessed by 24 h ambulatory measurements. Insulin sensitivity was determined using the hyperinsulinaemic euglycaemic clamp technique. Skin capillary recruitment after arterial occlusion was visualized with videomicroscopy and endothelium-(in)dependent vasodilation was evaluated with iontophoresis of acetylcholine and sodium nitroprusside combined with laser Doppler fluxmetry. Men were characterized by higher urinary cortisol excretion [median (interquartile range), 162 (130–194) compared with 118 (99–156) nmol/24 h, P
Published: 2007
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114. Does microvascular dysfunction link obesity with insulin resistance and hypertension?

Author: Renate T. de Jongh, Richard G. IJzerman, Erik H. Serné, Coen D.A. Stehouwer, Etto C. Eringa, Internal medicine, ACS - Diabetes & metabolism, ACS - Microcirculation, Physiology, AGEM - Endocrinology, metabolism and nutrition, Interne Geneeskunde, RS: NUTRIM School of Nutrition and Translational Research in Metabolism, and RS: CARIM School for Cardiovascular Diseases
Subjects: medicine.medical_specialty, Mechanism (biology), business.industry, Endocrinology, Diabetes and Metabolism, Adipose tissue, Adipokine, medicine.disease, Obesity, Nitric oxide, chemistry.chemical_compound, Endocrinology, Insulin resistance, chemistry, Internal medicine, medicine, Endocrine system, medicine.symptom, business, Vasoconstriction
Abstract: Obesity and obesity-associated clinical disorders are becoming an increasing public health burden. In this perspective, we postulate that impairment of microvascular function links obesity with insulin resistance and hypertension. Obesity is characterized by generalized microvascular dysfunction, which is associated with, and may precede, the development of insulin resistance and hypertension. Understanding of mechanisms involved in obesity-associated microvascular dysfunction may reveal new therapeutic targets. In obesity, cellular regulatory mechanisms of vasoreactivity are shifted towards vasoconstriction, with an increased role for endothelin-1 and a decreased role for nitric oxide. In addition, communicative pathways between adipose tissue and the microvasculature comprise increased release of adipokines and increased sympathetic activity. Although one mechanism may dominate, microvascular defects in obesity are probably caused by an integrated response consisting of endocrine, vasocrine and neurogenic mechanisms. This remains a fruitful area for future research.
Published: 2006
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115. Free fatty acid levels modulate microvascular function: relevance for obesity-associated insulin resistance, hypertension, and microangiopathy

Author: Renate T, de Jongh, Erik H, Serné, Richard G, Ijzerman, Greetje, de Vries, and Coen D A, Stehouwer
Subjects: Adult, Nitroprusside, Microcirculation, Blood Pressure, Fatty Acids, Nonesterified, Acetylcholine, Vasodilation, Heart Rate, Hypertension, Humans, Female, Obesity, Insulin Resistance, Biomarkers
Abstract: To test the hypothesis that free fatty acids (FFAs) modulate microvascular function and that this contributes to obesity-associated insulin resistance, hypertension, and microangiopathy, we examined the effects of both FFA elevation in lean women and FFA lowering in obese women on skin microvascular function. A total of 16 lean and 12 obese women underwent, respectively, Intralipid plus heparin (or saline) infusion and overnight acipimox (or placebo) treatment. We measured capillary recruitment with capillaroscopy and endothelium-(in)dependent vasodilation by iontophoresis of acetylcholine and sodium nitroprusside before and during hyperinsulinemia (40 mU . m(-2) . min(-1)). FFA elevation impaired capillary recruitment and acetylcholine-mediated vasodilation before (44.6 +/- 16.8 vs. 56.9 +/- 18.9%, P0.05; and 338 +/- 131 vs. 557 +/- 162%, P0.01, respectively) and during (54.0 +/- 21.3 vs. 72.4 +/- 25.4%, P0.01; and 264 +/- 186 vs. 685 +/- 199%, P0.01, respectively) hyperinsulinemia. FFA lowering improved capillary recruitment before (50.9 +/- 14.6 vs. 37.4 +/- 9.3%, P0.01) and during (66.8 +/- 20.6 vs. 54.8 +/- 15.4%, P0.05) hyperinsulinemia. Changes in FFA levels were inversely associated with changes in capillary recruitment and insulin sensitivity in lean (r = -0.46, P = 0.08; and r = -0.56, P = 0.03) and in obese (r = -0.70, P = 0.02; and r = -0.62, P = 0.04) women. Regression analyses showed that changes in capillary recruitment statistically explained approximately 29% of the association between changes in FFA levels and insulin sensitivity. In conclusion, FFA levels modulate microvascular function and may contribute to obesity-associated insulin resistance, hypertension, and microangiopathy.
Published: 2004

116. A man with diabetes and heart failure

Author: Jan H. Cornel, A.E.R. Arnold, J. Antonie Maassen, Erik H. Serné, Jan M Sepers, Robin Nijveldt, Cardiology, Internal medicine, ACS - Diabetes & metabolism, and ACS - Microcirculation
Subjects: Heart Failure, Male, medicine.medical_specialty, Mitochondrial Diseases, Heart disease, business.industry, General Medicine, Cardiomyopathy, Hypertrophic, Deafness, Middle Aged, medicine.disease, DNA, Mitochondrial, Surgery, Diabetes Mellitus, Type 2, Diabetes mellitus, Heart failure, medicine, Humans, Female, business, Intensive care medicine
Published: 2004
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117. 40(th) EASD Annual Meeting of the European Association for the Study of Diabetes : Munich, Germany, 5-9 September 2004

Author: S. Artigas, A V Dreval, Mark I. McCarthy, C Watson, Peter H. Bennett, M Quint, Y Ikeda, E Alpert, F Schiele, H Sekihara, Erik Gylfe, P Lowe, J Kuhlmann, Alain Golay, V Longo, Shahidul Alam Khan Akm., L G Mantovani, M Zawodniak-Szalapska, G Winkler, T Harrity, L Virág, U Johne, Kuo S-W., Linda C Tapsell, J Rodriguez, Michel Komajda, K Kankova, Carole A. Cull, M Sporna, E Estilles, U Ribel, M C Spruce, E Buzzigoli, T Prazak, J K McLaughlin, M K Lingohr, M Lim, F Calara, A Siebenhofer, G Meregalli, Roberto Anichini, A D Baron, R Kurashvili, P C Butler, G I Fantus, T. E. De Gooyer, Park Y-M., R. Walther, S Heinrich, Agnieszka Zawiejska, S Mukherjee, Nikolaos Papanas, G Wong, Ian D. Caterson, David M. Maahs, Shuichi Kaneko, Alexandra E. Butler, Francisco Javier Ampudia-Blasco, O N Kong, Attali J-R., C A Hedman, K Oshinyemi, Nicolle Müller, I C Cranston, N Okumus, M V Vlaiculescu, Balasubramanian Ravikumar, W W Cheatham, K Mukasa, K B Biswas, Annunziata Lapolla, Phil McEwan, G Mader, Gilles Chassot, Dragi Anevski, Werner A. Scherbaum, M Donath, C Hesselmann, R A Gandhi, David E. Moller, Ezio Bonifacio, C Garcia, V Ifandi, P Hornnes, Nieuwenhoven Fav., C Puech, S Pérez-Del-Pulgar, Kim S-R., G Hines, C Rubio Terrés, Michael Gaster, N. Hosszufalusi, A Scholze, Andrew A. Young, Stavros Liatis, F Hariri, S Tan, Paul Valensi, Allan E. Karlsen, J Kim, E. Moberg, J Kaiser, L Berman, G Nelson, A Altkrüger, P Kothare, D B Cook, S Doran, G. van Dijk, Shahnaz Shahinfar, Kim C-S., P Stahl, M Manousaki, S Sigrist, S K Lim, M. P. Stern, A Guberti, C Rezzani, J McKenney, Karl Thomaseth, Sofia Carlsson, M Julia, R Brillante, I Rubesova, T Darkow, E Matsumoto, Wendy M. Macfarlane, M Di Martino, G Bardini, Rossella Menghini, D Duhot, E Farcasiu, Annalisa Natalicchio, I Lindner, J Buvat, Christian L. Brand, Harry Dorchy, Iwona Pietrzak, Z T Luo, P Home, M Ekelund, Jesper Gromada, Kristine Færch, F Piarulli, H Kim, R Mentel, Zsuzsanna K. Zsengellér, Dullaart Rpf., Anton Luger, Thomas A. Pearson, V Manicardi, P Rösen, Feng Y-M., R Morganti, Lars Hansen, Demuth H-U., Haruo Kasai, A Shostak, Rudi Steffensen, G Taylor, Markolf Hanefeld, C Santini, E Hamaguchi, Roberto Miccoli, F Storms, M Cooper, Y Lee, Allison E. Aiello, P Smith, T Suehiro, K Treece, M Waluś, Timothy A Welborn, Simone Baltrusch, E Kontela, S Chai, J Crean, H Yokoyama, Johan G. Eriksson, Rafael Hernández Hernández, J Rodríguez-Saldaña, M P Tornero, G Formoso, D. Lovell, E Bingham, A Mylonakis, M Manteghetti, D Fedele, Antonio Martín-Duce, Ralph A. DeFronzo, D Salcedo, Kurt Højlund, Antonio Petrone, Sheu Whh., C Gutierrez, Flavia Pricci, S Kurita, Z G Abbas, M M Benedetti, Philippe A. Halban, Daniel J. Cox, O Ljungkvist, Justine Davies, J Palsgaard, Lars Sjöström, E Bosi, L Janin-Manificat, W. F. Kelly, M. Fernandez, E Colak, O V Mulyarchik, B Kronshage, F Lang, M Erfurth, Takashi Kadowaki, N Jendrike, U Walter, J Wishart, Y. Neye, D Kim, N Furuhashi, M Barsotti, D Florow, L Ke, L Borgquist, N C Jackson, Ffolliott M. Fisher, V Baskar, K Yoshioka, Bryan A. Wolf, G Chabrier, R Skoumal, Livio Luzi, H Kose, I Pharisien, B. Klein, H Winiarska, M C Johnson, L Griffiths, Nonna Kravchun, C Combe, Baptist Gallwitz, J Zdychova, L Skorda, Jorma Ilonen, W Gao, I N Steen, A Terrinoni, P D Ambery, W Kern, C M Kusminski, Cho M-H., Paolo Pozzilli, Louise G. Grunnet, E Schönle, David R Matthews, Robert W. Taylor, Y Cohen, Kim H-S., M P Eccles, N B Tutuncu, D McDowell, Richard M. Bergenstal, K Takamatsu, T Steiner, Jaan Palgi, Valdemar Grill, N Niculescu, G Federici, S Lehto, P. M. McKeigue, M Barone, Michael E. Trautmann, S Smirnov, J Mannion, M Eto, C Rousseau, M Conti, C S Ernest, Antonio Ceriello, D H Schweitzer, Jung E-D., Andreas Festa, Avijit Lahiri, A Shepelkevich, A Murro, A Kollmann, Jonathan R.S. Arch, R Landgraf, Son H-Y., I Engelsberger, E Agardh, S Rodríguez-Mulero, P J Kraml, K Lee, D. F. Du Toit, E Kim, G Fadini, Williams Ajk., Philip Home, M B Antcieferov, C Perlemoine, D Perrea, Song X-L., D Ruggieri, Krister Bokvist, Heidi Sørensen, Bilbao, G Yoshino, J P Taylor, Shen H-M., S M Furier, R Urquhart, J Wohlgelernter, Jianping Weng, T. Baba, Q Hong, C Silva, Castaigne J-P., M Felaco, X X Zhang, M Jaroň, Milla Rosengård-Bärlund, J G Papp, Toshio Miyata, Lervang H-H., Park M-K., I Kinalska, A Long, Oomen Phn., N Kogawa, Ippolita Patrizia Patera, S. Karadeniz, Dinesh Selvarajah, D S Chung, A Wensaas, Richard Imrich, M Recasens, J Ruxer, O Buchea, E Wilpart, S P Stepanenko, Le Ttd., H Ohgawara, Mariaconsuelo Valentini, A Mondok, M Peltonen, Marianne O. Larsen, K Chatzianagnostou, Agneta Ståhle, A L Ferrari, L Bordier, F Maingrette, A Matsuda, G Vukomanovic, Jakob D. Wikstrom, T Yamakita, E Gorostiaga, J Jin, B Gopalan, Heinz Drexel, S Hewitt, Rury R. Holman, C Dieterle, T L Ruchti, N Asatiani, M Sidira, A Iezzi, A J Sommerfield, D Châtenet, M L Olsen, R Bergemann, C Koehler, T L Kuraeva, B Balas, Christian Berne, E Santos-Mazo, G Smith, A Siejka, R Kožnarová, A Mattina, S Sheikh, A Adomeit, M Rasmussen, J. Fagerudd, N Busciantella Ricci, Nuria Vilarrasa, E Hammar, T L Thoms, L Aydın, Ron G. Rosenfeld, A Nikolajuk, R Gos, C L Morgan, H L Yu, D Dheelchand, S Ramrath, N Boudriga, Jerome I. Rotter, C Jahannault, W M Weston, Folke Lindgärde, M Hertlova, D Knight, A Monroy-Mayorga, E Pardini, A Chamson-Reig, B Franke, Janie McCluskey, Joseph Bryan, C Nikolopoulou, Christie M. Ballantyne, Fausto Santeusanio, L Pegoraro, M Lee, A Klimenko, S Jaiveer, K. Pettersson-Fernholm, Michael A. Nauck, A Ekbom-Schnell, G Deferrari, Riccardo Schiaffini, S. Pampanelli, Khan Aka., David Hopkins, Maija Wessman, M Kamarinos, Noh J-H., O Ebisui, K McCarroll, Jeppe Sturis, Peter Nowotny, N Gorbenko, Åke Sjöholm, David G. Maggs, A E Halseth, B Cresci, A A Ortiz-Gress, A Korakovouni, O Matejkova, C E Mogensen, C J Lin, Ramon Gomis, H Seaman, C Granier, Yang C-H., F Assah, O Sanchez, Fausto Machicao, Peter G. Morris, Alberto Ortiz, A Giardinelli, D Bracaglia, A Gonzalo, S Pavlatos, Andreas Lechner, F Canovic, L Sjolind, Allan Vaag, Birgitte Bruun Nielsen, David A. Ziegler, Vito Lampasona, R Gershoni-Baruch, A. Dei Cas, H Renz, E Mena, Matthew Waltham, Kim D-M., H Levanen, D D Mick, Valentina Alexandrovna Peterkova, E Meskhishvili, Sarah Nutland, R Bustani, John R. Lindsay, M Christoforidou, A Abicht, E Harno, K Cyganek, A Fitchet, S Neelotpol, P Nikishin, P Serradas, J Hinrichsen, M Halvorson, M Chovatia, B Voet, Jinny Willis, E Parretti, M Haslbeck, M Wellard, L Teng, Julio Wainstein, J S Fischer, K. Lalic, D Roggenland, I Gich, R Anwar, Maurizio Cassader, D Serota, X J Li, R J Schotzinger, Vilmundur Gudnason, Björn Zethelius, S A Wootton, W Andrzejewski, R Rezsohazy, R Gao, T Klimentova, T Mazurek, I Bruckner, C Dohrmann, R E James, G daSilva Xavier, Kim S-Y., A Dorca, Stuart J. Pocock, Terri J. Allen, I Giovos, P B Parab, N H Andersen, P Fotinakis, Miriam Cnop, H Lee, Norbert Tennagels, Omorodola I. Abatan, F Ailett, I. Lager, D Manzella, H Hut, Larry A. Distiller, G Lip, Lim S-K., Rong Zhang, T Tsuno, Steen Knudsen, M. Bajardi, Manuel Benito, Dai Sugimoto, Melvin J. Prince, D W Dunstan, D Rankins, K A Majali, G Ozansoy, Isabella Russo, S Uçak, G Annuzzi, R Talar-Wojnarowska, K Lange, S Neugebauer-Baba, Campbell H. Thompson, Eric Renard, P. D. Mountjoy, Z Morrison, Elizabeth A. Davis, Franco Cavallo, C Corvaja, R Antuña, Craig John Currie, H Linnebjerg, He Y-L., A J Palmer, Mariola R. Chacón, H Malinska, M. Jones, R Lichnovská, K Mandes, Paolo Tessari, T Mokhort, A Laina, H. L. Y. Chan, I Schmidt, R Banks, Richard G. IJzerman, L Ksinantova, G Setti, H Vaudry, A Gallo, V Spallone, Chen J-W., Thomas Danne, A Chong, M Hallschmid, S Aczel, S Hulme, N Islam, M Hosoi, P M Ternan, P Di Bartolo, N Bishara, T Shibasaki, Martin A. Osterhoff, Im S-S., M Jecht, T Hamaguchi, S Mattera, K Ways, Elizabeth Northam, U Rajala, Reinhard W. Holl, L Yang, S Panaiotopoulos, K Horvath, R Kluge, Thora B. Bodvarsdottir, Y Dong, Irene Alemanno, C McDougall, Reimar W. Thomsen, M Campbell, W Rabl, John Öhrvik, Yuichiro Yamada, Paola Ungaro, W Benzer, Mike Sampson, Roberto Trevisan, R G Radu, Aas A-M., P E Lobo, Ricardo Scott, S M Son, Josephine M. Forbes, T A Hillier, K L Wyne, Louis L. Nguyen, J Farmer, M H Tan, Kwon H-S., J Yang, L Sandvik, Franco Folli, A K Jenum, M Nguyen, W Pratipanawatr, A L Frederiksen, Rebecca Smith, Lee H-J., A Schäfer, C Manuelli, G S Denver, T Vukovich, B Maceira, K Matsumoto, K. Chokkalingam, Nurcan Üçeyler, P Modi, Timothy M. Morgan, S Mertens, B M Singh, Michaela Riedl, K Iso, C Cucurullo, G. F. Bottazzo, M Calvani, K Hur, J Wetzels, Kazuhiro Takahashi, Y Aso, H Stammer, M G Masding, Fitsum Guebre-Egziabher, J L González-Sánchez, L Armstrong, Alberto Maran, Peter G.F. Swift, S S Popovic, J Starczynski, E Vitacolonna, Luigi Laviola, R W Gelling, Marina Cardellini, D Barilla, Rosa de Diego Martínez, W H Landschulz, Anne Mette Rosenfalck, R K Wong, Kevin E. Schneider, K Peros, Giuseppe Nanni, F Zhang, I Rákóczi, T Iburi, M Nakhjavani, X Q Zhang, S Tournis, Per Lav Madsen, Graham A. Hitman, A. Tura, K Laubner, N D Kostic, Lawrence M. Dolan, R. Sinha Roy, J A Wagner, J. Tuomilehto, J Hauptman, M Abdel-Ghany, D Lacombe, Toralph Ruge, Johannes A Maassen, Triantafyllos Didangelos, K Sasaki, I Argüelles, Klaus Levin, C Popow, Emanuel Christ, R Chetty, L Baillet-Blanco, Jo-Ann Salmon, T Mine, James L. Trevaskis, I Franke, J Gorski, E A Andrianova, A Dayan, A Caballero, Aleksandra Gilis-Januszewska, M Yasujima, Z Kasalová, C.D.A. Stehouwer, F. K. Gorus, G A Nichols, A Glowania, David P. Strachan, P Fredlund, N. F. da Silva, P Reboldi, M Sausbier, K H Groenier, G Stuccio, N Guttman, K R Ahmed, A D Ristic, T Kapellen, J Coutcher, Aldo V. Greco, Oswald Wagner, A Zagayko, Maria Alevizaki, B B Zhang, W F Ferris, Jenny Fredriksson, Lois Jovanovic, J Hänninen, R De Giglio, Kazuo Yagui, O Potterat, P Hamliton, R E Scranton, B Mankovsky, A Stylianou, B Fellström, Abdel-Wahab Yha., M Kitagawa, Katherine L. Baldock, F R Johnson, F Baigts, S D'Addato, F J Sanz, A Mistry, S D Wise, T Pratipanawatr, U R Fölsch, James R.C. Parkinson, Claudia Sommer, C Park, F E Griffiths, M L Martí, R Demirtunc, S Taniguchi, J Lundkvist, T Siegmund, Juan Sztajzel, C Dienesch, F Baumgartner, L Scalone, T M Mckolanis, K Otake, Ullrik Pedersen-Bjergaard, T M Vriesendorp, Michael B. Wheeler, Henry Schmitt, Peter Hovind, S Lange, Stephane Roze, L. Van Gaal, B Klaproth, Anthony E. Civitarese, D Eckland, A Dagar, D F Hopkins, Kari Stefansson, C Gonzalez-Yanes, B Meyboom-de Jong, D. J. Betteridge, K Buhling, M Crepaldi, Ana M. Wägner, L Renna, L Volpe, R McBride, V Corbo, E O Brennesvik, R P Hayes, R Abdollahnia, G Viviani, C F Liew, Francisco Pérez-Bravo, Jeffrey Baron, Brian M. Frier, H H Samira, D Szentendrei, K. J. Schjoedt, W K Waldhäusl, D Gniuli, D Zou, G Tschank, V Urbančič, A L Nolan, Albertini J-P., J Malcomson, M Larbig, C Cheyssac, K Aurich, C M Kesson, S Heller, Maija E. Miettinen, R F Luco, Adrian J. Cameron, Luigi Mattiello, Z. Metelko, X E Zhang, M Parramón, I. G. Obrosova, J Fruchart, M Ilic, Björn Eliasson, Gilles Chatellier, M A Martín, D M Kendall, Holger Luthman, V F Varillas, D Maccubbin, Jang S-A., Amalia Gastaldelli, E Salzsieder, P. de Mol, A Yoshida, H D Lindner, D Gostiljac, M Just, Pan C-Y., J M Fujitaki, G Eiermann, K Bergenheim, A D Frick, A Agacdiken, K Varytimiadis, K Cseh, D A Jackson, S Calderari, Dena G. Hernandez, H M Liebich, K Min, F. de Zegher, Bernd Kulzer, K Han, Ulrich A. Müller, D Marrero, H Hatakeyama, René Koopman, Doo H-K., Petr Wohl, P. Sharp, P Forder, Thor Aspelund, N Meneveau, R M Schmülling, R Aubert, Thom Sam., H Youshikawa, M Ankelo, D Bowden, I Kelly, Frédéric Fumeron, M Sartini, Robert S. Sherwin, L Varadhan, A Criscimanna, John Betteridge, V Jelic, M Bartnik, N Lemke, B Ursø, A Bertoldo, A M Owona, H Okochi, L Pérez-Tamajó, S L Monfre, Daniel Brandhorst, K T Legg, Andries J. Smit, Veronica Sancho, Masashi Hirai, C Klein, Paul J. Thornalley, A Chaidaroglou, K Miura, B Zinman, O M Dvoynishnikova, J Plank, Jan Bolinder, C Lush, B Rubi, R Pozzilli, M Bashir, S A Shtandel, F Mosca, A Naskalska, Josef Vcelak, U Sausbier, P Cavaiani, T U Baehring, Michele Solimena, P Formisano, M Rastaldi, Bernard Thorens, J Ruzzin, E Arbit, M. Hori, Torkel B. Brismar, E Soltes Rak, A Filo, P Heinke, Matthew P. Coghlan, M Masotti, I Perevozskaya, K Ahn, I Moules, K Van Dyck, I Goldstein, Z Mathe, G Z Zhao, S Fajardo, J Taylor, S Chrul, J C Pareja, D Hadjidakis, A J Scheen, N Siddiqua, D C Cavan, R Grella, Krabbe S, H J Rochlitz, A E Hinkkanen, W Wilpshaar, Richard Stevens, M Dreyer, S Hara, X Wang, Melania Manco, D Gillen, Magalie A. Ravier, Olli Simell, John C. Lawrence, Kohnert K-D., Agardh C-D., A Berghold, L Kristensen, Grant Sfa., N Gursoy, Leif Groop, N Freemantle, Anja Schweizer, L Pala, Legros J-J., C. Di Pietro, N. Yamamoto, J Magyar, B Nikolovski, H Ikeda, D Lee, Bruce A. Buckingham, A O Wollitzer, I Kennedy, C Ernest, Neville H. McClenaghan, S Tanaka, Asimina Mitrakou, T Heinze, W Kerner, Moeenaldeen Al-Sayed, Charles Thivolet, L Klaff, A Miconi, Cristina Valeri, J. O. Christensen, K. Ekberg, A Jardine, T Endo, X Zhang, D F Child, A Kienitz, D K Seidel, H. Tada, Sylvie Abouna, Cyrus Cooper, Catherine R Chittleborough, Roberta Assaloni, S Corbi, A K Bose, K Ozawa, C Ahn, K A Deans, G Jackowski, Martin Gibson, Patrick McElduff, O A Mojiminiyi, Manuel Serrano-Ríos, O Dupuy, A L Davydov, Iwar Klimes, Sten-Anders Ivarsson, N Ichino, R Matsutomo, E R Smith, A Stefanovska, B Dehmel, K Koniavitou, E Agascioglu, M Hatazaki, J. M. Gibson, T Yada, P Ribaux, M Rupnik, K Fridell, G Scutaru, L Chugunova, Henrietta Mulnier, A Kendereski, H Lehnert, C Billi, M Sobczak, Francisco M-Mj., L K Archibald, S Sukumvanich, David B. Dunger, I. Benke, G Yillar, N Stingemore, J. M. Boavida, Y Shi, Jimmy D. Bell, L Bozzetto, Andrew J. Ahmann, E Jebens, J Keiding, Elena Henkel, Mark Fineman, J F McRae, Carol Forsblom, S Martemucci, Lourdes Ibáñez, P G Prieto, L Ringholm Nielsen, S Pratas, B von Stritzky, Julio Rosenstock, Lee K-W., J Stocks, L J Strow, I Samarguliani, L Wennekes, R Cheung, Abhishek Nag, Roberto Gambino, Y Suleymanoglu, E Murphy, T T Durck, M F Peyrot, Y Unno, Alexander Mayorov, Eleuterio Ferrannini, D. C. Rao, D Neely, H Karunajeewa, J Palmisano, Julia B. Lewis, M Ravid, G Pons, E Junca, P Vexiau, S Sailesh, D K Miloslavskiy, O N Bondarenko, U Smith, S Torri, Constantine Tsigos, Cesario Bianchi, Mattia Locatelli, D Jaquet, Virpi Lindi, M Moroi, M E Tushuizen, P Pelicci, R Scognamiglio, Pal Pacher, S M Thyssen, A Péterfalvi, Y Ho, S Guntram, L Romics, T Nakagami, Clive S. Cockram, Irina Kowalska, K Brodbeck, Gojka Roglic, J. Dörig, Lise Tarnow, Therese Tillin, A López-Alba, Martin Krššák, Moses Elisaf, S Hata, D P Snoeck, D Schmoll, O V Udovichenko, A Scaramuzza, J Paul, John H. Fuller, Nicholas Katsilambros, Michele Muggeo, Pia Ekbom, Piero Marchetti, V Melki, C Bailleau, H Stavrianos, A D'Errico, Geremia B. Bolli, Amabile Maier, Kelter A-R., Anders Green, Q J Morélis, Steffen Thiel, C Watkins, R C Cheung, A Clark, Elvira Fioriti, N Ari, Nam J-Y., Y Cottin, L G Krinelke, H Al Mohammedi, Simon C. Fleming, C Jones, Z Kerényi, Ahn Y-H., Meile M-J., P Nánási, M Graner, V Canonico, Gangnerau M-N., Hugh R. Taylor, Giovanni Sartore, A. Dejgaard, Carol Kelley, S. Ali, Stéphane Dalle, Jeffrey S. Gonzalez, Elena Šeböková, Alexander Beck, Ingo B. Leibiger, M Rosu, C Pencea, Werner Waldhäusl, Kaltenbacher M-C., R Butzer, S Thore, Adam G. Tabak, Angelo Avogaro, E Standi, Boris Kovatchev, O Bradescu, Patrizia Dentelli, A Fujita, C Verri, R Chlup, Prasad Ydm., S V Hörsten, van der Merwe M-T., D Hilliard, W Klein, D Worthley, M Udvardy, Berit R. Jensen, A D'Avanzo, J Monaghan, K P Yeo, Guivarch P-H., B Bauduceau, D Weghuber, P Tatti, J Ybarra, S Gwozdziewiczová, E Gasparini, B Saltin, Charlotte Granhall, Howard Leventhal, R Marin, M Tumiati, Cicero Afg., L Csémy, B Berger, S Mikros, D Dall'Asta, M Shahmanesh, Y G Vasiljev, F Potthoff, H S Randeva, G De Berardis, J O Logan, K Warncke, P Uitterlinden, E Rehring, K Gilmore, K Shankhdhar, V V Bojko, M Vahatalo, E A Korolyova, D Wiemann, P G Lankisch, D Hendrie, F Galtier, M Rybarczyk, Gisela Dahlquist, N N Rudovich, G Stein, A Liebl, F Tan, A Westerlund, S Gronemann, I Franklin, Jonathan A. Prince, Peter Arner, E Skliros, T. Sparre, M Vigas, Maddalena Trombetta, L. Bjerre Knudsen, A C Sima, I Dubroca, Alastair Gray, I Weets, R Ferraresi, Schauer Ujw., E. Leinonen, S Corazza, Jonathan Levy, P K Prakash, R Guzder, S. Barnhill, John Blangero, J Herreros, G. de Vries, Cheng Ptw., A Macías-Batista, K. Capito, R Thomas, G Thomas, G Boemi, Lotte Pietraszek, Pierre Fontaine, I Holme, J Smedegaard, C A Harrop, U Helwig, B Levy, A P Gribben, Hiroto Furuta, P Beckett, S Giannini, Ruth L. Coleman, Eva Fernqvist-Forbes, N Cugnardey, A Dumas, Jane Pinaire, S E Hofer, D Shimono, Erik H. Serné, Alain D. Baron, C Battista, M Tanen, M Klementova, V Adams, J Komorowski, Antonio Nicolucci, E. C. Burns, H Sydall, M G Fanara, M G Giovannitti, N Okabayashi, Magdalena Szurkowska, I A Eroshkin, M. I. J. Uusitupa, D Ma, C C Dieguez, J Sutcliffe-Goulden, A V Gaddi, Michał Arabski, Serge Halimi, Wendy C. Burns, S Seclén, H Sugano, A Vinterby, K Backx, L F Diaconu, Fernando Gomez-Peralta, O'Harte Fpm., G Lepeniotis, D Laune, H Kvasničková, N H Wallén, G Boner, G Cieślik, Robert Hermann, Paul Q. Thomas, Y Kumon, Maria Maiello, M Atkins, Kenneth A. Earle, Guowang Xu, H Y Bae, I Reynisdottir, D Perez, D E Cannon, P Fabietti, I Geronooz, J Østergaard, K J Jeitler, S Skourtis, A Zambanini, A Saemann, K Kuboki, Helen L. Lutgers, A C Thai, Arne Melander, D Pinkowski, S G Straub, S A Wolfe-Coote, A Totora, Hayley Dickinson, A Lindenmair, A Ginis, I Faturos, F Van Eylen, C Huard, F Fu, N Wang, B M Rasmussen, Angela Napoli, L Granato, Markus M. Lerch, M. Frandsen, A Lyras, Lawrence S. Phillips, J Mabley, R Goldschmeding, B K Kilhovd, W Liu, Greg Poffenberger, P Cipriano, Anna Maria Charlotte K Lindqvist, A Matsuzawa, J Wang, T Yu, M S Pepper, Lena M. Thorn, Y Sakamoto, Blanche Schwappach, Anna L. Gloyn, P Dupraz, A. M. Schmidt, M Psallas, V Tsirimbis, Carl D. Langefeld, D Sass, H E Scholtz, M. Cailleau, Lauren Julia Brown, K Phillips, M. Iezzi, C Jayawarna, Eleni Anastasiou, R Lobmann, R Lundershausen, H Fujiwara, H R Nan, I C Smith, I A Karpova, A Navazio, S Kang, T. 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D, Torjesen, P, Kilhovd, B, Berg, T, Sandvik, L, Hanssen, K, Mentink, C, Donchenko, G, Stepanenko, S, Maingrette, F, Deng, H, Lindenmair, A, Freudenthaler, A, Baumgartner parzer, S, Nizheradze, K, Khoruzhenko, A, Tronko, N, Sheu, W, Ou, H, Shen, H, Lin, T, Wu, H, Yang, C, Mogylnytska, L, Schmoelzer, I, Davies, J, Band, M, Struthers, A, Prázný, M, Škrha, J, Kasalová, Z, Neelotpol, S, Jahan, P, Kauschke, S, Harrop, C, Schäfer, A, Widder, J, Eigenthaler, M, Walter, U, Uchimura, I, Ikebukuro, M, Kaibara, M, Hirata, M, Helal, R, Pervin, F, Yang, X, Jansson, P, Nagaev, I, Jack, M, Carvalho, E, Sunnerhagen, K, Cam, M, Cushman, S, Smith, U, Creely, S, Farmer, J, Gustafson, B, Kusminski, C, Krusinova, E, Wohl, P, Klementova, M, Lanska, V, Mcdougall, C, Kelly, I, Abbas, Z, Lutale, J, Archibald, L, Karunajeewa, H, Stingemore, N, Stuccio, G, Mcgechie, D, Muller, L, Hak, E, Goudzwaard, W, Montorsi, F, Homering, M, Sprenger, K, Goldstein, I, Asnaghi, V, Ferrari, G, Rastaldi, M, Gabellini, D, Dell'Antonio, G, Maestroni, A, Ruggieri, D, Luzi, L, Piemonti, L, Zerbini, G, Anafaroglu, I, Tutuncu, N, Sultana, M, Siddiqua, N, Iwasaki, T, Nakajima, A, Yoneda, M, Mukasa, K, Tanaka, S, and Sekihara, H
Subjects: 0303 health sciences, medicine.medical_specialty, business.industry, EASD, Endocrinology, Diabetes and Metabolism, Human physiology, medicine.disease, 03 medical and health sciences, 0302 clinical medicine, Diabetes mellitus, Family medicine, Internal Medicine, Medicine, business, 030217 neurology & neurosurgery, 030304 developmental biology
Published: 2004

118. The effect of calcium dobesilate on vascular endothelial function, blood pressure, and markers of oxidation in obese male smokers:A placebo-controlled randomised clinical trial

Author: Coen D.A. Stehouwer, Rob A.J.M. Van Dijk, Frank Stam, Erik H. Serné, Miranda T. Schram, Casper G. Schalkwijk, Ad M Kamper, Prabath W. B. Nanayakkara, Renate T. de Jongh, Peter G. Scheffer, Greetje de Vries, Maarten E. Tushuizen, Deva Lampe, Internal medicine, ACS - Diabetes & metabolism, ACS - Microcirculation, Gastroenterology and hepatology, Laboratory Medicine, and Human genetics
Subjects: Male, Vasodilator Agents, Calcium dobesilate, Blood Pressure, Vasodilation, Calcium Dobesilate, Hemostatics, chemistry.chemical_compound, Diastole, Heart Rate, Reference Values, Medicine, Enzyme Inhibitors, Brachial artery, Ketocholesterols, Smoking, Alanine Transaminase, Blood Pressure Monitoring, Ambulatory, Middle Aged, Lipoproteins, LDL, Forearm, Treatment Outcome, medicine.anatomical_structure, Cardiology and Cardiovascular Medicine, Oxidation-Reduction, Flow-Mediated Vasodilation, medicine.drug, Adult, Nitroprusside, medicine.medical_specialty, Adolescent, Endothelium, Systole, Nitric oxide, Microcirculation, Double-Blind Method, medicine.artery, Internal medicine, Humans, Nitric Oxide Donors, Obesity, omega-N-Methylarginine, business.industry, Capillaries, Blood pressure, Endocrinology, chemistry, Regional Blood Flow, Patient Compliance, Endothelium, Vascular, business, Biomarkers, Follow-Up Studies
Abstract: This randomised double-blind, placebo-controlled, clinical trial investigated the effect of 3 months of treatment with calcium dobesilate on endothelium-dependent vasodilation, markers of endothelial function, blood pressure, and markers of oxidation in obese, male smokers. Vascular effects may depend on the type of vessel and we, therefore, investigated both smaller arteries, i.e. resistance arteries and small arterioles, and large conduit arteries. Vascular function was measured by acetylcholine- and sodium-nitroprusside-mediated vasodilation, and capillary recruitment, in the skin microcirculation; by forearm blood flow (FBF) responses to several agonists and to N-G-monomethyl L-arginine (L-NMMA) in the forearm vascular bed; by flow-mediated vasodilation in the brachial artery; and by determination of soluble levels of vascular cell adhesion molecule-1 (sVCAM-1), intercellular adhesion molecule-1 (sICAM-1) and E-selectin. Twenty-eight individuals received dobesilate and 24 placebo. No effect of calcium dobesilate on endothelial function, blood pressure or markers of oxidation was observed compared with placebo. The difference in acetylcholine-mediated vasodilation in the microcirculation was -52.1%-point (95% confidence interval -132.8 to 28.1); in sodium-nitroprusside-mediated vasodilation in the microcirculation, 2.6%-point (-95.1 to 100.2); in capillary recruitment, 2.5%-point (-6.8 to 11.7); in acetylcholine-induced increases in FBF (n=28), 23%-point (-173 to 126); in L-NMMA-induced reduction of basal FBF, -2.8%-point (-29.3 to 23.8); in flow-mediated vasodilation of the brachial artery, 0.3%-points (-2.7 to 3.3); in 24-h systolic blood pressure, 2.1 mmHg (-1.3 to 5.5); in soluble VCAM-1, 54 ng/ml (-8 to 115); in soluble ICAM-1, 9 ng/ml (-49 to 67); in sE-selectin, -17 ng/ml (-44 to 11); in ketocholesterol 5 nM (-17 to 26); and in oxidised LDL -1. 6 U/l (-6.7 to 3.5). We have shown that endothelial function, blood pressure, and markers of oxidation were not affected by 3 months of treatment with calcium dobesilate in mildly obese, smoking men. Thus, our data provide no evidence of an effect on vascular function of calcium dobesilate in humans.
Published: 2003
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119. PS14 - 74. Microvascular insulin sensitivity in human skeletal muscle and skin are related and both are associated with metabolic insulin sensitivity

Author: Martine R. Groen, Erik H. Serné, Etto C. Eringa, Rick I. Meijer, Yvo M. Smulders, and Michiel P. de Boer
Subjects: medicine.medical_specialty, business.industry, Insulin, medicine.medical_treatment, Insulin sensitivity, Skeletal muscle, medicine.disease, Microcirculation, Endocrinology, Insulin resistance, medicine.anatomical_structure, Internal medicine, Diabetes mellitus, medicine, Percentage difference, business, Contrast-enhanced ultrasound
Abstract: Insulin recruits microvascular vessels to increase the available surface area for exchange of insulin with the interstitium. Insulin-induced microvascular recruitment is perturbed in insulin resistance, and may even be the culprit of insulin resistance. As such, insulin-induced microvascular recruitment has received increasing attention. The study of the human microcirculation has however been hampered by a perceived lack of appropriate techniques. Skin microcirculation has been used as a model for the muscle microcirculation, even though the skin is an insulin sensitive organ, doubt remained whether skin microcirculation is indeed a good model for the muscle microcirculation. In recent years, Contrast Enhanced UltraSound (CEUS) emerged as a novel tool to study muscle microcirculation. In this study, we set out to clarify the relation between insulin-induced capillary recruitment in skin and microvascular recruitment in muscle.
Published: 2011
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120. Renal sodium handling and haemodynamics are equally affected by hyperinsulinaemia in salt-sensitive and salt-resistant hypertensives

Author: Ajm Donker, Stephan J. L. Bakker, Erik H. Serné, Reinold O. B. Gans, ter Jan Maaten, Internal medicine, ACS - Diabetes & metabolism, and ACS - Microcirculation
Subjects: Adult, Male, medicine.medical_specialty, Physiology, medicine.medical_treatment, Sodium, Drug Resistance, Renal function, chemistry.chemical_element, Natriuresis, Sodium Chloride, Kidney, Renal Circulation, Insulin resistance, Internal medicine, Hyperinsulinism, Internal Medicine, medicine, Humans, Insulin, Renal sodium reabsorption, business.industry, Hemodynamics, Middle Aged, medicine.disease, medicine.anatomical_structure, Endocrinology, chemistry, Renal blood flow, Hypertension, Female, Cardiology and Cardiovascular Medicine, business, Glomerular Filtration Rate
Abstract: Objective. It is well-known that insulin induces renal sodium retention. It is not yet known whether insulin's renal effects are involved in the development of salt-sensitive hypertension. We assessed the effects of insulin on renal sodium handling and haemodynamics in 10 salt-sensitive (SS) and 10 salt-resistant (SR) essential hypertensives. Design. After a baseline period of 90 min, all subjects underwent a euglycaemic clamp with sequential infusion of a physiological and supraphysiological dose of insulin (50 and 150 mU/kg per h) during 90 min periods each. Time-control studies were performed in the same subjects. Clearances of 131l-hippuran, 125l-iothalamate, sodium and lithium were used to evaluate renal plasma flow (RPF), C Na/glomerular filtration rate (GFR) and fractional proximal and distal sodium reabsorption. Results. Plasma insulin levels and insulin-mediated glucose uptake did not differ between both groups. RPF and GFR showed similar increases during both insulin infusions in both groups. During physiological hyperinsulinaemia, fractional sodium excretion decreased 38% (P = 0.009) in the SS group and 36% (P = 0.002) in the SR group. During supraphysiological hyperinsulinaemia, fractional sodium excretion decreased 49% (P = 0.01) in the SS group and 19% (P = 0.2) in the SR group, not statistically different between both groups. Fractional proximal sodium reabsorption was unaffected and fractional distal sodium reabsorption increased to a similar magnitude in both groups. Conclusion. The comparable renal effects of acute exogenous hyperinsulinaemia in SS and SR hypertensives do not support a role for insulin in the development of salt-sensitive hypertension. However, the results do not yet exclude a role for chronic hyperinsulinaemia.
Published: 2001
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121. Effects of insulin on glucose uptake and leg blood flow in patients with sickle cell disease and normal subjects

Author: Jan C. ter Maaten, Stephan J. L. Bakker, Ab J.M. Donker, Erik H. Serné, Gans Ro, Wim Statius van Eps, Internal medicine, ACS - Diabetes & metabolism, ACS - Microcirculation, Groningen Institute for Organ Transplantation (GIOT), Lifestyle Medicine (LM), and Groningen Kidney Center (GKC)
Subjects: STIMULATION, Adult, Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Glucose uptake, Hemodynamics, HYPERINSULINEMIA, Anemia, Sickle Cell, PRESSURE, Endocrinology, Insulin resistance, Internal medicine, medicine, Hyperinsulinemia, Humans, Hypoglycemic Agents, Insulin, Infusions, Intravenous, Muscle, Skeletal, Pancreatic hormone, Microvascular occlusion, Leg, business.industry, Microangiopathy, SALT SENSITIVITY, HUMAN SKELETAL-MUSCLE, medicine.disease, SODIUM, Glucose, Regional Blood Flow, Glucose Clamp Technique, Female, business, RESISTANCE, HEALTHY-VOLUNTEERS
Abstract: The hemodynamic concept of insulin resistance assumes that vasodilatory effects of insulin determine glucose uptake. Sickle cell disease (SCD) is characterized by microangiopathy and microvascular occlusion. Therefore, we hypothesized that patients with SCD have a reduced insulin-mediated glucose uptake. In 8 patients with SCD and 8 matched normal controls, we studied the effects of a 4-hour insulin infusion (50 mU/kg/h) on glucose uptake and leg blood flow (LBF) using the euglycemic clamp technique and venous occlusion plethysmography. Time-control experiments were performed in the same subjects. Insulin-mediated glucose uptake (M value, mg/kg/min) did not differ between patients with SCD and control subjects during the second (6.3 +/- 4.6 and 7.6 +/- 2.6, P = .5), third (7.5 +/- 4.6 and 9.3 +/- 3.4, P = .4) and fourth hour (8.6 +/- 4.7 and 11.0 +/- 2.9, P = .2) of the clamp. At baseline, LBF was higher in the patients with SCD than in the controls (3.28 +/- 1.68 and 1.37 +/- 0.47 mL/min/dL, respectively; P = .005). Insulin-induced increases in LBF in patients with SCD and in normal subjects were not different (P = .9). Respectively, 56% and 24% of the changes in glucose uptake could be explained from changes in LBF in the course of the insulin infusion in the patients with SCD and controls. We suppose that the comparable insulin sensitivity between both groups is due to a compensatory hemodynamic state in SCD characterized by vasodilation and increased flow. Copyright (C) 2001 by W.B. Saunders Company.
Published: 2001
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122. Capillary recruitment is impaired in essential hypertension and relates to insulin's metabolic and vascular actions

Author: Erik H. Serné, Jan C. ter Maaten, Reinold O. B. Gans, Piet M. ter Wee, Coen D.A. Stehouwer, Ab J.M. Donker, Internal medicine, ACS - Diabetes & metabolism, ACS - Microcirculation, VU University medical center, Nephrology, AII - Inflammatory diseases, Lifestyle Medicine (LM), and Groningen Kidney Center (GKC)
Subjects: Adult, Male, RAREFACTION, medicine.medical_specialty, Ambulatory blood pressure, Physiology, medicine.medical_treatment, Hemodynamics, ENDOTHELIUM-DEPENDENT VASODILATION, BLOOD-PRESSURE, Vasodilation, Blood Pressure, Essential hypertension, Insulin resistance, endothelial function, Heart Rate, Physiology (medical), Internal medicine, medicine, blood flow, Humans, Insulin, Aged, Skin, business.industry, Middle Aged, medicine.disease, Arterial occlusion, Capillaries, Endocrinology, Blood pressure, Hypertension, Linear Models, SKELETAL-MUSCLE, MICROVASCULAR FUNCTION, Regression Analysis, Female, FATTY-ACIDS, SENSITIVITY, Cardiology and Cardiovascular Medicine, business, RESISTANCE, MEDIATED GLUCOSE-UPTAKE
Abstract: Objective: In patients with essential hypertension, defects in both the metabolic and vascular actions of insulin have been described. Impaired microvascular function, a well-established abnormality in essential hypertension, may explain part of these defects. In the present study we investigated whether microvascular function is impaired in essential hypertension and relates to insulin's metabolic and vasodilatatory actions. Methods: We measured 24-h ambulatory blood pressure, capillary recruitment after arterial occlusion, and skin blood flow responses to iontophoresis of acetylcholine and sodium nitroprusside in 18 subjects with untreated essential hypertension and in 18 control subjects. Whole body insulin sensitivity and leg insulin-mediated vasodilatation were assessed with the hyperinsulinaemic clamp technique and plethysmography. Results: Hypertensive, as compared to normotensive, subjects had a decreased insulin sensitivity (0.8±0.3 vs. 1.7±0.6 mg kg-1 min-1 per pmol l-1; P
Published: 2001
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123. Birth weight relates to blood pressure and microvascular function in normal subjects

Author: Reinold O. B. Gans, Jan C. ter Maaten, Ab J.M. Donker, Erik H. Serné, Piet M. ter Wee, Coen D.A. Stehouwer, Internal medicine, ACS - Diabetes & metabolism, ACS - Microcirculation, VU University medical center, Nephrology, and AII - Inflammatory diseases
Subjects: Adult, Male, medicine.medical_specialty, Ambulatory blood pressure, Physiology, medicine.medical_treatment, Birth weight, Blood Pressure, Essential hypertension, Microcirculation, Insulin resistance, Heart Rate, Internal medicine, Internal Medicine, Birth Weight, Humans, Medicine, business.industry, Insulin, Middle Aged, medicine.disease, Capillaries, Low birth weight, Endocrinology, Blood pressure, Body Composition, Regression Analysis, Female, Insulin Resistance, medicine.symptom, Cardiology and Cardiovascular Medicine, business
Abstract: Objective The relationship between low birth weight and elevated blood pressure in adult life is well established but presently unexplained. Both microvascular dysfunction and insulin resistance have been proposed as a possible explanation. We have examined the relation between birth weight and blood pressure in 30 healthy subjects exhibiting a wide range of insulin sensitivity, and assessed whether microvascular function and/or insulin resistance may underlie this relationship. Methods Birth weight data were obtained from birth announcements. Blood pressure was measured with an ambulatory blood pressure monitor and insulin sensitivity was assessed by the hyperinsulinaemic, euglycaemic clamp technique. Microvascular function, i.e. capillary recruitment and endothelium-dependent and -independent vasodilatation in the skin, was evaluated by videomicroscopy and iontophoresis of acetylcholine and sodium nitroprusside. Results Birth weight was significantly associated with blood pressure (r = -0.50; P
Published: 2000
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124. Microvascular function relates to insulin sensitivity and blood pressure in normal subjects

Author: Ab J.M. Donker, Jan A. Rauwerda, Erik H. Serné, Reinold O. B. Gans, Coen D.A. Stehouwer, Piet M. ter Wee, Jan C. ter Maaten, Internal medicine, ACS - Diabetes & metabolism, ACS - Microcirculation, VU University medical center, Nephrology, AII - Inflammatory diseases, and Surgery
Subjects: Adult, Male, medicine.medical_specialty, Ambulatory blood pressure, medicine.medical_treatment, Blood Pressure, Vasodilation, Essential hypertension, Microcirculation, Heart Rate, Reference Values, Physiology (medical), Internal medicine, Humans, Medicine, Skin, business.industry, Insulin, Middle Aged, Laser Doppler velocimetry, medicine.disease, Capillaries, Blood pressure, Endocrinology, Regression Analysis, Female, Endothelium, Vascular, Sodium nitroprusside, Insulin Resistance, Cardiology and Cardiovascular Medicine, business, medicine.drug
Abstract: Background —A strong but presently unexplained inverse association between blood pressure and insulin sensitivity has been reported. Microvascular vasodilator capacity may be a common antecedent linking insulin sensitivity to blood pressure. To test this hypothesis, we studied 18 normotensive and glucose-tolerant subjects showing a wide range in insulin sensitivity as assessed with the hyperinsulinemic, euglycemic clamp technique. Methods and Results —Blood pressure was measured by 24-hour ambulatory blood pressure monitoring. Videomicroscopy was used to measure skin capillary density and capillary recruitment after arterial occlusion. Skin blood flow responses after iontophoresis of acetylcholine and sodium nitroprusside were evaluated by laser Doppler flowmetry. Insulin sensitivity correlated with 24-hour systolic blood pressure (24-hour SBP; r =−0.50, P r =0.84, P r =0.78, P r =−0.53, P R 2 =38%) and insulin sensitivity ( R 2 =71%) could be explained by microvascular function. Conclusions —Insulin sensitivity and blood pressure are associated well within the physiological range. Microvascular function strongly relates to both, consistent with a central role in linking these variables.
Published: 1999
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125. PS9 - 9. Human coronary artery disease is characterized by defects in coronary insulin signaling

Author: Yvo M. Smulders, Mariam Abbas, Erik H. Serné, Jolanda van der Velden, Cristobal G. dos Remedios, Etto C. Eringa, and Victor W.M. Hinsbergh
Subjects: medicine.medical_specialty, biology, business.industry, medicine.disease, Coronary artery disease, Coronary arteries, Insulin receptor, Endocrinology, Insulin resistance, medicine.anatomical_structure, Internal medicine, Diabetes mellitus, medicine, biology.protein, Cardiology, cardiovascular diseases, business
Abstract: Insulin resistance has been linked to coronary artery disease (CAD), but the underlying mechanisms have not been elucidated. Here, we assessed whether insulin signaling is impaired in coronary arteries of human subjects with coronary artery disease (CAD), and whether these defects are related to endothelial signaling.
Published: 2013
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126. FRI0427 Tumor necrosis factor blocking agents inhibit the progression of preclinical atherosclerosis in patients with ankylosing spondylitis

Author: Erik H. Serné, Michael T. Nurmohamed, Mike J L Peters, Yvo M. Smulders, I. H. van der Horst-Bruinsma, A.M. van Sijl, and I C van Eijk
Subjects: medicine.medical_specialty, Ankylosing spondylitis, business.industry, Immunology, Carotid ultrasonography, Odds ratio, Disease, medicine.disease, Gastroenterology, General Biochemistry, Genetics and Molecular Biology, Confidence interval, Surgery, Rheumatology, Rheumatoid arthritis, Internal medicine, medicine, Immunology and Allergy, Tumor necrosis factor alpha, business, Cohort study
Abstract: Background Ankylosing spondylitis (AS) is associated with an increased cardiovascular (CV) risk that might be due to the chronic underlying inflammatory process, but is still unknown whether treatment with TNF inhibitors reduce the increased CV risk. Objectives We investigated whether preclinical atherosclerosis of the carotid arteries in patients with AS were reduced after use of TNF inhibitors in an observational cohort study. Methods 67 out of 82 AS patients who underwent ultrasonography at baseline returned for follow-up. Of the 67 remaining AS patients, 11 discontinued use of TNF inhibitors. Assessments of AS related factors and CV risk factors were measured at baseline and repeated at follow-up. B-mode carotid ultrasonography was used to investigate arterial wall parameters, including intima-media thickness (IMT) and Young’s elastic modulus (YEM). Results After 5 years of follow-up, IMT did not change significantly (+0.012, p-value= 0.561) in those who continued the use of TNF inhibitors, whereas IMT increased significantly (+0.060, p-value=0.025) in AS patients who discontinued use of TNF inhibitors. Compared to prior studies in rheumatoid arthritis (a disease with comparable CV risk as in AS) AS patients who discontinued TNF inhibitors had a comparable yearly increase in IMT, while patients who continued use of TNF inhibitors had a 5-fold lower increase in IMT. Duration of use of TNF inhibitors (in years) was associated with stabilization or regression of IMT, odds ratio (95%>confidence interval): 1.67 (1.04-2.63). Also, YEM improved significantly in patients who continued TNF inhibitors (+0.037, p-value=0.002) but not in patients who discontinued TNF inhibitors. Image/graph Conclusions (Continuous) use of TNF inhibitors might stabilize or slow down IMT progression in AS patients, reflecting a decreased CV risk in these patients. Unfavourable changes in IMT were associated with equally unfavourable changes in AS related factors, while unfavourable changes in YEM were associated with unfavourable changes in lipid levels. More research is needed to investigate the relationship between improvement in AS-related disease acitivity indices and improvement in IMT or vascular stiffness. Disclosure of Interest None Declared
Published: 2013
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127. Blood pressure and insulin resistance: role for microvascular function? [Cardiovasc Res 2002;53:271–276]

Author: Richard G. IJzerman, Renate T. de Jongh, Erik H. Serné, and Coen D.A. Stehouwer
Subjects: medicine.medical_specialty, Physiology, business.industry, Cardiovascular research, Blood flow, medicine.disease, Elevated blood, Hyperaemia, Endocrinology, Blood pressure, Insulin resistance, Physiology (medical), Dilator, Internal medicine, medicine, medicine.symptom, Cardiology and Cardiovascular Medicine, business, Acetylcholine, medicine.drug
Abstract: In a recent issue of Cardiovascular Research , Irving et al. [1] reported on the relationships among microvascular function, blood pressure, and insulin resistance in healthy men. The main objective was to test the hypothesis that defects in microvascular function could explain the relationship between elevated blood pressure and insulin resistance. They report that higher systolic blood pressure was associated with insulin resistance, lower dermal capillary density at rest and during venous occlusion, and impaired maximum dermal blood flow after heating, but not with dilator responses to acetylcholine. Insulin resistance, as assessed by HOMA, did not correlate with indices of microvascular function or structure. It is concluded that the association between hypertension and insulin resistance is unlikely to be explained by altered microvascular function and structure. In contrast, we have demonstrated that higher systolic blood pressure was associated with insulin resistance, capillary recruitment during post-occlusive reactive hyperaemia (PRH), and dilator responses to acetylcholine in both normotensive [2] and hypertensive subjects …
Published: 2002
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128. PS6 - 34. Microvascular function and Body Mass Index development over time, the Amsterdam Growth and Health Longitudinal Study

Author: Jos W. R. Twisk, Trynke Hoekstra, Erik H. Serné, Nienke J. Wijnstok, Etto C. Eringa, and Yvo M. Smulders
Subjects: medicine.medical_specialty, Longitudinal study, business.industry, Cvd risk, Peripheral resistance, Insulin sensitivity, Disease, medicine.disease, Obesity, Endocrinology, Internal medicine, Diabetes mellitus, medicine, business, Body mass index
Abstract: Obesity is associated with cardiovascular disease (CVD). Microvascular function is hypothesized to be the link between obesity and cardiovascular damage via decreased insulin sensitivity and an increased peripheral resistance. Whether duration of apparent obesity is associated with CVD risk remains unclear. This study examines the existence of distinct development patterns of BMI and the relation of these distinct patterns with microvascular function.
Published: 2011
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129. PS3 - 16. Insulin induced vasoreactivity is dependent on perivascular adipose tissue as well as resistance artery properties after a two-week high fat diet in mice

Author: Erik H. Serné, Caro-Lynn F. Alta, Etto C. Eringa, John S Yudkin, Rick I. Meijer, Victor W.M. van Hinsbergh, Yvo M. Smulders, and Eugene J. Barrett
Subjects: medicine.medical_specialty, business.industry, Insulin, medicine.medical_treatment, Adipose tissue, High fat diet, Vasodilation, White adipose tissue, medicine.disease, Obesity, Resistance artery, Endocrinology, Internal medicine, Diabetes mellitus, medicine, business
Abstract: Obesity is a major risk factor for microvascular dysfunction, a determinant of insulin sensitivity. Perivascular adipose tissue (PVAT) regulates insulin induced vasodilation. The effects of a short high fat diet on PVAT and resistance arteries (RA) are however unkown.
Published: 2011
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130. Urinary cortisol is inversely associated with capillary recruitment in women: a potential explanation for the cortisol–blood pressure relationship.

Author: Renate T. de jongh, Richard G. Ijzerman, Erik H. Serné, Mirjam M. van weissenbruch, Jasper J. Voordouw, Henriette A. Delemarre-van de waal, and Coen D. A. Stehouwer
Subjects: HYDROCORTISONE, EXCRETION, BLOOD pressure, DISEASES in women, INSULIN resistance, SKIN blood-vessels, MICROCIRCULATION disorders, VASODILATION, MICROSCOPY, LASER Doppler blood flowmetry
Abstract: The relationships of cortisol with elevated blood pressure and insulin resistance are likely to be the result of a complex interplay of different mechanisms. We hypothesize that cortisol is associated with impaired microvascular function and that this contributes to cortisol-associated high blood pressure and insulin resistance. We examined 24 h urinary free cortisol excretion in 56 healthy adults (26 women). Blood pressure was assessed by 24 h ambulatory measurements. Insulin sensitivity was determined using the hyperinsulinaemic euglycaemic clamp technique. Skin capillary recruitment after arterial occlusion was visualized with videomicroscopy and endothelium-(in)dependent vasodilation was evaluated with iontophoresis of acetylcholine and sodium nitroprusside combined with laser Doppler fluxmetry. Men were characterized by higher urinary cortisol excretion [median (interquartile range), 162 (130–194) compared with 118 (99–156) nmol/24 h, P<0.05]. In women, but not in men, urinary cortisol excretion was associated with impaired capillary recruitment (r=−0.66, P<0.001), higher systolic blood pressure (r=0.64, P<0.001) and lower insulin sensitivity (r=−0.43, P<0.05). Urinary cortisol excretion was not associated with endothelium-(in)dependent vasodilation in men or women. Regression analysis demonstrated that capillary recruitment statistically explained 37% of the association between urinary cortisol and blood pressure in women. Capillary recruitment did not explain part of the association between urinary cortisol and insulin sensitivity. In conclusion, urinary cortisol excretion is inversely associated with capillary recruitment in women, but not in men, and capillary recruitment explains part of the cortisol–blood pressure relationship. These data suggest that, in women, impairment of capillary function mediates some of the adverse effects of cortisol and thus may provide a target to prevent such adverse effects. [ABSTRACT FROM AUTHOR]
Published: 2007
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131. Perivascular Fat and the Microcirculation: Relevance to Insulin Resistance, Diabetes, and Cardiovascular Disease

Author: Etto C. Eringa, Yvo M. Smulders, Alphons J.H.M. Houben, Erik H. Serné, A.M. Jonk, Coen D.A. Stehouwer, Physiology, Internal medicine, ICaR - Circulation and metabolism, and Kinesiology
Subjects: medicine.medical_specialty, Adipokine, Adipose tissue, Disease, Type 2 diabetes, Microcirculation, Insulin resistance, SDG 3 - Good Health and Well-being, Diabetes mellitus, Internal medicine, Medicine, Pharmacology (medical), Obesity, Pharmacology, business.industry, Diabetes, Perivascular adipose tissue, medicine.disease, Diabetes and Insulin Resistance (JB Meigs and M Rutter, Section Editors), Endocrinology, Microvascular dysfunction, Hypertension, business
Abstract: Type 2 diabetes and its major risk factor, obesity, are a growing burden for public health. The mechanisms that connect obesity and its related disorders, such as insulin resistance, type 2 diabetes, and hypertension, are still undefined. Microvascular dysfunction may be a pathophysiologic link between insulin resistance and hypertension in obesity. Many studies have shown that adipose tissue-derived substances (adipokines) interact with (micro)vascular function and influence insulin sensitivity. In the past, research focused on adipokines from perivascular adipose tissue (PVAT). In this review, we focus on the interactions between adipokines, predominantly from PVAT, and microvascular function in relation to the development of insulin resistance, diabetes, and cardiovascular disease. © 2011 The Author(s).
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132. [Glycemia reduction in type 2 diabetes patients with low cardiovascular risk].

Author: Serné EH, Sikkens JJ, and IJzerman RG
Subjects: Humans, Hypoglycemic Agents therapeutic use, Blood Glucose, Risk Factors, Heart Disease Risk Factors, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 drug therapy, Diabetes Mellitus, Type 2 prevention & control, Cardiovascular Diseases prevention & control, Cardiovascular Diseases complications
Abstract: In persons with type 2 diabetes without established cardiovascular complications data are lacking on the comparative effectiveness of commonly used glucose-lowering medications, when added to metformin, with respect to glycemic outcomes as well as microvascular and cardiovascular disease outcomes. The GRADE trial compared the ability of four glucose-lowering remedies to achieve and maintain a defined glycated hemoglobin target and to protect the participant from microvascular and macrovascular complications. In this article, we comment on the relevance of this trial with specific attention for the notion that GLP-1 receptor agonists seem to have a primary preventive effect.
Published: 2023

133. [Round Table Diabetes Care: a collaboration for appropriate care].

Author: Serné EH
Subjects: Humans, Quality of Health Care, Netherlands, Diabetes Mellitus therapy
Abstract: The provision of appropriate care is the cornerstone of the Integrated Care Agreement (IZA) in the Netherlands. Appropriate care is presented as a way of working together to ensure that everyone continues to have access to reimbursed and good quality health care in the future. A method that has been successfully used within the diabetes field since 2016 and has taken shape as the Round Table Diabetes Care. The current article describes this approach.
Published: 2023

134. [Prevalence and drug treatment of people with type 2 diabetes mellitus and a very high risk of cardiovascular disease].

Author: Serné EH, Overbeek JA, Palmen J, de Jong HJI, and Stehouwer CDA
Subjects: Humans, Female, Aged, Male, Prevalence, Cross-Sectional Studies, Cardiovascular Diseases epidemiology, Diabetes Mellitus, Type 2 complications, Diabetes Mellitus, Type 2 drug therapy, Diabetes Mellitus, Type 2 epidemiology, Heart Failure drug therapy, Heart Failure epidemiology, Renal Insufficiency, Chronic drug therapy, Renal Insufficiency, Chronic epidemiology
Abstract: Objective: Dutch diabetes guidelines have been updated to incorporate specific therapies with cardiovascular and kidney outcomes benefit in type 2 diabetes patients (T2D) at very high risk for cardiorenal complications. This is part of a comprehensive approach to reduce the risk of diabetes-related complications, including management of glycemia, blood pressure, and lipids. The current study examines the prevalence of T2D at very high cardiorenal risk and the deployment of evidence-based approaches to lower this risk., Design: Cross-sectional, observational study., Method: A representative population) with T2D in primary care (N= 64,224) was selected from the PHARMO Data Network. A very high risk of CVD was defined as: 1) established CVD, 2) CKD with (very) high cardiovascular risk and 3) heart failure. Drug treatment was determined according to prescriptions in 2019., Results: 25,901 subjects with T2D had a very high risk of CVD (mean age 73.3 years; 42% female). Established CVD, CKD with (very) high cardiovascular risk, and heart failure were observed in 82%, 26% and 22% of patients, respectively. Low-dose salicylates, lipid-lowering and blood pressure-lowering medication were used by 39%, 70% and 69%, respectively. Glucose-lowering medication use included metformin (53%), sulfonylurea-derivatives (24%), and insulin (19%). 2% of the population used a SGLT2 inhibitor or GLP1-receptor agonist., Conclusion: 40% of people with DM2 have a very high risk of CVD. Although our findings reflect the recommendations of the previous treatment guideline for DM2, they also show that the new guideline has significant implications for the treatment of a large proportion of people with DM2.
Published: 2023

135. [Important alteration of the Dutch treatment algorithm in patients with type 2 diabetes mellitus].

Author: Serné EH, IJzerman RG, Krijger-Dijkema JM, Burger KNJ, Hart HE, Klein Woolthuis EP, Janssen PGH, and Wiersma T
Subjects: Algorithms, Humans, Hypoglycemic Agents therapeutic use, Stroke Volume, Diabetes Mellitus, Type 2 drug therapy, Heart Failure drug therapy, Sodium-Glucose Transporter 2 Inhibitors therapeutic use
Abstract: Recent trials of two classes of glucose-lowering drugs (SGLT2 inhibitors and GLP1RAs) have shown consistent cardiovascular and renal benefits that appear independent of glycaemic control. These results have prompted the Dutch College of General Practitioners (NHG) together with the Dutch Society of Internal Medicine (NIV) to update the treatment algorithm in patients with type 2 diabetes mellitus (T2D) at very high CVD risk. The use of SGLT2 inhibitors or GLP1RAs is now recommended in 3 groups of people with T2D. 1. patients with established CVD; 2. Patients with chronic kidney disease and a moderately to high CVD risk according to KDIGO; 3. patients with heart failure with reduced ejection fraction (HFrEF). Treatment algorithms differ for drug-naïve and drug-treated patients with T2D. In both drug-naïve and drug-treated patients the use of a SGLT2 inhibitor respectively as monotherapy or add-on is recommended as first step. If HbA1c is above the individual target, metformin will be added in drug-naive patients whereas GLP1-RAs could be considered in drug-treated patients. GLP1-RAs should also be considered when SGLT2-inhibitors are contraindicated.
Published: 2021

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135 results on '"Erik H, Serné"'

101. Premature aging of the microcirculation in patients with advanced chronic kidney disease

102. Comment on: A multicentre study on the reliability of qualitative and quantitative nailfold videocapillaroscopy assessment: reply

103. Meal-related increases in microvascular vasomotion are impaired in obese individuals: a potential mechanism in the pathogenesis of obesity-related insulin resistance

104. Obesity is associated with impaired endothelial function in the postprandial state

105. Microvascular function is preserved in newly diagnosed rheumatoid arthritis and low systemic inflammatory activity

106. Angiotensin II Enhances Insulin-Stimulated Whole-Body Glucose Disposal but Impairs Insulin-Induced Capillary Recruitment in Healthy Volunteers

107. Sunitinib-induced reduction in skin microvascular density is a reversible phenomenon

108. [Raynaud's phenomenon; diagnosis and treatment]

109. Commentary on viewpoint: the human cutaneous circulation as a model of generalized microvascular function

110. Protein kinase C theta activation induces insulin-mediated constriction of muscle resistance arteries

111. Microvascular function: a potential link between salt sensitivity, insulin resistance and hypertension

112. Regulation of vascular function and insulin sensitivity by adipose tissue: focus on perivascular adipose tissue

113. Urinary cortisol is inversely associated with capillary recruitment in women: A potential explanation for the cortisol-blood pressure relationship

114. Does microvascular dysfunction link obesity with insulin resistance and hypertension?

115. Free fatty acid levels modulate microvascular function: relevance for obesity-associated insulin resistance, hypertension, and microangiopathy

116. A man with diabetes and heart failure

117. 40(th) EASD Annual Meeting of the European Association for the Study of Diabetes : Munich, Germany, 5-9 September 2004

118. The effect of calcium dobesilate on vascular endothelial function, blood pressure, and markers of oxidation in obese male smokers:A placebo-controlled randomised clinical trial

119. PS14 - 74. Microvascular insulin sensitivity in human skeletal muscle and skin are related and both are associated with metabolic insulin sensitivity

120. Renal sodium handling and haemodynamics are equally affected by hyperinsulinaemia in salt-sensitive and salt-resistant hypertensives

121. Effects of insulin on glucose uptake and leg blood flow in patients with sickle cell disease and normal subjects

122. Capillary recruitment is impaired in essential hypertension and relates to insulin's metabolic and vascular actions

123. Birth weight relates to blood pressure and microvascular function in normal subjects

124. Microvascular function relates to insulin sensitivity and blood pressure in normal subjects

125. PS9 - 9. Human coronary artery disease is characterized by defects in coronary insulin signaling

126. FRI0427 Tumor necrosis factor blocking agents inhibit the progression of preclinical atherosclerosis in patients with ankylosing spondylitis

127. Blood pressure and insulin resistance: role for microvascular function? [Cardiovasc Res 2002;53:271–276]

128. PS6 - 34. Microvascular function and Body Mass Index development over time, the Amsterdam Growth and Health Longitudinal Study

129. PS3 - 16. Insulin induced vasoreactivity is dependent on perivascular adipose tissue as well as resistance artery properties after a two-week high fat diet in mice

130. Urinary cortisol is inversely associated with capillary recruitment in women: a potential explanation for the cortisol–blood pressure relationship.

131. Perivascular Fat and the Microcirculation: Relevance to Insulin Resistance, Diabetes, and Cardiovascular Disease

132. [Glycemia reduction in type 2 diabetes patients with low cardiovascular risk].

133. [Round Table Diabetes Care: a collaboration for appropriate care].

134. [Prevalence and drug treatment of people with type 2 diabetes mellitus and a very high risk of cardiovascular disease].

135. [Important alteration of the Dutch treatment algorithm in patients with type 2 diabetes mellitus].

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135 results on '"Erik H, Serné"'

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