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103. Central opiate mu-receptor-mediated suppression of tissue protein synthesis

Author

Hashiguchi, Yojiro, Molina, Patricia E., Dorton, Simon, McNurlan, Margaret A., Garlick, Peter J., Reddy, Dasari, and Abumrad, Naji N.

Subjects
Proteins -- Synthesis, Morphine -- Physiological aspects, Chemical inhibitors -- Research, Endorphins -- Receptors, Biological sciences
Abstract

The mu-opioid receptor-mediated effects of morphine on tissue protein synthesis and tissue content of high-energy compounds were examined using the specific agonist (D-Ala2,N-Me-Phe4,Gly5-ol)enkephalin (DAGO). Intracerebroventricular injection of DAGO reduced protein synthesis in kidney, spleen, liver, gut mucosa and gastrocnemius muscle while there were no significant changes in the brain, heart and soleus muscle. The results indicated that the inhibition of protein synthesis is greatly mediated by activation of mu-receptors.

Published
1997

104. Histaminergic contribution to the metabolic effects of neuroglucopenia

Author

Molina, Patricia E., Williams, Phillip, and Abumrad, Naji N.

Subjects
Catecholamines -- Physiological aspects, Glucose metabolism -- Physiological aspects, Histamine -- Physiological aspects, Biological sciences
Abstract

The activity of two histaminergic receptors in modulating glucoregulatory responses during central nervous system glucopenia was analyzed in 2-deoxy-D-glucose (2-DG)-treated dogs. Intracerebroventricular infusion of cerebrospinal fluid did not alter plasma glucose concentrations in dogs. However, intracerebroventricular infusions of 2-DG elevated plasma glucose concentrations which was not affected by histaminergic H1 and H2 blockers. Furthermore, histamine receptor activation mediated hyperglycemic response and enhanced rate of hepatic glucose production.

Published
1997

105. Role of the kidney in plasma glucose regulation during hypoglycemia

Author

Cersosimo, Eugenio, Ajmal, Mohammed, Naukam, Rebecca J., Molina, Patricia E., and Abumrad, Naji N.

Subjects
Hypoglycemia -- Physiological aspects, Glucose metabolism -- Physiological aspects, Kidneys -- Physiological aspects, Biological sciences
Abstract

The effects of hypoglycemia on the utilization of glucose in the kidneys were analyzed in conscious, fasted dogs subjected to intrarenal or peripheral dextrose infusions. Analysis of renal glucose metabolism in fasted dogs exhibiting hypoglycemia indicated the role of the kidney in mediating plasma glucose disappearance in the postabsorptive state. On the other hand, renal glucose utilization did not change during hypoglycemia which was induced by peripheral dextrose infusions in dogs.

Published
1997

106. Central effects of morphine and morphine-6-glucuronide on tissue protein synthesis

Author

Hashiguchi, Yojiro, Molina, Patricia E., Preedy, Victor R., Sugden, Peter H., McNurlan, Margaret A., Garlick, Peter J., and Abumrad, Naji N.

Subjects
Morphine -- Physiological aspects, Proteins -- Synthesis, Rats -- Physiological aspects, Biological sciences
Abstract

Opiates are known to inhibit RNA and protein synthesis in mammalian cells but the mechanism of this inhibition has not been elucidated. Herein, intracerebroventricular injection of morphine and morphine-6-glucuronide (M6G) into Sprague-Dawley rats inhibited protein synthesis through a central mechanism which involved suppression of the circulation of arterial blood gases and hormones for tissue protein synthesis.

Published
1996

108. Genome-wide Association Study of Change in Fasting Glucose over time in 13,807 non-diabetic European Ancestry Individuals

Author

Liu, C.-T. (Ching-Ti), Merino, J. (Jordi), Rybin, D. (Denis), DiCorpo, D. (Daniel), Benke, P.J. (Paul), Bragg-Gresham, J.L. (Jennifer L.), Canouil, M. (Mickaël), Corre, T. (Tanguy), Grallert, H. (Harald), Isaacs, A.J. (Aaron), Kutalik, Z. (Zoltán), Lahti, J. (Jari), Marullo, L. (Letizia), Marzi, C. (Carola), Rasmussen-Torvik, L.J. (Laura), Rocheleau, G. (Ghislain), Rueedi, R. (Rico), Scapoli, C. (Chiara), Verweij, N. (Niek), Vogelzangs, N. (Nicole), Willems, S.M. (Sara), Yengo, L. (Loic), Bakker, S.J.L. (Stephan), Beilby, J.P. (John), Hui, J. (Jennie), Kajantie, E. (Eero), Müller-Nurasyid, M. (Martina), Rathmann, W. (Wolfgang), Balkau, B. (Beverley), Bergmann, S.M. (Sven), Hagen, K. (Knut), Florez, J.C. (Jose), Froguel, P. (Philippe), Harris, T.B. (Tamara), Hung, J. (Joseph), James, A. (Alan), Kavousi, M. (Maryam), Miljkovic, I. (Iva), Musk, A.W. (Arthur W.), Palmer, L.J. (Lyle J.), Peters, A. (Annette), Roussel, R. (Ronan), Harst, P. (Pim) van der, Duijn, C.M. (Cornelia) van, Vollenweider, P. (Peter), Barroso, I.E. (Inês), Prokopenko, I. (Inga), Amin, N. (Najaf), Meigs, J.B. (James), Bouatia-Naji, N. (Nabila), Liu, C.-T. (Ching-Ti), Merino, J. (Jordi), Rybin, D. (Denis), DiCorpo, D. (Daniel), Benke, P.J. (Paul), Bragg-Gresham, J.L. (Jennifer L.), Canouil, M. (Mickaël), Corre, T. (Tanguy), Grallert, H. (Harald), Isaacs, A.J. (Aaron), Kutalik, Z. (Zoltán), Lahti, J. (Jari), Marullo, L. (Letizia), Marzi, C. (Carola), Rasmussen-Torvik, L.J. (Laura), Rocheleau, G. (Ghislain), Rueedi, R. (Rico), Scapoli, C. (Chiara), Verweij, N. (Niek), Vogelzangs, N. (Nicole), Willems, S.M. (Sara), Yengo, L. (Loic), Bakker, S.J.L. (Stephan), Beilby, J.P. (John), Hui, J. (Jennie), Kajantie, E. (Eero), Müller-Nurasyid, M. (Martina), Rathmann, W. (Wolfgang), Balkau, B. (Beverley), Bergmann, S.M. (Sven), Hagen, K. (Knut), Florez, J.C. (Jose), Froguel, P. (Philippe), Harris, T.B. (Tamara), Hung, J. (Joseph), James, A. (Alan), Kavousi, M. (Maryam), Miljkovic, I. (Iva), Musk, A.W. (Arthur W.), Palmer, L.J. (Lyle J.), Peters, A. (Annette), Roussel, R. (Ronan), Harst, P. (Pim) van der, Duijn, C.M. (Cornelia) van, Vollenweider, P. (Peter), Barroso, I.E. (Inês), Prokopenko, I. (Inga), Amin, N. (Najaf), Meigs, J.B. (James), and Bouatia-Naji, N. (Nabila)

Abstract

Type 2 diabetes (T2D) affects the health of millions of people worldwide. The identification of genetic determinants associated with changes in glycemia over time might illuminate biological features that precede the development of T2D. Here we conducted a genome-wide association study of longitudinal fasting glucose changes in up to 13,807 non-diabetic individuals of European descent from nine cohorts. Fasting glucose change over time was defined as the slope of the line defined by multiple fasting glucose measurements obtained over up to 14 years of observation. We tested for associations of genetic variants with inverse-normal transformed fasting glucose change over time adjusting for age at baseline, sex, and principal components of genetic variation. We found no genome-wide significant association (P < 5 × 10−8) with fasting glucose change over time. Seven loci previously associated with T2D, fasting glucose or HbA1c were nominally (P < 0.05) associated with fasting glucose change over time. Limited power influences unambiguous interpretation, but these dat

Published
2019
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110. Contribution of central and peripheral adrenergic stimulation to IL-1alpha-mediated glucoregulation

Author

Petit, Felix, Jarrous, Ammar, Dickinson, Richard D., Molina, Patricia E., Abumrad, Naji N., and Lang, Charles H.

Subjects
Glucose metabolism -- Analysis, Interleukins -- Research, Blood plasma -- Composition, Biological sciences
Abstract

Central infusion of interleukin (IL)-1alpha into rats generates temporary hyperinsulinemia and strongly enhances the whole body glucose metabolism and plasma concentrations of insulin corticosterone and glucagon catecholamines. Injection of IL-1alpha, when regulated by improved sympathoadrenal activity, enhances whole body glucose metabolism. Central adrenoreceptors regulate the IL-1alpha-initiated enhancement of pancreatic insulin and glucagon secretion.

Published
1994

111. Effects of chronic hypercortisolemia on carbohydrate metabolism during insulin deficiency

Author

Goldstein, Richard E., Cherrington, Alan D., Reed, George W., Lacy, D.B., Wasserman, David H., and Abumrad, Naji N.

Subjects
Carbohydrate metabolism -- Physiological aspects, Insulin -- Physiological aspects, Biological sciences
Abstract

A study of the influence of chronic selective insulin deficiency on gluconeogenesis and glycogenolysis during acute physiological hypercortisolemia in conscious dogs which are fasted overnight reveals that deficiency of insulin influences glycogenolysis more significantly than gluconeogenesis during acute hypercortisolemia. Increase in glycogenolysis during insulin deficiency plays an important role in worsening the hyperglycemia.

Published
1994

112. Removal of glycylglutamine from plasma by individual tissues: mechanism and impact on amino acid fluxes in postabsorption and starvation

Author

Adibi, Siamak A., Lochs, Herbert, Abumrad, Naji N., Daniel, Hannelore, and Vazquez, Jorge A.

Subjects
Amino acids in human nutrition -- Research, Glutamine -- Physiological aspects, Amino acid metabolism -- Research, Food/cooking/nutrition
Abstract

A possible source of glutamine, for inclusion in the parenteral solutions, is glycylglutamine. The aim of this article is to review briefly the information on metabolism of glycylglutamine when administered intravenously. The fact that there is efficient utilization of intravenously infused glycylglutamine was evident with very little excretion in the urine. Although all the tissues examined, except brain, participated in the removal of glycylglutamine from plasma, kidney predominated in this regard. This may be related to the presence of carrier-mediated systems for cellular uptake of glycylglutamine in the kidney and the lack of them in other tissues. Starvation did not alter the metabolic clearance of glycylglutamine, although it reduced the removal by the kidney. Renal metabolism of glycylglutamine resulted in the release of constituent amino acids that were largely utilized by the liver in the postabsorptive state and by skeletal muscle in starvation. This alteration was accompanied by a selective inhibition of muscle release of amino acids that are substrates for enhanced hepatic gluconeogenesis and renal ammoniagenesis in starvation. Because there was no change either in plasma glucose level or ammonia excretion during the infusion of glycylglutamine in starved human subjects, apparently the amino acid residues of glycylglutamine fulfilled the substrate needs for these functions. These results provide a metabolic basis for further investigations of the possible nutritional benefit of including glycylglutamine in parenteral nutrition.

Published
1993

113. Effects of chronic elevation in plasma cortisol on hepatic carbohyrate metabolism

Author

Goldstein, Richard E., Wasserman, David H., McGuinness, Owen P., Lacy, D. Brooks, Cherrington, Alan D., and Abumrad, Naji N.

Subjects
Stress (Physiology) -- Endocrine aspects, Carbohydrate metabolism -- Physiological aspects, Hydrocortisone -- Physiological aspects, Biological sciences
Abstract

A study of the effects of chronically elevated plasma cortisol level on glycogenolysis and gluconeogenesis is presented. The study protocol included the use of dyes to monitor glucose production and continuous hydrocortisone infusions of ovenight-fasted dogs. The results showed that cortisol promotes hepatic gluconeogenesis by enhancing substrate delivery to the liver, raises plasma insulin levels to inhibit intrahepatic gluconeogenesis and enhances glucose cycling through glycogen. It also inhibits non-hepatic glucose utilization. These effects indicate a role for cortisol in stress response.

Published
1993

115. Jejunal administration of glucose enhances acyl ghrelin suppression in obese humans

Author

Joseph Antoun, James M. Isbell, Vance L. Albaugh, Reem M. Sidani, Naji N. Abumrad, Anna E. Garcia, and Robyn A. Tamboli

Subjects
Adult, Blood Glucose, Male, 0301 basic medicine, medicine.medical_specialty, Physiology, Endocrinology, Diabetes and Metabolism, Gastric bypass, Gastric Bypass, Incretin, 030209 endocrinology & metabolism, Gastric Inhibitory Polypeptide, Carbohydrate metabolism, Biology, 03 medical and health sciences, 0302 clinical medicine, Glucagon-Like Peptide 1, Physiology (medical), Internal medicine, medicine, Humans, Insulin, Acyl ghrelin, Obesity, Infusions, Intravenous, digestive, oral, and skin physiology, Articles, Ghrelin, Glucose, Jejunum, 030104 developmental biology, Endocrinology, Glucose Clamp Technique, Female, Hormone
Abstract

Ghrelin is a gastric hormone that stimulates hunger and worsens glucose metabolism. Circulating ghrelin is decreased after Roux-en-Y gastric bypass (RYGB) surgery; however, the mechanism(s) underlying this change is unknown. We tested the hypothesis that jejunal nutrient exposure plays a significant role in ghrelin suppression after RYGB. Feeding tubes were placed in the stomach or jejunum in 13 obese subjects to simulate pre-RYGB or post-RYGB glucose exposure to the gastrointestinal (GI) tract, respectively, without the confounding effects of caloric restriction, weight loss, and surgical stress. On separate study days, the plasma glucose curves obtained with either gastric or jejunal administration of glucose were replicated with intravenous (iv) infusions of glucose. These “isoglycemic clamps” enabled us to determine the contribution of the GI tract and postabsorptive plasma glucose to acyl ghrelin suppression. Plasma acyl ghrelin levels were suppressed to a greater degree with jejunal glucose administration compared with gastric glucose administration ( P < 0.05). Jejunal administration of glucose also resulted in a greater suppression of acyl ghrelin than the corresponding isoglycemic glucose infusion ( P ≤ 0.01). However, gastric and isoglycemic iv glucose infusions resulted in similar degrees of acyl ghrelin suppression ( P > 0.05). Direct exposure of the proximal jejunum to glucose increases acyl ghrelin suppression independent of circulating glucose levels. The enhanced suppression of acyl ghrelin after RYGB may be due to a nutrient-initiated signal in the jejunum that regulates ghrelin secretion.

Published
2016
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116. High Dose Omega-3 Fatty Acid Administration and Skeletal Muscle Protein Turnover in Maintenance Hemodialysis Patients

Author

Cindy Booker, Serpil Muge Deger, T. Alp Ikizler, Adriana M. Hung, Aihua Bian, Naji N. Abumrad, Charles D. Ellis, and Guanhua Chen

Subjects
0301 basic medicine, medicine.medical_specialty, Epidemiology, 030232 urology & nephrology, Muscle Proteins, Critical Care and Intensive Care Medicine, Systemic inflammation, Placebo, 03 medical and health sciences, 0302 clinical medicine, Interquartile range, Internal medicine, Fatty Acids, Omega-3, medicine, Humans, Renal Insufficiency, Chronic, Omega 3 fatty acid, Transplantation, biology, business.industry, C-reactive protein, Protein turnover, Skeletal muscle, Original Articles, Protein catabolism, 030104 developmental biology, Endocrinology, medicine.anatomical_structure, Nephrology, biology.protein, medicine.symptom, business
Abstract

Background and Objectives Protein energy wasting and systemic inflammation are prevalent in maintenance hemodialysis (MHD) patients. Omega-3 (ω-3) fatty acids have anti-inflammatory properties and have been shown to improve protein homeostasis. We hypothesized that administration of high-dose (2.9 g/d) ω-3 would be associated with decreased muscle protein breakdown in MHD patients with systemic inflammation. Design, setting, participants & measurements This is a substudy from a randomized, placebo-controlled study (NCT00655525). Patients were recruited between September 2008 and June 2011. Primary inclusion criteria included signs of chronic inflammation (average C-reactive protein of ≥5 mg/L over three consecutive measurements), lack of active infectious or inflammatory disease, no hospitalization within 1 month prior to the study, and not receiving steroids (>5 mg/d) and/or immunosuppressive agents. The primary outcomes were forearm muscle and whole body protein breakdown and synthesis before and after the intervention. The patients received ω-3 (n=11) versus placebo (n=9) for 12 weeks. Analysis of covariance was used to compare outcome variables at 12 weeks. Models were adjusted for a propensity score that was derived from age, sex, race, baseline high sensitivity C-reactive protein, diabetes mellitus, and fat mass because the groups were not balanced for several characteristics. Results Compared with placebo, ω-3 supplementation was significantly associated with decreased muscle protein breakdown at 12 weeks (−31, [interquartile range, −98–−13] versus 26 [interquartile range, 13–87] µg/100 ml per min; P=0.01), which remained significant after multivariate adjustment (−46, [95% confidence interval, −102 to −1] µg/100 ml per min). ω-3 Supplementation resulted in decreased forearm muscle protein synthesis while the rate in the placebo group increased; however, there is no longer a statistically significant difference in skeletal muscle protein synthesis or in net protein balance after multivariate adjustment. There was no statistically significant effect of ω-3 supplementation on whole body protein synthesis or breakdown. Conclusions High-dose ω-3 supplementation over 12 weeks in MHD patients with systemic inflammation was associated with attenuation of forearm muscle protein breakdown but did not influence skeletal muscle protein synthesis, skeletal muscle net protein balance or any component of the whole-body protein balance. These results should be interpreted cautiously given the imbalance in the two groups and the short duration of the intervention.

Published
2016
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117. In vitro safety pharmacology evaluation of 2-hydroxybenzylamine acetate

Author

Naji N. Abumrad, John C. Fuller, J. Scott Daniels, Olivier Boutaud, Charles R. Flynn, John A. Oates, Lisa M. Pitchford, Ryan D. Morrison, and John A. Rathmacher

Subjects
0301 basic medicine, Adult, Male, Salmonella typhimurium, Benzylamines, ERG1 Potassium Channel, Low protein, Erythrocytes, CYP2B6, hERG, Pharmacology, Toxicology, medicine.disease_cause, 030226 pharmacology & pharmacy, Article, Gene Expression Regulation, Enzymologic, 03 medical and health sciences, 0302 clinical medicine, Cytochrome P-450 Enzyme System, medicine, Humans, biology, CYP3A4, Chemistry, Mutagenicity Tests, Safety pharmacology, CYP1A2, Cytochrome P450, General Medicine, Blood Proteins, Middle Aged, 030104 developmental biology, biology.protein, Hepatocytes, Female, Oxidative stress, Food Science
Abstract

2-hydroxybenzylamine (2-HOBA), a compound found in buckwheat, is a potent scavenger of reactive γ-ketoaldehydes, which are increased in diseases associated with inflammation and oxidative stress. While the potential of 2-HOBA is promising, studies were needed to characterize the safety of the compound before clinical trials. In a series of experiments, the risks of 2-HOBA-mediated mutagenicity and cardio-toxicity were assessed in vitro. The effects of 2-HOBA on the mRNA expression of select cytochrome P450 (CYP) enzymes were also assessed in cryopreserved human hepatocytes. Further, the distribution and metabolism of 2-HOBA in blood were determined. Our results indicate that 2-HOBA is not cytotoxic or mutagenic in vitro and does not induce the expression of CYP1A2, CYP2B6, or CYP3A4 in human hepatocytes. The results of the hERG testing showed a low risk of cardiac QT wave prolongation. Plasma protein binding and red blood cell distribution characteristics indicate low protein binding and no preferential distribution into erythrocytes. The major metabolites identified were salicylic acid and the glycoside conjugate of 2-HOBA. Together, these findings support development of 2-HOBA as a nutritional supplement and provide important information for the design of further preclinical safety studies in animals as well as for human clinical trials with 2-HOBA.

Published
2018

118. Subchronic (90-day) repeated dose oral toxicity study of 2-hydroxybenzylamine acetate in rabbit

Author

John C. Fuller, Lisa M. Pitchford, Naji N. Abumrad, and John A. Rathmacher

Subjects
0301 basic medicine, Male, Benzylamines, No-Observed-Adverse-Effect Level, Toxicity Tests, Subchronic, Administration, Oral, General Medicine, Toxicology, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Functional Food, Dietary Supplements, Animals, Female, Rabbits, 030217 neurology & neurosurgery
Abstract

2-hydroxybenzylamine (2-HOBA), a naturally occurring compound found in buckwheat, has potential for use as a nutrition supplement due to its ability to protect against the damaging effects of oxidative stress. In a series of rodent toxicity studies, 2-HOBA acetate was well-tolerated and did not produce any toxic effects over 28 or 90 days of repeated oral administration. However, it remained necessary to test the potential toxicity of 2-HOBA acetate in a non-rodent species. In this investigation, 2-HOBA acetate was orally administered to male and female New Zealand White Rabbits for 90 days at doses of 100, 500, and 1000 mg·kg BW

Published
2018

119. Insulin resistance is a significant determinant of sarcopenia in advanced kidney disease

Author

Cindy Mamnungu, Adriana M. Hung, Charles D. Ellis, Feng Sha, Thomas G. Stewart, Serpil Muge Deger, Aihua Bian, Edward D. Siew, T. Alp Ikizler, Jorge L. Gamboa, Naji N. Abumrad, and Jennifer R. Hewlett

Subjects
Adult, Male, medicine.medical_specialty, Sarcopenia, Anabolism, Physiology, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, 030232 urology & nephrology, 030204 cardiovascular system & hematology, 03 medical and health sciences, 0302 clinical medicine, Insulin resistance, Renal Dialysis, Physiology (medical), Internal medicine, medicine, Humans, Insulin, Phosphorylation, Renal Insufficiency, Chronic, Muscle, Skeletal, business.industry, Skeletal muscle, Middle Aged, medicine.disease, Endocrinology, medicine.anatomical_structure, Cross-Sectional Studies, Glucose, Body Composition, Glucose Clamp Technique, Female, Hemodialysis, Insulin Resistance, business, Hormone, Kidney disease, Research Article
Abstract

Maintenance hemodialysis (MHD) patients display significant nutritional abnormalities. Insulin is an anabolic hormone with direct effects on skeletal muscle (SM). We examined the anabolic actions of insulin, whole-body (WB), and SM protein turnover in 33 MHD patients and 17 participants without kidney disease using hyperinsulinemic-euglycemic-euaminoacidemic (dual) clamp. Gluteal muscle biopsies were obtained before and after the dual clamp. At baseline, WB protein synthesis and breakdown rates were similar in MHD patients. During dual clamp, controls had a higher increase in WB protein synthesis and a higher suppression of WB protein breakdown compared with MHD patients, resulting in statistically significantly more positive WB protein net balance [2.02 (interquartile range [IQR]: 1.79 and 2.36) vs. 1.68 (IQR: 1.46 and 1.91) mg·kg fat-free mass−1·min−1 for controls vs. for MHD patients, respectively, P < 0.001]. At baseline, SM protein synthesis and breakdown rates were higher in MHD patients versus controls, but SM net protein balance was similar between groups. During dual clamp, SM protein synthesis increased statistically significantly more in controls compared with MHD patients ( P = 0.03), whereas SM protein breakdown decreased comparably between groups. SM net protein balance was statistically significantly more positive in controls compared with MHD patients [67.3 (IQR: 46.4 and 97.1) vs. 15.4 (IQR: −83.7 and 64.7) μg·100 ml−1·min−1 for controls and MHD patients, respectively, P = 0.03]. Human SM biopsy showed a positive correlation between glucose and leucine disposal rates, phosphorylated AKT to AKT ratio, and muscle mitochondrial markers in controls but not in MHD patients. Diminished response to anabolic actions of insulin in the stimulated setting could lead to muscle wasting in MHD patients.

Published
2018

120. Acute and 28-day repeated dose toxicity evaluations of 2-hydroxybenzylamine acetate in mice and rats

Author

Jodi D. Smith, Lisa M. Pitchford, John C. Fuller, Naji N. Abumrad, and John A. Rathmacher

Subjects
0301 basic medicine, Male, Benzylamines, Administration, Oral, Pharmacology, Acetates, Toxicology, medicine.disease_cause, Median lethal dose, 03 medical and health sciences, Mice, 0302 clinical medicine, Weight loss, Oral administration, medicine, Toxicity Tests, Acute, Animals, Dosing, Palatability, Rats, Wistar, Adverse effect, business.industry, General Medicine, 030104 developmental biology, Toxicity Tests, Subacute, Toxicity, Female, medicine.symptom, business, 030217 neurology & neurosurgery, Oxidative stress
Abstract

2-hydroxybenzylamine (2-HOBA), a compound naturally found in buckwheat, has been shown to protect cells and tissues from the damaging effects of oxidative stress. The purpose of this report was to evaluate 2-HOBA in preclinical oral rodent toxicity studies. This report includes the results from three oral toxicity studies in rodents: a preliminary 28-day feeding study in mice, a 14-day acute oral toxicity study in rats, and a 28-day repeated dose oral toxicity study in rats. The preliminary mouse feeding study showed no adverse effects of 2-HOBA at concentrations up to 0.456% by weight in feed, but decreased food intake and weight loss were observed at 1.56% 2-HOBA in the diet, likely due to poor palatability. In the acute dosing study, 2000 mg/kg BW 2-HOBA resulted in mortality in one of the six tested female rats, indicating a median lethal dose of 2500 mg/kg BW. In the 28-day repeated oral dose study, small differences were observed between 2-HOBA treated and control group rats, but none of these differences were determined to be of toxicological significance. Together, these studies support the lack of toxicity of oral administration of 2-HOBA acetate at doses up to 1000 mg/kg BW d−1 in rodents.

Published
2018

121. CD36 Modulates Fasting and Preabsorptive Hormone and Bile Acid Levels

Author

Nada A. Abumrad, Yan Wei, Naji N. Abumrad, Cyndya A. Shibao, Reem M. Sidani, Yanhua Xiong, Robyn A. Tamboli, Charles R. Flynn, Jorge E Celedonio, Terri A. Pietka, and Latisha Love-Gregory

Subjects
0301 basic medicine, Adult, CD36 Antigens, medicine.medical_specialty, Genotype, medicine.drug_class, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Clinical Biochemistry, Biochemistry, Polymorphism, Single Nucleotide, Bile Acids and Salts, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Endocrinology, Internal medicine, Medicine, Humans, Clinical Research Articles, Bile acid, business.industry, Insulin, Biochemistry (medical), FGF19, Fasting, Middle Aged, medicine.disease, Hormones, Black or African American, 030104 developmental biology, Postprandial, Glycodeoxycholic acid, chemistry, Intestinal Absorption, Case-Control Studies, Ghrelin, Female, Metabolic syndrome, business, Energy Metabolism, 030217 neurology & neurosurgery, Hormone
Abstract

Context Abnormal fatty acid (FA) metabolism contributes to diabetes and cardiovascular disease. The FA receptor CD36 has been linked to risk of metabolic syndrome. In rodents CD36 regulates various aspects of fat metabolism, but whether it has similar actions in humans is unknown. We examined the impact of a coding single-nucleotide polymorphism in CD36 on postprandial hormone and bile acid (BA) responses. Objective To examine whether the minor allele (G) of coding CD36 variant rs3211938 (G/T), which reduces CD36 level by ∼50%, influences hormonal responses to a high-fat meal (HFM). Design Obese African American (AA) women carriers of the G allele of rs3211938 (G/T) and weight-matched noncarriers (T/T) were studied before and after a HFM. Setting Two-center study. Participants Obese AA women. Intervention HFM. Main Outcome Measures Early preabsorptive responses (10 minutes) and extended excursions in plasma hormones [C-peptide, insulin, incretins, ghrelin fibroblast growth factor (FGF)19, FGF21], BAs, and serum lipoproteins (chylomicrons, very-low-density lipoprotein) were determined. Results At fasting, G-allele carriers had significantly reduced cholesterol and glycodeoxycholic acid and consistent but nonsignificant reductions of serum lipoproteins. Levels of GLP-1 and pancreatic polypeptide (PP) were reduced 60% to 70% and those of total BAs were 1.8-fold higher. After the meal, G-allele carriers displayed attenuated early (−10 to 10 minute) responses in insulin, C-peptide, GLP-1, gastric inhibitory peptide, and PP. BAs exhibited divergent trends in G allele carriers vs noncarriers concomitant with differential FGF19 responses. Conclusions CD36 plays an important role in the preabsorptive hormone and BA responses that coordinate brain and gut regulation of energy metabolism.

Published
2018

122. New-Onset Post-Transplant Diabetes Mellitus after Allogeneic Hematopoietic Celltransplant Is Initiated By Insulin Resistance, Not Iatrogenesis

Author

Robert F. Cornell, Dae Kwang Jung, Michael Byrne, Alvin C. Powers, Katie S. Gatwood, Kathryn A. Culos, Naji N. Abumrad, Stacey Goodman, Brian G. Engelhardt, James E. Crowe, Adetola A. Kassim, Ujjawal Savani, and Madan Jagasia

Subjects
Transplantation, medicine.medical_specialty, business.industry, Mortality rate, medicine.medical_treatment, Immunosuppression, Hematology, medicine.disease, Impaired fasting glucose, Gastroenterology, Calcineurin, Iatrogenesis, Haematopoiesis, Insulin resistance, Internal medicine, Diabetes mellitus, Medicine, business
Abstract

The mortality rate triples for the 50% of allogeneic hematopoietic cell transplant (HCT) recipients diagnosed new-onset post-transplant diabetes mellitus (PTDM). Calcineurin inhibitors and corticosteroids are assumed the cause for hyperglycemia, however patients developing PTDM have elevated fasting C-peptide levels before HCT. We tested the hypotheses that an oral glucose tolerance test (OGTT) would predict new-onset PTDM and that PTDM progresses from established insulin resistance present before HCT. Glucose tolerance and insulin sensitivity were quantified with OGTTs and euglycemic hyperinsulinemic clamps before and 90 days after matched related donor peripheral blood HCT in 20 patients without diabetes. PTDM was diagnosed by a weekly fasting BG ≥126mg/dL or random BG ≥200mg/dL from day 0 to day+100. PTDM was diagnosed in 11 (55%) patients at a median of 22 days post-HCT (range, 0-88 days). Table 1 outlines patient characteristics and OGTT results. PTDM preceded grade 2-4 acute GVHD or corticosteroids in 9 (82%) and 11 (100%) patients, respectively. Pre-transplant 2-hour, post-prandial OGTT plasma glucose values did not discriminate between patients developing PTDM and those maintaining euglycemia after HCT. However, fasting pre-transplant glucose and C-peptide levels were elevated in patients developing PTDM. All 5 patients with impaired fasting glucose (100-125mg/dl) compared to 6 out of 15 individuals with normal fasting glucose levels ( PTDM risk is dependent on pre-transplant insulin resistance and independent of immunosuppression. Impaired fasting glucose levels identified PTDM susceptibility. Peripheral insulin resistance could be targeted for the prevention/treatment of PTDM.

Published
2019
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125. Iatrogenic Hyperinsulinemia, Not Hyperglycemia, Drives Insulin Resistance in Type 1 Diabetes as Revealed by Comparison With GCK-MODY (MODY2)

Author

Gregory, Justin M., primary, Smith, T. Jordan, additional, Slaughter, James C., additional, Mason, Holly R., additional, Hughey, Curtis C., additional, Smith, Marta S., additional, Kandasamy, Balamurugan, additional, Greeley, Siri Atma W., additional, Philipson, Louis H., additional, Naylor, Rochelle N., additional, Letourneau, Lisa R., additional, Abumrad, Naji N., additional, Cherrington, Alan D., additional, and Moore, Daniel J., additional

Published
2019
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127. New-Onset Post-Transplant Diabetes Mellitus after Allogeneic Hematopoietic Celltransplant Is Initiated By Insulin Resistance, Not Iatrogenesis

Author

Savani, Ujjawal B., primary, Jung, Dae Kwang, additional, Crowe, James E., additional, Abumrad, Naji N., additional, Powers, Alvin C., additional, Jagasia, Madan, additional, Cornell, Robert F., additional, Goodman, Stacey, additional, Kassim, Adetola A., additional, Culos, Kathryn Ann A., additional, Gatwood, Katie S., additional, Byrne, Michael T., additional, and Engelhardt, Brian G., additional

Published
2019
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133. Early Increases in Bile Acids Post Roux-en-Y Gastric Bypass Are Driven by Insulin-Sensitizing, Secondary Bile Acids

Author

Naji N. Abumrad, Yi Xiao, Charles R. Flynn, Steven Cai, Vance L. Albaugh, and Robyn A. Tamboli

Subjects
Adult, Blood Glucose, Male, medicine.medical_specialty, Adolescent, medicine.drug_class, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Clinical Biochemistry, Gastric Bypass, Context (language use), Hot Topics in Translational Endocrinology, Biochemistry, Body Mass Index, Bile Acids and Salts, Young Adult, Endocrinology, Insulin resistance, Weight loss, Diabetes mellitus, Internal medicine, Weight Loss, medicine, Humans, Insulin, Bile acid, business.industry, Biochemistry (medical), nutritional and metabolic diseases, Fasting, Middle Aged, medicine.disease, Roux-en-Y anastomosis, Obesity, Morbid, Treatment Outcome, Female, Insulin Resistance, medicine.symptom, business, Body mass index, Follow-Up Studies
Abstract

Roux-en-Y gastric bypass (RYGB) is the most effective treatment for morbid obesity and resolution of diabetes. Over the last decade, it has become well accepted that this resolution of diabetes occurs before significant weight loss; however, the mechanisms behind this effect remain unknown and could represent novel therapeutic targets for obesity and diabetes. Bile acids have been identified as putative mediators of these weight loss-independent effects.To identify the longitudinal changes in bile acids after RYGB, which may provide mechanistic insight into the weight loss-independent effects of RYGB.Observational study before/after intervention.Academic medical center.Samples were collected from morbidly obese patients (n = 21) before and after RYGB.RYGB.Seventeen individual bile acid species were measured preoperatively and at 1, 6, 12, and 24 months postoperatively. Anthropometric, hormonal, and hyperinsulinemic-euglycemic clamp data were also examined to identify physiological parameters associated with bile acid changes.Fasting total plasma bile acids increased after RYGB; however, increases were bimodal and were observed only at 1 (P.05) and 24 months (P.01). One-month increases were secondary to surges in ursodeoxycholic acid and its glycine and taurine conjugates, bacterially derived bile acids with putative insulin-sensitizing effects. Increases at 24 months were due to gradual rises in primary unconjugated bile acids as well as deoxycholic acid and its glycine conjugate. Plasma bile acid changes were not significantly associated with any anthropometric or hormonal measures, although hepatic insulin sensitivity was significantly improved at 1 month.Overall findings suggest that bacterially derived bile acids may mediate the early improvements at 1 month after RYGB. Future studies should examine the changes in specific bile acid chemical species after bariatric procedures and bile acid-specific signaling changes.

Published
2015
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135. Population Pharmacokinetics of Dasatinib in Healthy Subjects

Author

Walaa B. Hassouneh, Mutasim A. Al-Ghazawi, Mohammad I. Saleh, and Naji Najib

Subjects
dasatinib, population pharmacokinetics, body mass index, absorption rate constant, obesity, overweight, Medicine, Pharmacy and materia medica, RS1-441
Abstract

Background and Objectives: Dasatinib is one of the tyrosine kinase inhibitors. The main use of these agents is inhibition of cancerous cell proliferation. The therapeutic importance of tyrosine kinase inhibitors raises the necessity of many types of investigations, especially the pharmacokinetic analysis of these drugs in humans. This analysis, along with other investigations and clinical research, will contribute to the overall knowledge of the drug. This study focused on the population pharmacokinetics of dasatinib. The objective of the study was to investigate the sources of the variability of dasatinib in a population pharmacokinetics study in healthy participants. Methods: We utilized 4180 plasma observations from 110 subjects who were administered SPRYCEL® on two separate occasions under fasting conditions; data from 20% of the subjects (22 subjects) were extracted for the purpose of internal model evaluation and data from 88 subjects were used in modeling. The model was evaluated by visual predictive check of three different datasets. A two-compartmental model with first order absorption and transit compartment was considered the simplest base model to describe the data based on the corrected Bayesian information criterion evaluation. Covariates were tested through conditional sampling for the stepwise approach-screening procedure in Monolix 2020R1 version. Conditional sampling for the stepwise approach was used to include the correlated covariates within the base model in the forward inclusion step and then to eliminate them backwardly to ensure that the key covariates were kept in the model at the final stage. Results: The effect of body mass index on the absorption rate constant was considered as significant covariate in the final established model. Visual predictive check for simulations, 20% of the original dataset (internal dataset) and an external dataset demonstrated the appropriateness of the final model. Conclusions: Population pharmacokinetic modeling was performed to describe dasatinib pharmacokinetics in healthy subjects. Body mass index was considered as a factor that might be used in the future along with studies on patients to adjust the dosing regimens. Key Points: Dasatinib is classified as a highly variable drug; this variability was demonstrated in the study by the effect of body mass index on the absorption rate constant.

Published
2024
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136. New genetic loci link adipose and insulin biology to body fat distribution

Author

Shungin, D, Winkler, T, Croteau Chonka, D, Ferreira, T, Locke, A, Mägi, R, Strawbridge, R, Pers, T, Fischer, K, Justice, A, Workalemahu, T, Wu, J, Buchkovich, M, Heard Costa, N, Roman, T, Drong, A, Song, C, Gustafsson, S, Day, F, Esko, T, Fall, T, Kutalik, Z, Luan, J, Randall, J, Scherag, A, Vedantam, S, Wood, A, Chen, J, Fehrmann, R, Karjalainen, J, Kahali, B, Liu, C, Schmidt, E, Absher, D, Amin, N, Anderson, D, Beekman, M, Bragg Gresham, J, Buyske, S, Demirkan, A, Ehret, G, Feitosa, M, Goel, A, Jackson, A, Johnson, T, Kleber, M, Kristiansson, K, Mangino, M, Leach, I, Medina Gomez, C, Palmer, C, Pasko, D, Pechlivanis, S, Peters, M, Prokopenko, I, Stanca'Kova', A, Sung, Y, Tanaka, T, Teumer, A, Van Vliet Ostaptchouk, J, Yengo, L, Zhang, W, Albrecht, E, Ärnlöv, J, Arscott, G, Bandinelli, S, Barrett, A, Bellis, C, Bennett, A, Berne, C, Blüher, M, Böhringer, S, Bonnet, F, Böttcher, Y, Bruinenberg, M, Carba, D, Caspersen, I, Clarke, R, Daw, E, Deelen, J, Deelman, E, Delgado, G, Doney, A, Eklund, N, Erdos, M, Estrada, K, Eury, E, Friedrich, N, Garcia, M, Giedraitis, V, Gigante, B, Go, A, Golay, A, Grallert, H, Grammer, T, Gräsler, J, Grewal, J, Groves, C, Haller, T, Hallmans, G, Hartman, C, Hassinen, M, Hayward, C, Heikkilä, K, Herzig, K, Helmer, Q, Hillege, H, Holmen, O, Hunt, S, Isaacs, A, Ittermann, T, James, A, Johansson, I, Juliusdottir, T, Kalafati, I, Kinnunen, L, Koenig, W, Kooner, I, Kratzer, W, Lamina, C, Leander, K, Lee, N, Lichtner, P, Lind, L, Lindström, J, Lobbens, S, Lorentzon, M, Mach, F, Magnusson, P, Mahajan, A, Mcardle, W, Menni, C, Merger, S, Mihailov, E, Milani, L, Mills, R, Moayyeri, A, Monda, K, Mooijaart, S, Mühleisen, T, Mulas, A, Müller, G, Müller Nurasyid, M, Nagaraja, R, Nalls, M, Narisu, N, Glorioso, N, Nolte, I, Olden, M, Rayner, N, Renstrom, F, Ried, J, Robertson, N, Rose, L, Sanna, S, Scharnagl, H, Scholtens, S, Sennblad, B, Seufferlein, T, Sitlani, C, Smith, A, Stirrups, K, Stringham, H, Sundström, J, Swertz, M, Swift, A, Syvänen, A, Tayo, B, Thorand, B, Thorleifsson, G, Tomaschitz, A, Troffa, C, Van Oort, F, Verweij, N, Vonk, J, Waite, L, Wennauer, R, Wilsgaard, T, Wojczynski, M, Wong, A, Zhang, Q, Zhao, J, Brennan, E, Choi, M, Eriksson, P, Folkersen, L, Franco Cereceda, A, Gharavi, A, Hedman, A, Hivert, M, Huang, J, Kanoni, S, Karpe, F, Keildson, S, Kiryluk, K, Liang, L, Lifton, R, Ma, B, Mcknight, A, Mcpherson, R, Metspalu, A, Min, J, Moffatt, M, Montgomery, G, Murabito, J, Nicholson, G, Nyholt, D, Olsson, C, Perry, J, Reinmaa, E, Salem, R, Sandholm, N, Schadt, E, Scott, R, Stolk, L, Vallejo, E, Westra, H, Zondervan, K, Amouyel, P, Arveiler, D, Bakker, S, Beilby, J, Bergman, R, Blangero, J, Brown, M, Burnier, M, Campbell, H, Chakravarti, A, Chines, P, Claudi Boehm, S, Collins, F, Crawford, D, Danesh, J, De Faire, U, De Geus, E, Dörr, M, Erbel, R, Eriksson, J, Farrall, M, Ferrannini, E, Ferrières, J, Forouhi, N, Forrester, T, Franco, O, Gansevoort, R, Gieger, C, Gudnason, V, Haiman, C, Harris, T, Hattersley, A, Heliövaara, M, Hicks, A, Hingorani, A, Hoffmann, W, Hofman, A, Homuth, G, Humphries, S, Hyppönen, E, Illig, T, Jarvelin, M, Johansen, B, Jousilahti, P, Jula, A, Kaprio, J, Kee, F, Keinanen Kiukaanniemi, S, Kooner, J, Kooperberg, C, Kovacs, P, Kraja, A, Kumari, M, Kuulasmaa, K, Kuusisto, J, Lakka, T, Langenberg, C, Le Marchand, L, Lehtimäki, T, Lyssenko, V, Männistö, S, Marette, A, Matise, T, Mckenzie, C, Mcknight, B, Musk, A, Möhlenkamp, S, Morris, A, Nelis, M, Ohlsson, C, Oldehinkel, A, Ong, K, Palmer, L, Penninx, B, Peters, A, Pramstaller, P, Raitakari, O, Rankinen, T, Rao, D, Rice, T, Ridker, P, Ritchie, M, Rudan, I, Salomaa, V, Samani, N, Saramies, J, Sarzynski, M, Schwarz, P, Shuldiner, A, Staessen, J, Steinthorsdottir, V, Stolk, R, Strauch, K, Tönjes, A, Tremblay, A, Tremoli, E, Vohl, M, Völker, U, Vollenweider, P, Wilson, J, Witteman, J, Adair, L, Bochud, M, Boehm, B, Bornstein, S, Bouchard, C, Cauchi, S, Caulfield, M, Chambers, J, Chasman, D, Cooper, R, Dedoussis, G, Ferrucci, L, Froguel, P, Grabe, H, Hamsten, A, Hui, J, Hveem, K, Jöckel, K, Kivimaki, M, Kuh, D, Laakso, M, Liu, Y, März, W, Munroe, P, Njolstad, I, Oostra, B, Pedersen, N, Perola, M, Pe'Russe, L, Peters, U, Power, C, Quertermous, T, Rauramaa, R, Rivadeneira, F, Saaristo, T, Saleheen, D, Sinisalo, J, Slagboom, P, Snieder, H, Spector, T, Thorsteinsdottir, U, Stumvoll, M, Tuomilehto, J, Uitterlinden, A, Uusitupa, M, Van Der Harst, P, Veronesi, G, Walker, M, Wareham, N, Watkins, H, Wichmann, H, Abecasis, G, Assimes, T, Berndt, S, Boehnke, M, Borecki, I, Deloukas, P, Franke, L, Frayling, T, Groop, L, Hunter, D, Kaplan, R, O'Connell, J, Qi, L, Schlessinger, D, Strachan, D, Stefansson, K, Van Duijn, C, Willer, C, Visscher, P, Yang, J, Hirschhorn, J, Zillikens, M, Mccarthy, M, Speliotes, E, North, K, Fox, C, Barroso, I, Franks, P, Ingelsson, E, Heid, I, Loos, R, Cupples, L, Lindgren, C, Mohlke, K, Dastani, Z, Timpson, N, Yuan, X, Henneman, P, Kizer, J, Lyytikainen, L, Fuchsberger, C, Small, K, Coassin, S, Lohman, K, Pankow, J, Uh, H, Wu, Y, Bidulescu, A, Rasmussen Torvik, L, Greenwood, C, Ladouceur, M, Grimsby, J, Manning, A, Mooser, V, Kapur, K, Frants, R, Willemsvan vanDijk, K, Willems, S, Psaty, B, Tracy, R, Brody, J, Chen, I, Viikari, J, Kähönen, M, Evans, D, St Pourcain, B, Sattar, N, Carlson, O, Egan, J, van Heemst, D, Kedenko, L, Nuotio, M, Loo, B, Kanaya, A, Haun, M, Klopp, N, Katsareli, E, Couper, D, Duncan, B, Kloppenburg, M, Borja, J, Musani, S, Guo, X, Semple, R, Teslovich, T, Allison, M, Redline, S, Buxbaum, S, Meulenbelt, I, Ballantyne, C, Hu, F, Paulweber, B, Florez, J, Smith, G, Siscovick, D, Kronenberg, F, van Duijn, C, Waterworth, D, Meigs, J, Dupuis, J, Richards, J, Willenborg, C, Thompson, J, Erdmann, J, Goldstein, B, König, I, Cazier, J, Johansson, Å, Hall, A, Lee, J, Grundberg, E, Havulinna, A, Ho, W, Hopewell, J, Eriksson, N, Lundmark, P, Lyytikäinen, L, Rafelt, S, Tikkanen, E, Van Zuydam, N, Voight, B, Ziegler, A, Altshuler, D, Balmforth, A, Braund, P, Burgdorf, C, Cox, D, Dimitriou, M, Do, R, El Mokhtari, N, Fontanillas, P, Hager, J, Han, B, Kang, H, Kessler, T, Knowles, J, Kolovou, G, Langford, C, Lokki, M, Lundmark, A, Meisinger, C, Melander, O, Maouche, S, Nikus, K, Peden, J, Rasheed, A, Rosinger, S, Rubin, D, Rumpf, M, Schäfer, A, Sivananthan, M, Stewart, A, Tan, S, Thorgeirsson, G, van der Schoot, C, Wagner, P, Wells, G, Wild, P, Yang, T, Basart, H, Boerwinkle, E, Brambilla, P, Cambien, F, Cupples, A, de Faire, U, Dehghan, A, Diemert, P, Epstein, S, Evans, A, Ferrario, M, Gauguier, D, Goodall, A, Hazen, S, Holm, H, Iribarren, C, Jang, Y, Kim, H, Laaksonen, R, Ouwehand, W, Parish, S, Park, J, Rader, D, Shah, S, Stark, K, Trégouët, D, Virtamo, J, Wallentin, L, Zimmermann, M, Nieminen, M, Hengstenberg, C, Sandhu, M, Pastinen, T, Hovingh, G, Zalloua, P, Siegbahn, A, Schreiber, S, Ripatti, S, Blankenberg, S, O'Donnell, C, Reilly, M, Collins, R, Kathiresan, S, Roberts, R, Schunkert, H, Pattaro, C, Köttgen, A, Garnaas, M, Böger, C, Chen, M, Tin, A, Taliun, D, Li, M, Gao, X, Gorski, M, Yang, Q, Hundertmark, C, Foster, M, O'Seaghdha, C, Glazer, N, Struchalin, M, Li, G, Johnson, A, Gierman, H, Hwang, S, Atkinson, E, Cornelis, M, Chouraki, V, Holliday, E, Sorice, R, Deshmukh, H, Ulivi, S, Chu, A, Murgia, F, Trompet, S, Imboden, M, Kollerits, B, Pistis, G, Launer, L, Aspelund, T, Eiriksdottir, G, Mitchell, B, Schmidt, H, Cavalieri, M, Rao, M, de Andrade, M, Turner, S, Ding, J, Andrews, J, Freedman, B, Döring, A, Kolcic, I, Zemunik, T, Boban, M, Minelli, C, Wheeler, H, Igl, W, Zaboli, G, Wild, S, Wright, A, Ellinghaus, D, Nöthlings, U, Jacobs, G, Biffar, R, Endlich, K, Ernst, F, Kroemer, H, Nauck, M, Stracke, S, Völzke, H, Aulchenko, Y, Polasek, O, Hastie, N, Vitart, V, Helmer, C, Wang, J, Ruggiero, D, Bergmann, S, Nikopensius, T, Province, M, Ketkar, S, Colhoun, H, Robino, A, Giulianini, F, Krämer, B, Portas, L, Ford, I, Buckley, B, Adam, M, Thun, G, Sala, C, Metzger, M, Mitchell, P, Ciullo, M, Kim, S, Gasparini, P, Pirastu, M, Jukema, J, Probst Hensch, N, Toniolo, D, Coresh, J, Schmidt, R, Kardia, S, Curhan, G, Gyllensten, U, Franke, A, Rettig, R, Parsa, A, Goessling, W, Kao, W, de Boer, I, Peralta, C, Akylbekova, E, Kramer, H, van der Harst, P, Arking, D, Franceschini, N, Hernandez, D, Townsend, R, Lumley, T, Kestenbaum, B, Haritunians, T, Waeber, G, Lu, X, Leak, T, Aasarød, K, Skorpen, F, Baumert, J, Devuyst, O, Mychaleckyj, J, Hallan, S, Navis, G, Shlipak, M, Bull, S, Paterson, A, Rotter, J, Beckmann, J, Dreisbach, A, Styrkarsdottir, U, Evangelou, E, Hsu, Y, Duncan, E, Ntzani, E, Oei, L, Albagha, O, Kemp, J, Koller, D, Minster, R, Vandenput, L, Willner, D, Xiao, S, Yerges Armstrong, L, Zheng, H, Alonso, N, Kammerer, C, Kaptoge, S, Leo, P, Wilson, S, Aalto, V, Alen, M, Aragaki, A, Center, J, Dailiana, Z, Duggan, D, Garcia Giralt, N, Giroux, S, Hocking, L, Husted, L, Jameson, K, Khusainova, R, Kim, G, Koromila, T, Kruk, M, Laaksonen, M, Lacroix, A, Lee, S, Leung, P, Lewis, J, Masi, L, Mencej Bedrac, S, Nguyen, T, Nogues, X, Patel, M, Prezelj, J, Scollen, S, Siggeirsdottir, K, Svensson, O, Trummer, O, van Schoor, N, Woo, J, Zhu, K, Balcells, S, Brandi, M, Cheng, S, Christiansen, C, Cooper, C, Frost, M, Goltzman, D, González Macías, J, Karlsson, M, Khusnutdinova, E, Koh, J, Kollia, P, Langdahl, B, Leslie, W, Lips, P, Ljunggren, Ö, Lorenc, R, Marc, J, Mellström, D, Obermayer Pietsch, B, Olmos, J, Pettersson Kymmer, U, Reid, D, Riancho, J, Rousseau, F, Tang, N, Urreizti, R, Van Hul, W, Zarrabeitia, M, Castano Betancourt, M, Herrera, L, Ingvarsson, T, Johannsdottir, H, Kwan, T, Li, R, Luben, R, Medina Gómez, C, Palsson, S, Reppe, S, Sigurdsson, G, van Meurs, J, Verlaan, D, Williams, F, Zhou, Y, Gautvik, K, Raychaudhuri, S, Cauley, J, Clark, G, Cummings, S, Danoy, P, Dennison, E, Eastell, R, Eisman, J, Jackson, R, Jones, G, Khaw, K, Mccloskey, E, Nandakumar, K, Peacock, M, Pols, H, Prince, R, Reid, I, Robbins, J, Sambrook, P, Sham, P, Tylavsky, F, Econs, M, Kung, A, Reeve, J, Streeten, E, Karasik, D, Ralston, S, Ioannidis, J, Kiel, D, Forsblom, C, Isakova, T, Mckay, G, Williams, W, Sadlier, D, Mäkinen, V, Swan, E, Boright, A, Ahlqvist, E, Keller, B, Huang, H, Ahola, A, Fagerholm, E, Gordin, D, Harjutsalo, V, He, B, Heikkilä, O, Hietala, K, Kytö, J, Lahermo, P, Lehto, M, Österholm, A, Parkkonen, M, Pitkäniemi, J, Rosengård Bärlund, M, Saraheimo, M, Sarti, C, Söderlund, J, Soro Paavonen, A, Syreeni, A, Thorn, L, Tikkanen, H, Tolonen, N, Tryggvason, K, Wadén, J, Gill, G, Prior, S, Guiducci, C, Mirel, D, Taylor, A, Hosseini, M, Parving, H, Rossing, P, Tarnow, L, Ladenvall, C, Alhenc Gelas, F, Lefebvre, P, Rigalleau, V, Roussel, R, Tregouet, D, Maestroni, A, Maestroni, S, Falhammar, H, Gu, T, Möllsten, A, Cimponeriu, D, Mihai, I, Mota, M, Mota, E, Serafinceanu, C, Stavarachi, M, Hanson, R, Nelson, R, Kretzler, M, Panduru, N, Gu, H, Brismar, K, Zerbini, G, Hadjadj, S, Marre, M, Lajer, M, Waggott, D, Savage, D, Bain, S, Martin, F, Godson, C, Groop, P, Maxwell, A, Sengupta, S, Peloso, G, Ganna, A, Mora, S, Chang, H, Den Hertog, H, Donnelly, L, Fraser, R, Freitag, D, Gurdasani, D, Kaakinen, M, Kettunen, J, Li, X, Montasser, M, Petersen, A, Saxena, R, Service, S, Sidore, C, Surakka, I, Van den Herik, E, Volcik, K, Asiki, G, Been, L, Bolton, J, Bonnycastle, L, Burnett, M, Cesana, G, Elliott, P, Eyjolfsson, G, Goodarzi, M, Gravito, M, Hartikainen, A, Hung, Y, Jones, M, Kaleebu, P, Kastelein, J, Kim, E, Komulainen, P, Lin, S, Nieminen, T, Nsubuga, R, Olafsson, I, Palotie, A, Papamarkou, T, Pomilla, C, Pouta, A, Ruokonen, A, Seeley, J, Silander, K, Stančáková, A, Tiret, L, van Pelt, L, Wainwright, N, Wijmenga, C, Willemsen, G, Young, E, Bennett, F, Boomsma, D, Bovet, P, Chen, Y, Feranil, A, Freimer, N, Hsiung, C, Järvelin, M, Kesäniemi, A, Koudstaal, P, Krauss, R, Kyvik, K, Martin, N, Meneton, P, Moilanen, L, Njølstad, I, Price, J, Sanghera, D, Sheu, W, Whitfield, J, Wolffenbuttel, B, Ordovas, J, Rich, S, Johnson, L, Larson, M, Levy, D, Newton Cheh, 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Abstract

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, we conducted genome-wide association meta-analyses of waist and hip circumference-related traits in up to 224,459 individuals. We identified 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (WHRadjBMI) and an additional 19 loci newly associated with related waist and hip circumference measures (P<5×10-8). Twenty of the 49 WHRadjBMI loci showed significant sexual dimorphism, 19 of which displayed a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation, and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms.

Published
2015

137. Genetic studies of body mass index yield new insights for obesity biology

Author

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M., Adam M., Thun G. A., Paulweber B., Haun M., Sala C., Metzger M., Mitchell P., Ciullo M., Kim S. K., Vollenweider P., Palmer C., Gasparini P., Pirastu M., Probst-Hensch N. M., Kronenberg F., Toniolo D., Coresh J., Schmidt R., Siscovick D. S., Kardia S. L., Curhan G., Franke A., Parsa A., Goessling W., Kao W. H., de Boer I. H., Peralta C. A., Akylbekova E., Kramer H., Arking D. E., Franceschini N., Egan J., Hernandez D. G., Townsend R. R., Lumley T., Psaty B. M., Kestenbaum B., Haritunians T., Mooser V., Florez J. C., Meigs J. B., Lu X., Leak T. S., Aasarod K., Skorpen F., Baumert J., Devuyst O., Mychaleckyj J. C., Kedenko L., Coassin S., Hallan S., Navis G., Shlipak M. G., Bull S. B., Paterson A. D., Rotter J. I., Dreisbach A. W., Anderson C. A., Guo Q., Henders A., Lambert A., Lee S. H., Kraft P., Kennedy S. H., Macgregor S., Missmer S. A., Painter J. N., Roseman F., Treloar S. A., Wallace L., Forsblom C., Isakova T., McKay G. J., Williams W. W., Sadlier D. M., Makinen V. P., Swan E. J., Boright A. P., Ahlqvist E., Keller B. J., Huang H., Ahola A., Fagerholm E., Gordin D., Harjutsalo V., He B., Heikkila O., Hietala K., Kyto J., Lahermo P., Lehto M., Osterholm A. M., Parkkonen M., Pitkaniemi J., Rosengard-Barlund M., Saraheimo M., Sarti C., Soderlund J., Soro-Paavonen A., Syreeni A., Thorn L. M., Tikkanen H., Tolonen N., Tryggvason K., Waden J., Gill G. V., Prior S., Guiducci C., Mirel D. B., Taylor A., Hosseini M., Parving H. H., Rossing P., Tarnow L., Ladenvall C., Alhenc-Gelas F., Lefebvre P., Rigalleau V., Roussel R., Maestroni A., Maestroni S., Falhammar H., Gu T., Mollsten A., Cimponeriu D., Mihai I., Mota M., Mota E., Serafinceanu C., Stavarachi M., Hanson R. L., Nelson R. G., Kretzler M., Panduru N. M., Gu H. F., Brismar K., Zerbini G., Hadjadj S., Marre M., Lajer M., Waggott D., Savage D. A., Bain S. C., Martin F., Godson C., Groop P. H., Maxwell A. P., Sengupta S., Peloso G. M., Ganna A., Mora S., Chang H. Y., Den Hertog H. M., Donnelly L. A., Freitag D. F., Gurdasani D., Heikkila K., Johnson T., Kaakinen M., Kettunen J., Li X., Montasser M. E., Petersen A. K., Saxena R., Service S. K., Sidore C., Surakka I., Teslovich T. M., Van den Herik E. G., Volcik K. A., Wu Y., Asiki G., Been L. F., Burnett M. S., Elliott P., Eyjolfsson G. I., Goodarzi M. O., Gravito M. L., Hartikainen A. L., Hung Y. J., Jones M. R., Kaleebu P., Khaw K. T., Kim E., Komulainen P., Lin S. Y., Narisu N., Nieminen T. V., Nsubuga R. N., Olafsson I., Palotie A., Papamarkou T., Pomilla C., Pouta A., Ruokonen A., Seeley J., Silander K., Tiret L., van Pelt L., Wainwright N., Wijmenga C., Young E. H., Bennett F., Boomsma D. I., Burnier M., Chen Y. D., Feranil A. B., Freimer N. B., Hsiung C. A., Kesaniemi A., Koudstaal P. J., Krauss R. M., Kyvik K. O., Meneton P., Moilanen L., Sanghera D. K., Sheu W. H., Whitfield J. B., Wolffenbuttel B. H., Ordovas J. M., Rich S. S., Johnson A., Johnson L., Larson M., Levy D., Newton-Cheh C., O'reilly P., Palmas W., Rice K., Smith A., Snider H., Tobin M., Verwoert G., Rice K. M., Verwoert G. C., Pihur V., Heath S., Sober S., Arora P., Zhang F., Lucas G., Milaneschi Y., Parker A. N., Fava C., Fox E. R., Go M. J., Sjogren M., Vinay D., Alexander M., Tabara Y., Shaw-Hawkins S., Whincup P. H., Shi G., Seielstad M., Sim X., Nguyen K. D., Matullo G., Gaunt T. R., Onland-Moret N. C., Cooper M. N., Platou C. G., Org E., Hardy R., Dahgam S., Palmen J., Kuznetsova T., Uiterwaal C. S., Adeyemo A., Ludwig B., Tomaszewski M., Tzoulaki I., Palmer N. D., Chang Y. P., Steinle N. I., Grobbee D. E., Morrison A. C., Najjar S., Hadley D., Brown M. J., Connell J. M., Day I. N., Lawlor D. A., Lawrence R. W., Ongen H., Li Y., Young J. H., Bis J. C., Bolton J. A., Chaturvedi N., Islam M., Jafar T. H., Kulkarni S. R., Howard P., Guarrera S., Ricceri F., Emilsson V., Plump A., Weder A. B., Sun Y. V., Scott L. J., Peltonen L., Vartiainen E., Brand S. M., Staessen J. A., Wang T. J., Burton P. R., Artigas M. S., Dong Y., Wang X., Zhu H., Rudock M. E., Heckbert S. R., Smith N. L., Wiggins K. L., Doumatey A., Shriner D., Veldre G., Viigimaa M., Kinra S., Prabhakaran D., Tripathy V., Langefeld C. D., Rosengren A., Thelle D. S., Corsi A. M., Singleton A., Hilton G., Salako T., Iwai N., Kita Y., Ogihara T., Ohkubo T., Okamura T., Ueshima H., Umemura S., Eyheramendy S., Meitinger T., Cho Y. S., Kim H. L., Scott J., Sehmi J. S., Hedblad B., Nilsson P., Smith G. D., Raffel L. J., Yao J., Schwartz S. M., Ikram M., W L., Mosley T. H., Seshadri S., Shrine N. R., Wain L. V., Zitting P., Cooper J. A., van Gilst W. H., Janipalli C. S., Mani K., Yajnik C. S., Mattace-Raso F. U., Lakatta E. G., Orru M., Scuteri A., Ala-Korpela M., Kangas A. J., Soininen P., Tukiainen T., Wurtz P., Ong R. T., Dorr M., Galan P., Hercberg S., Lathrop M., Zelenika D., Zhai G., Meschia J. F., Sharma P., Terzic J., Kumar M., Denniff M., Zukowska-Szczechowska E., Wagenknecht L. E., Fowkes F., Charchar F. J., Guo X., Rotimi C., Bots M. L., Brand E., Talmud P. J., Nyberg F., Laan M., Palmer L. J., van der Schouw Y. T., Casas J. P., Vineis P., Ganesh S. K., Wong T. Y., Tai E. S., Morris R. W., Marmot M. G., Miki T., Chandak G. R., Zhu X., Elosua R., Soranzo N., Sijbrands E. J., Uda M., Vasan R. S., Alizadeh B. Z., de Boer R. A., Boezen H. M., Hillege H. L., van der Klauw M. M., Ormel J., Rosmalen J. G., Slaets J. P., Lagou V., Welch R. P., Wheeler E., Rehnberg E., Rasmussen-Torvik L. J., Lecoeur C., Johnson P. C., Sennblad B., Salo P., Timpson N. J., Evans D. M., St Pourcain B., Bielak L. F., Horikoshi M., Navarro P., Raychaudhuri S., Chen H., Rybin D., Willems S. M., Song K., An P., Marullo L., Jansen H., Pankow J. S., Edkins S., Varga T. V., Oksa H., Antonella M., Kong A., Herder C., Antti J., Small K., Miljkovic I., Atalay M., Kiess W., Smit J. H., Campbell S., Fowkes G. R., Rathmann W., Maerz W., Watanabe R. M., de Geus E. J., Penninx B. W., Toenjes A., Peyser P. A., Korner A., Dupuis J., Cucca F., Balkau B., Bouatia-Naji N., Purcell S., Musunuru K., Ardissino D., Mannucci P. M., Anand S., Engert J. C., Morgan T., Spertus J. A., Stoll M., Girelli D., McKeown P. P., Patterson C. C., Merlini P. A., Berzuini C., Bernardinelli L., Peyvandi F., Tubaro M., Celli P., Fetiveau R., Marziliano N., Casari G., Galli M., Ribichini F., Rossi M., Bernardi F., Zonzin P., Piazza A., Yee J., Friedlander Y., Marrugat J., Subirana I., Sala J., Ramos R., Williams G., Nathan D. M., Macrae C. A., Berglund G., Asselta R., Duga S., Spreafico M., Daly M. J., Nemesh J., Korn J. M., Surti A., Gianniny L., Parkin M., Burtt N., Gabriel S. B., Wright B. J., Ball S. G., Schunkert I., Linsel-Nitschke P., Lieb W., Fischer M., Grosshennig A., Preuss M., Scholz M., Chen Z., Wilensky R., Matthai W., Qasim A., Hakonarson H. H., Devaney J., Pichard A. D., Kent K. M., Satler L., Lindsay J. M., Waksman R., Knouff C. W., Scheffold T., Berger K., Huge A., Martinelli N., Olivieri O., Corrocher R., Xie C., Ahmadi K. R., Ainali C., Bataille V., Bell J. T., Buil A., Dermitzakis E. T., Dimas A. S., Durbin R., Glass D., Hassanali N., Ingle C., Knowles D., Krestyaninova M., Lowe C. E., Meduri E., Di Meglio P., Montgomery S. B., Nestle F. O., Nica A. C., Nisbet J., O'rahilly S., Parts L., Potter S., Sekowska M., Shin S. Y., Surdulescu G., Travers M. E., Tsaprouni L., Tsoka S., Wilk A., Yang T. P., Higashio J., Williams R., Nato A., Ambite J. L., Deelman E., Manolio T., Heiss G., Taylor K., Avery C., Graff M., Lin D., Quibrera M., Cochran B., Kao L., Umans J., Cole S., Maccluer J., Person S., Gross M., Fornage M., Durda P., Jenny N., Patsy B., Arnold A., Buzkova P., Haines J., Murdock D., Glenn K., Brown-Gentry K., Thornton-Wells T., Dumitrescu L., Bush W. S., Mitchell S. L., Goodloe R., Wilson S., Boston J., Malinowski J., Restrepo N., Oetjens M., Fowke J., Spencer K., Pendergrass S., Le Marchand L., Park L., Tiirikainen M., Kolonel L., Cheng I., Wang H., Shohet R., Stram D., Henderson B., Monroe K., Anderson G., Carlson C., Prentice R., Lacroix A., Wu C., Carty C., Rosse S., Young A., Kocarnik J., Lin Y., Jackson R., Duggan D., Kuller L., He C., Sulem P., Barbalic M., Broer L., Byrne E. M., Gudbjartsson D. F., McArdle P. F., Porcu E., van Wingerden S. W., Zhuang W. V., Lauc L. B., Broekmans F. J., Burri A., Chen C., Corre T., Coviello A. D., D'adamo P., Davies G., Deary I. J., Ebrahim S., Fauser B. C., Ferreli L., Folsom A. R., Hankinson S. E., Hass M., Janssens A. C., Karasik D., Keyzer J., Kiel D. P., Lahti J., Lai S., Laisk T., Laven J. S., Liu J., Lopez L. M., Louwers Y. V., Marongiu M., Klaric I. M., Masciullo C., Melzer D., Newman A. B., Pare G., Peeters P. H., Pop V. J., Raikkonen K., Salumets A., Stacey S. N., Starr J. M., Stathopoulou M. G., Styrkarsdottir U., Tenesa A., Tryggvadottir L., Tsui K., van Dam R. M., van Gils C. H., van Nierop P., Vink J. M., Voorhuis M., Widen E., Wijnands-Van Gent C. J., Yerges-Armstrong L. M., Zgaga L., Zygmunt M., Buring J. E., Crisponi L., Demerath E. W., Streeten E. A., Murray A., Visser J. A., Lunetta K. L., Elks C. E., Cousminer D. L., Koller D. L., Lin P., Smith E. N., Warrington N. M., Alavere H., Berenson G. S., Blackburn H., Busonero F., Chen W., Couper D., Easton D. F., Eriksson J., Foroud T., Kilpelainen T. O., Li S., Murray S. S., Ness A. R., Northstone K., Peacock M., Pennell C. E., Pharoah P., Rafnar T., Rice J. P., Ring S. M., Schork N. J., Segre A. V., Sovio U., Srinivasan S. R., Tammesoo M. L., van Meurs J. B., Young L., Bierut L. J., and Econs M. J.

Abstract

Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 × 10-8), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ∼2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20 % of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.

Published
2015

139. Thiamin deficiency impairs endotoxin-induced increases in hepatic glucose output

Author

Molina, Patricia E., Yousef, Khalil A., Smith, Rita M., Tepper, Patrick G., Lang, Charles H., and Abumrad, Naji N.

Subjects
Vitamin B1 deficiency -- Physiological aspects, Glucose metabolism -- Physiological aspects, Endotoxins -- Physiological aspects, Food/cooking/nutrition, Health
Abstract

We addressed the role of thiamin, a cofactor for several enzymes involved in glucose metabolism, in the glucose metabolic response to endotoxin. Characterized by hyperglycemia, increased hepatic glucose production exceeding elevated rates of whole-body glucose utilization, this response is mediated by hormones and cytokines and is dependent on the immune and nutritional status of the hose. We hypothesized that a thiamin-deficient state would impair the metabolic response to endotoxin. Rats were fed a thiamin-deficient or control diet for 6 wk before in vivo assessment of glucose kinetics. In control rats, Escherichia coli endotoxin increased the rate of glucose appearance (+76%), disappearance (+ 70%), and metabolic clearance (+50%). Thiamin deficiency resulted in increased plasma glucose (18%) and lactate (3- to 4-fold) as well as in a 30% decrease in insulin and an increase in glucagon (2.6-fold) and corticosterone (3.6-fold). Thiamin deficiency inhibited the endotoxin-induced hyperglycemia and the rise in hepatic glucose production, glucose utilization, and metabolic clearance rate.

Published
1994

140. Caloric restriction-induced decreases in dopamine receptor availability are associated with leptin concentration

Author

Dunn, Julia P., Abumrad, Naji N., Kessler, Robert M., Patterson, Bruce W., Li, Rui, Marks-Shulman, Pamela, and Tamboli, Robyn A.

Subjects
Adult, Leptin, Receptors, Dopamine D2, Brain, Humans, Female, Obesity, Article, Caloric Restriction
Abstract

It has been previously reported that early after Roux-en-Y-gastric bypass, dopamine (DA) type 2 and 3 receptor (D2/3R) binding potential (BPFifteen females with obesity (BMI = 39 ± 6 kg/mWith the VLCD, weight decreased slightly (-3 kg). Insulin, glucose, and leptin decreased significantly, but there was no change in acyl ghrelin or measures from OMM. SN D2/3R BPIn obesity, reductions in regional D2/3R availability after VLCD are suggestive of increased endogenous DA competing with the radioligand. Changes in regional D2/3R availability were associated with decreases in leptin concentrations that occurred before clinically significant weight loss.

Published
2017

141. Role of Bile Acids and GLP-1 in Mediating the Metabolic Improvements of Bariatric Surgery

Author

Naji N. Abumrad, Jie Ping, Joseph Antoun, Yan Guo, Charles R. Flynn, Vance L. Albaugh, Muhammed Alikhan, Yanhua Xiong, Babak Banan, and Blake Austin Clements

Subjects
0301 basic medicine, Blood Glucose, Male, Bariatric Surgery, Receptors, Cytoplasmic and Nuclear, Type 2 diabetes, Receptors, G-Protein-Coupled, Mice, 0302 clinical medicine, Glucagon-Like Peptide 1, Glucose homeostasis, Mice, Knockout, Bile acid, biology, Anticholesteremic Agents, digestive, oral, and skin physiology, Anastomosis, Surgical, Gastroenterology, Gallbladder, G protein-coupled bile acid receptor, Intestines, 030211 gastroenterology & hepatology, Lymph, Akkermansia muciniphila, medicine.drug, Signal Transduction, medicine.medical_specialty, medicine.drug_class, Cholestyramine Resin, Diet, High-Fat, Glucagon-Like Peptide-1 Receptor, Bile Acids and Salts, 03 medical and health sciences, Verrucomicrobia, Bile acid sequestrant, Ileum, Weight Loss, medicine, Animals, Cholestyramine, Hepatology, business.industry, Glucose Tolerance Test, biology.organism_classification, medicine.disease, Surgery, Mice, Inbred C57BL, 030104 developmental biology, Farnesoid X receptor, Insulin Resistance, business
Abstract

Background & aims Bile diversion to the ileum (GB-IL) has strikingly similar metabolic and satiating effects to Roux-en-Y gastric bypass (RYGB) in rodent obesity models. The metabolic benefits of these procedures are thought to be mediated by increased bile acids, although parallel changes in body weight and other confounding variables limit this interpretation. Methods Global G protein–coupled bile acid receptor-1 null (Tgr5−/−) and intestinal-specific farnesoid X receptor null (FxrΔ/E) mice on high-fat diet as well as wild-type C57BL/6 and glucagon-like polypeptide 1 receptor deficient (Glp-1r−/−) mice on chow diet were characterized following GB-IL. Results GB-IL induced weight loss and improved oral glucose tolerance in Tgr5−/−, but not FxrΔ/E mice fed a high-fat diet, suggesting a role for intestinal Fxr. GB-IL in wild-type, chow-fed mice prompted weight-independent improvements in glycemia and glucose tolerance secondary to augmented insulin responsiveness. Improvements were concomitant with increased levels of lymphatic GLP-1 in the fasted state and increased levels of intestinal Akkermansia muciniphila. Improvements in fasting glycemia after GB-IL were mitigated with exendin-9, a GLP-1 receptor antagonist, or cholestyramine, a bile acid sequestrant. The glucoregulatory effects of GB-IL were lost in whole-body Glp-1r−/− mice. Conclusions Bile diversion to the ileum improves glucose homeostasis via an intestinal Fxr-Glp-1 axis. Altered intestinal bile acid availability, independent of weight loss, and intestinal Akkermansia muciniphila appear to mediate the metabolic changes observed after bariatric surgery and might be manipulated for treatment of obesity and diabetes.

Published
2017

142. Systemic inflammation is associated with exaggerated skeletal muscle protein catabolism in maintenance hemodialysis patients

Author

Serpil Muge Deger, Haiming Li, Charles D. Ellis, Aihua Bian, Roy Zent, Feng Sha, Edward D. Siew, Cindy Booker, T. Alp Ikizler, Jorge L. Gamboa, Adriana M. Hung, Thomas G. Stewart, William E. Mitch, and Naji N. Abumrad

Subjects
0301 basic medicine, Nephrology, Adult, Male, medicine.medical_specialty, Ubiquitin-Protein Ligases, Muscle Proteins, Systemic inflammation, Tripartite Motif Proteins, 03 medical and health sciences, Mice, Renal Dialysis, Diabetes mellitus, Internal medicine, medicine, Animals, Homeostasis, Humans, Renal Insufficiency, Chronic, Muscle, Skeletal, Wasting, Inflammation, Mice, Knockout, SKP Cullin F-Box Protein Ligases, business.industry, Integrin beta1, Protein turnover, Skeletal muscle, General Medicine, Middle Aged, medicine.disease, Protein catabolism, Disease Models, Animal, Kinetics, 030104 developmental biology, Endocrinology, medicine.anatomical_structure, C-Reactive Protein, Multivariate Analysis, Cytokines, Regression Analysis, Female, medicine.symptom, Clinical Medicine, business, Biomarkers, Kidney disease
Abstract

BACKGROUND. Systemic inflammation and muscle wasting are highly prevalent and coexist in patients on maintenance hemodialysis (MHD). We aimed to determine the effects of systemic inflammation on skeletal muscle protein metabolism in MHD patients. METHODS. Whole body and skeletal muscle protein turnover were assessed by stable isotope kinetic studies. We incorporated expressions of E1, E214K, E3αI, E3αII, MuRF-1, and atrogin-1 in skeletal muscle tissue from integrin β1 gene KO CKD mice models. RESULTS. Among 129 patients with mean (± SD) age 47 ± 12 years, 74% were African American, 73% were male, and 22% had diabetes mellitus. Median high-sensitivity C-reactive protein (hs-CRP) concentration was 13 (interquartile range 0.8, 33) mg/l. There were statistically significant associations between hs-CRP and forearm skeletal muscle protein synthesis, degradation, and net forearm skeletal muscle protein balance (P < 0.001 for all). The associations remained statistically significant after adjustment for clinical and demographic confounders, as well as in sensitivity analysis, excluding patients with diabetes mellitus. In attempting to identify potential mechanisms involved in this correlation, we show increased expressions of E1, E214K, E3αI, E3αII, MuRF-1, and atrogin-1 in skeletal muscle tissue obtained from an animal model of chronic kidney disease. CONCLUSION. These data suggest that systemic inflammation is a strong and independent determinant of skeletal muscle protein homeostasis in MHD patients, providing rationale for further studies using anticytokine therapies in patients with underlying systemic inflammation. FUNDING. This study was in part supported by NIH grants R01 DK45604 and 1K24 DK62849, the Clinical Translational Science Award UL1-TR000445 from the National Center for Advancing Translational Sciences, the Veterans Administration Merit Award I01 {"type":"entrez-nucleotide","attrs":{"text":"CX000414","term_id":"56271831","term_text":"CX000414"}}CX000414, the SatelliteHealth Normon Coplon Extramural Grant Program, and the FDA grant 000943.

Published
2017

143. Bile Acids and Bariatric Surgery

Author

Charles R. Flynn, Hana Ajouz, Babak Banan, Vance L. Albaugh, and Naji N. Abumrad

Subjects
0301 basic medicine, Sleeve gastrectomy, medicine.medical_specialty, medicine.drug_class, medicine.medical_treatment, Clinical Biochemistry, Gastric Bypass, Receptors, Cytoplasmic and Nuclear, 030209 endocrinology & metabolism, Rodentia, Biology, Biochemistry, Article, Receptors, G-Protein-Coupled, Bile Acids and Salts, 03 medical and health sciences, 0302 clinical medicine, Gastrectomy, Internal medicine, Enterohepatic Circulation, medicine, Glucose homeostasis, Animals, Homeostasis, Humans, Molecular Biology, Enterohepatic circulation, Bile acid, Lipid metabolism, General Medicine, Metabolism, G protein-coupled bile acid receptor, Surgery, Gastrointestinal Microbiome, Obesity, Morbid, 030104 developmental biology, Endocrinology, Glucose, Diabetes Mellitus, Type 2, Gene Expression Regulation, Molecular Medicine, Farnesoid X receptor, Insulin Resistance, Signal Transduction
Abstract

Bariatric surgery, specifically Roux-en-Y gastric bypass (RYGB) and vertical sleeve gastrectomy (VSG), are the most effective and durable treatments for morbid obesity and potentially a viable treatment for type 2 diabetes (T2D). The resolution rate of T2D following these procedures is between 40 and 80% and far surpasses that achieved by medical management alone. The molecular basis for this improvement is not entirely understood, but has been attributed in part to the altered enterohepatic circulation of bile acids. In this review we highlight how bile acids potentially contribute to improved lipid and glucose homeostasis, insulin sensitivity and energy expenditure after these procedures. The impact of altered bile acid levels in enterohepatic circulation is also associated with changes in gut microflora, which may further contribute to some of these beneficial effects. We highlight the beneficial effects of experimental surgical procedures in rodents that alter bile secretory flow without gastric restriction or altering nutrient flow. This information suggests a role for bile acids beyond dietary fat emulsification in altering whole body glucose and lipid metabolism strongly, and also suggests emerging roles for the activation of the bile acid receptors farnesoid x receptor (FXR) and G-protein coupled bile acid receptor (TGR5) in these improvements. The limitations of rodent studies and the current state of our understanding is reviewed and the potential effects of bile acids mediating the short- and long-term metabolic improvements after bariatric surgery is critically examined.

Published
2017

145. Short-term effects of dietary-fat ingestion on energy expenditure and nutrient balance

Author

Bennett, Chuck, Reed, George W., Peters, John C., Abumrad, Naji N., Sun, Ming, and Hill, James O.

Subjects
Dietary fat -- Physiological aspects, Energy metabolism -- Physiological aspects, Nutrient interactions -- Physiological aspects, Food/cooking/nutrition, Health
Abstract

Joule for joule, dietary fat may promote obesity more than protein or carbohydrate. In this study we determined whether the addition of 50 g dietary fat to a standard breakfast would increase energy expenditure or fat oxidation during the immediate 6-h postprandial period or over the ensuing 18 h. We also determined whether subjects with a high level of aerobic physical fitness would show a greater increase in fat oxidation after the ingestion of the extra fat than would less fit subjects. Adding fat did not increase fat oxidation or energy expenditure either during the immediate 6-h postprandial period or over the following 18 h. This was true regardless of the subject's fitness level. Acutely, dietary fat ingested in excess of its usual rate of oxidation appears to be stored in the body. Being physically fit does not appear to provide an advantage in avoiding short-term storage of excess dietary fat. Am J Clin Nutr 1992;55: 1071-7.

Published
1992

146. Nutrient balance and energy expenditure during ad libitum feeding of high-fat and high-carbohydrate diets in humans

Author

Thomas, Cecilia D., Peters, John C., Reed, George W., Abumrad, Naji N., Sun, Ming, and Hill, James O.

Subjects
Thermogenesis -- Health aspects, Weight loss -- Health aspects, High-carbohydrate diet -- Health aspects, Dietary fat -- Health aspects, Energy metabolism -- Physiological aspects, Food/cooking/nutrition, Health
Abstract

To study the influence of diet composition on regulation of body weight, we fed 21 weight-stable subjects (11 lean, 10 obese) high-carbohydrate (HC) and high-fat (HF) diets for 1 wk each. Although diet composition was fixed, total energy intake was unrestricted. Subject had a higher energy intake on the HF (11 039 [+ or -] 2700 kJ/d) than on the HC (10672 [+ or -] 2617 kJ/d) diet (P < 0.05), but energy expenditure was not different between diets. On day 7 of the HC diet, carbohydrate (CHO) oxidation was significantly related to CHO intake with the slope of the regression line 0.99, suggesting the overall CHO balance was near zero. However, the slope of the regression line was greater for obese than for lean subjects. On day 7 of the HF diet, fat oxidation was significantly related to fat intake but the slope of the line was 0.50, suggesting that overall fat balance was positive. However, this relationship was due entirely to lean subjects, with obese subjects showing no relationship between fat intake and oxidation.

Published
1992

147. Autonomic Blockade Improves Insulin Sensitivity in Obese Subjects

Author

Sachin Y. Paranjape, Satish R. Raj, Naji N. Abumrad, Luis E. Okamoto, André Diedrich, Alfredo Gamboa, Ginnie Farley, Amy C. Arnold, Italo Biaggioni, and Rocio A. Figueroa

Subjects
Adult, Blood Glucose, Male, medicine.medical_specialty, Ganglionic Blockers, medicine.medical_treatment, Glucose uptake, Ganglionic blocker, Blood Pressure, Autonomic Nervous System, Article, Insulin resistance, Internal medicine, Internal Medicine, medicine, Humans, Insulin, Resting energy expenditure, Obesity, Enzyme Inhibitors, Cross-Over Studies, omega-N-Methylarginine, business.industry, Muscles, Middle Aged, Glucose clamp technique, medicine.disease, Autonomic nervous system, Endocrinology, Glucose Clamp Technique, Omega-N-Methylarginine, Female, Insulin Resistance, Nitric Oxide Synthase, Trimethaphan, business
Abstract

Obesity is an important risk factor for the development of insulin resistance. Initial compensatory mechanisms include an increase in insulin levels, which are thought to induce sympathetic activation in an attempt to restore energy balance. We have previously shown, however, that sympathetic activity has no beneficial effect on resting energy expenditure in obesity. On the contrary, we hypothesize that sympathetic activation contributes to insulin resistance. To test this hypothesis, we determined insulin sensitivity using a standard hyperinsulinemic euglycemic clamp protocol in obese subjects randomly assigned in a crossover design 1 month apart to receive saline (intact day) or trimetaphan (4 mg/min IV, autonomic blocked day). Whole-body glucose uptake ( M BW in mg/kg per minute) was used as index of maximal muscle glucose use. During autonomic blockade, we clamped blood pressure with a concomitant titrated intravenous infusion of the nitric oxide synthase inhibitor N -monomethyl-L-arginine. Of the 21 obese subjects (43±2 years; 35±2 kg/m 2 body mass index) studied, 14 were insulin resistant; they were more obese, had higher plasma glucose and insulin, and had higher muscle sympathetic nerve activity (23.3±1.5 versus 17.2±2.1 burst/min; P =0.03) when compared with insulin-sensitive subjects. Glucose use improved during autonomic blockade in insulin-resistant subjects ( M BW 3.8±0.3 blocked versus 3.1±0.3 mg/kg per minute intact; P =0.025), with no effect in the insulin-sensitive group. These findings support the concept that sympathetic activation contributes to insulin resistance in obesity and may result in a feedback loop whereby the compensatory increase in insulin levels contributes to greater sympathetic activation.

Published
2014
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148. Striatal Dopamine Homeostasis is Altered in Mice Following Roux-en-Y Gastric Bypass Surgery

Author

Aurelio Galli, Naji N. Abumrad, Alyssa H. Hasty, India A. Reddy, Julio E. Ayala, and David H. Wasserman

Subjects
Male, obesity, Physiology, striatum, Dopamine, medicine.medical_treatment, medicine.disease_cause, Biochemistry, Norepinephrine, 0302 clinical medicine, Weight loss, Homeostasis, Phosphorylation, bypass, Adiposity, media_common, Mitogen-Activated Protein Kinase 1, 2. Zero hunger, 0303 health sciences, Mitogen-Activated Protein Kinase 3, biology, General Medicine, medicine.symptom, Research Article, medicine.drug, insulin, medicine.medical_specialty, Tyrosine 3-Monooxygenase, brain, Cognitive Neuroscience, media_common.quotation_subject, Immunoblotting, Gastric Bypass, Diet, High-Fat, 03 medical and health sciences, RYGB, Internal medicine, medicine, Animals, Caloric Restriction, 030304 developmental biology, Tyrosine hydroxylase, Gastric bypass surgery, Insulin, Body Weight, nutritional and metabolic diseases, Anastomosis, Roux-en-Y, Appetite, Cell Biology, Corpus Striatum, Receptor, Insulin, Mice, Inbred C57BL, Insulin receptor, Monoamine neurotransmitter, Endocrinology, biology.protein, 030217 neurology & neurosurgery
Abstract

Roux-en-Y gastric bypass (RYGB) is an effective treatment for obesity. Importantly, weight loss following RYGB is thought to result in part from changes in brain-mediated regulation of appetite and food intake. Dopamine (DA) within the dorsal striatum plays an important role in feeding behavior; we therefore hypothesized that RYGB alters DA homeostasis in this subcortical region. In the current study, obese RYGB-operated mice consumed significantly less of a high-fat diet, weighed less by the end of the study, and exhibited lower adiposity than obese sham-operated mice. Interestingly, both RYGB and caloric restriction (pair feeding) resulted in elevated DA and reduced norepinephrine (NE) tissue levels compared with ad libitum fed sham animals. Consequently, the ratio of NE to DA, a measure of DA turnover, was significantly reduced in both of these groups. The RYGB mice additionally exhibited a significant increase in phosphorylation of tyrosine hydroxylase at position Ser31, a key regulatory site of DA synthesis. This increase was associated with augmented expression of extracellular-signal-regulated kinases ERK1/2, the kinase targeting Ser31. Additionally, RYGB has been shown in animal models and humans to improve insulin sensitivity and glycemic control. Curiously, we noted a significant increase in the expression of insulin receptor-β in RYGB animals in striatum (a glucosensing brain region) compared to sham ad libitum fed mice. These data demonstrate that RYGB surgery is associated with altered monoamine homeostasis at the level of the dorsal striatum, thus providing a critical foundation for future studies exploring central mechanisms of weight loss in RYGB.

Published
2014
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149. Early weight regain after gastric bypass does not affect insulin sensitivity but is associated with elevated ghrelin

Author

Robyn A. Tamboli, Naji N. Abumrad, Igal Breitman, Willie Melvin, Kareem Jabbour, Brandon Williams, Irene D. Feurer, Ronald H. Clements, and Pam Marks-Shulman

Subjects
medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, Medicine (miscellaneous), 030209 endocrinology & metabolism, medicine.disease_cause, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Insulin resistance, Internal medicine, medicine, 030212 general & internal medicine, Nutrition and Dietetics, Gastric bypass surgery, business.industry, Leptin, nutritional and metabolic diseases, Insulin sensitivity, medicine.disease, Obesity, Peripheral, Ghrelin, medicine.symptom, business, Weight gain
Abstract

Objectives—We sought to determine: 1) if early weight regain between one and two years after RYGB is associated with worsened hepatic and peripheral insulin sensitivity, and 2) if preoperative levels of ghrelin and leptin are associated with early weight regain after RYGB. Design and Methods—Hepatic and peripheral insulin sensitivity and ghrelin and leptin plasma levels were assessed longitudinally in 45 subjects before RYGB and at one month, six months, one year, and two years post operatively. Weight regain was defined as ≥ 5% increase in body weight between one and two years after RYGB. Results—Weight regain occurred in 33% of subjects, with an average increase in body weight of 10 ± 5 % (8.5 ± 3.3 kg). Weight regain was not associated with worsening of peripheral or hepatic insulin sensitivity. Subjects with weight regain after RYGB had higher preoperative and postoperative levels of ghrelin compared to those who maintained or lost weight during this time. Conversely, the trajectories of leptin levels corresponded with the trajectories of fat mass in both groups. Conclusions—Early weight regain after RYGB is not associated with a reversal of improvements in insulin sensitivity. Higher preoperative ghrelin levels might identify patients that are more susceptible to weight regain after RYGB.

Published
2014
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150. Regulation of novelty seeking by midbrain dopamine D2/D3 signaling and ghrelin is altered in obesity

Author

Julia P. Dunn, Robert M. Kessler, Naji N. Abumrad, David H. Zald, Nora D. Volkow, Pamela A. Marks-Shulman, Shane W. Savage, and Ronald L. Cowan

Subjects
0303 health sciences, medicine.medical_specialty, Nutrition and Dietetics, Endocrinology, Diabetes and Metabolism, Novelty seeking, Medicine (miscellaneous), Substantia nigra, Biology, Midbrain, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, nervous system, Dopamine, Internal medicine, Dopamine receptor D2, medicine, Ghrelin, Signal transduction, Receptor, 030217 neurology & neurosurgery, 030304 developmental biology, medicine.drug
Abstract

Objective To investigate the relationship of novelty seeking traits (NS) with midbrain dopamine (DA) receptors and acyl ghrelin levels (AG) in normal weight (NW) and obese females. NS predict addictive behaviors and are hypothesized to contribute to eating behaviors. In healthy, NS are negatively associated with DA receptors in the substantia nigra (SN). We hypothesized that obesity would influence the regulation of NS by DA signaling and AG.

Published
2014
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