150 results on '"Hother-Nielsen O"'
Search Results
2. METFORMIN INCREASES THE HEPATIC GLUCOSE PRODUCTION IN FATING HEALTHY INDIVIDUALS INDEPENDENTLY OF THE OCT1 GENOTYPE: 792
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Christensen, M., Højlund, K., Stage, T., Hother-Nielsen, O., Nielsen, F., Andersen, Brasch C., Damkier, P., Beck-Nielsen, H., and Brosen, K.
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- 2014
3. Overall Health, Daily Functioning, and Quality of Life in Acute Hepatic Porphyria Patients: ENVISION, a Phase 3 Global, Multicenter, Randomized, Double-Blind, Placebo-Controlled Trial
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Sardh, E., primary, Gouya, L., additional, Rees, D.C., additional, Stein, P., additional, Stölzel, U., additional, Aguilera Peiro, P., additional, Bissell, D.M., additional, Bonkovsky, H.L., additional, Keel, S., additional, Parker, C., additional, Phillips, J.D., additional, Silver, S., additional, Windyga, J., additional, D’Avola, D., additional, Ross, G., additional, Stewart, P., additional, Ritchie, B., additional, Oh, J., additional, Harper, P., additional, Wang, J.D., additional, Langendonk, J.G., additional, Ivanova, A., additional, Horie, Y., additional, Anderson, K.E., additional, Ventura, P., additional, Kauppinen, R., additional, Vassiliou, D., additional, Wang, B., additional, Hother-Nielsen, O., additional, Nakahara, T., additional, Lee, M.J., additional, Sasapu, A., additional, Scalera, S., additional, Lin, T., additional, Penz, C., additional, Simon, A., additional, Ko, J., additional, and Balwani, M., additional
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- 2020
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4. Pathogenesis of Type 2 (non-insulin-dependent) diabetes mellitus: the role of skeletal muscle glucose uptake and hepatic glucose production in the development of hyperglycaemia. A critical comment
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Beck-Nielsen, H., Hother-Nielsen, O., Vaag, A., and Alford, F.
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- 1994
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5. Impact of injection sites for soluble insulin on glycaemic control in Type 1 (insulin-dependent) diabetic patients treated with a multiple insulin injection regimen
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Henriksen, J. E., Djurhuus, M. S., Vaag, A., Thye-Rønn, P., Knudsen, D., Hother-Nielsen, O., and Beck-Nielsen, H.
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- 1993
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6. Hyperglycaemia compensates for the defects in insulin-mediated glucose metabolism and in the activation of glycogen synthase in the skeletal muscle of patients with Type 2 (non-insulin-dependent) diabetes mellitus
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Vaag, A., Damsbo, P., Hother-Nielsen, O., and Beck-Nielsen, H.
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- 1992
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7. Effect of insulin on renal sodium handling in hyperinsulinaemic Type 2 (non-insulin-dependent) diabetic patients with peripheral insulin resistance
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Skøtt, P., Vaag, A., Bruun, N. E., Hother-Nielsen, O., Gall, M.-A., Beck-Nielsen, H., and Parving, H.-H.
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- 1991
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8. Reduced glycogen synthase activity in skeletal muscle from obese patients with and without Type 2 (non-insulin-dependent) diabetes mellitus
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Damsbo, P., Vaag, A., Hother-Nielsen, O., and Beck-Nielsen, H.
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- 1991
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9. Does overnight normalization of plasma glucose by insulin infusion affect assessment of glucose metabolism in Type 2 diabetes?
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Staehr, P., Hojlund, K., Hother-Nielsen, O., Holst, J. J., and Beck-Nielsen, H.
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- 2003
10. On the determination of basal glucose production rate in patients with Type 2 (non-insulin-dependent) diabetes mellitus using primed-continuous 3-3H-glucose infusion
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Hother-Nielsen, O. and Beck-Nielsen, H.
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- 1990
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11. Hepatic glucose production: therapeutic target in type 2 diabetes?
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Staehr, P., Hother-Nielsen, O., and Beck-Nielsen, H.
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- 2002
12. Enhanced hepatic insulin sensitivity, but peripheral insulin resistance in patients with Type 1 (insulin-dependent) diabetes
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Hother-Nielsen, O., Schmitz, O., Bak, J., and Beck-Nielsen, H.
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- 1987
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13. Effects of insulin on kidney function and sodium excretion in healthy subjects
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Skøtt, P., Hother-Nielsen, O., Bruun, N. E., Giese, J., Nielsen, M. D., Beck-Nielsen, H., and Parving, H. -H.
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- 1989
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14. Effect of troglitazone in young firstdegree relatives of patients with type 2 diabetes
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Levin, K., Hother-Nielsen, O., Henriksen, Jan Erik, and Beck-Nielsen, Henning
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- 2004
15. Effects of free fatty acids per se on glucose production, gluconeogenesis, and glycogenolysis
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Stæhr, P., Hother-Nielsen, O., Landau, B.R., Chandramulli, V., Holst, J.J., Beck-Nielsen, H., and Beck-Nielsen, Henning
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- 2003
16. The Combined effect of (Triple Therapy( with Rosiglitazone, Metformin and Insulin Aspart in Type 2 diabetic patients
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Poulsen, M.K., Henriksen, J.E., Hother-Nielsen, O., and Beck-Nielsen, H.
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- 2003
17. Is hepatic glucose production increased, in Type 2 diabetes mellitus ?
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Beck-Nielsen, H., Hother-Nielsen, O., Staehr, P., Davidson, M, and Kelley, D S
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- 2002
18. Assessment of hepatic insulin action in obese Type 2 diabetic patients -:Evidence for impaired direct as well as indirect effects of insulin
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Staehr, P., Hother-Nielsen, O., Levin, K., Holst, J.J., and Beck-Nielsen, Henning
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- 2001
19. Obesity in Type 2 diabetes mellitus YYYY No org found YYY
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Beck-Nielsen, H., Hother-Nielsen, O., LeRoith, D., Taylor, S.I., and Olefsky, J.M.
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- 2000
20. Hyperglycaemia enhance renal magnesium excretion in Type 1 diabetic patients
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Djurhuus, M.S., Skøtt, P., Vaag, A., Hother-Nielsen, O., Andersen, P., Parving, H.H., and Klitgaard, N.A.H.
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- 2000
21. Impact on ubiquinone (coenzyme Q10) treatment on glycaemic control, insulin requirement and well-being in patients with Type 1 diabetes mellitus
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Henriksen, J.E., Andersen, C.B., Hother-Nielsen, O., Vaag, A., Mortensen, S.A., and Beck-Nielsen, H.
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- 1999
22. Hepatic autoregulation: response of glucose production and gluconeogenesis to increased glycogenolysis
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Stæhr, Peter Anton, Hother-Nielsen, O., Beck-Nielsen, H., Roden, M., Stingl, H., Holst, J.J., Jones, P.K., Chandramouli, V., Landau, B.R., Stæhr, Peter Anton, Hother-Nielsen, O., Beck-Nielsen, H., Roden, M., Stingl, H., Holst, J.J., Jones, P.K., Chandramouli, V., and Landau, B.R.
- Abstract
Udgivelsesdato: 2007/5
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- 2007
23. The Combined Effect of Triple Therapy With Rosiglitazone, Metformin, and Insulin Aspart in Type 2 Diabetic Patients
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Poulsen, M. K., primary, Henriksen, J. E., additional, Hother-Nielsen, O., additional, and Beck-Nielsen, H., additional
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- 2003
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24. Impaired insulin-stimulated nonoxidative glucose metabolism in pancreas-kidney transplant recipients. Dose-response effects of insulin on glucose turnover.
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Christiansen E, Vestergaard H, Tibell A, Hother-Nielsen O, Holst JJ, Pedersen O, Madsbad S, Christiansen, E, Vestergaard, H, Tibell, A, Hother-Nielsen, O, Holst, J J, Pedersen, O, and Madsbad, S
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- 1996
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25. Glucose-mediated glucose disposal in insulin-resistant normoglycemic relatives of type 2 diabetic patients.
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Henriksen, J E, primary, Levin, K, additional, Thye-Rønn, P, additional, Alford, F, additional, Hother-Nielsen, O, additional, Holst, J J, additional, and Beck-Nielsen, H, additional
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- 2000
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26. Hyperglycaemia enhances renal magnesium excretion in Type 1 diabetic patients
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Djurhuus, M. S., primary, Skøtt, P., additional, Vaag, A., additional, Hother-Nielsen, O., additional, Andersen, P., additional, Parving, H.-H., additional, and Klitgaard, N. A. H., additional
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- 2000
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27. Impact of ubiquinone (coenzyme Q 10 ) treatment on glycaemic control, insulin requirement and well‐being in patients with Type 1 diabetes mellitus
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Henriksen, J. E., primary, Andersen, C. Bruun, additional, Hother‐Nielsen, O., additional, Vaag, A., additional, Mortensen, S. Aage, additional, and Beck‐Nielsen, H., additional
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- 1999
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28. Irreversibility of the Defect in Glycogen Synthase Activity in Skeletal Muscle From Obese Patients With NIDDM Treated With Diet and Metformin
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Damsbo, P., primary, Hermann, L. S., additional, Vaag, A., additional, Hother-Nielsen, O., additional, and Beck-Nielsen, H., additional
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- 1998
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29. The effect of coenzyme Q10 on blood glucose and insulin requirement in patients with insulin dependent dlabetes mellitus
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Andersen, C.B., primary, Henriksen, J.E., additional, Hother-Nielsen, O., additional, Vaag, A., additional, Mortensen, S.A., additional, and Beck-Nielsen, H., additional
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- 1997
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30. Insulin Increases Renal Magnesium Excretion: A Possible Cause of Magnesium Depletion in Hyperinsulinaemic States
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Djurhuus, M.S., primary, Skøtt, P., additional, Hother-Nielsen, O., additional, Klitgaard, N.A.H., additional, and Beck-Nielsen, H., additional
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- 1995
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31. Assessment of Glucose Turnover Rates in Euglycaemic Clamp Studies using Primed‐constant [3‐3H]‐glucose Infusion and Labelled or Unlabelled Glucose Infusates
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Hother‐Nielsen, O., primary, Møngel, A., additional, Møller, J., additional, Rasmussen, O., additional, Schmitz, O., additional, and Beck‐Nielsen, H., additional
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- 1992
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32. Effect of acute hyperglycemia on glucose metabolism in skeletal muscles in IDDM patients
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Vaag, A., primary, Hother-Nielsen, O., additional, Skott, P., additional, Andersen, P., additional, Richter, E. A., additional, and Beck-Nielsen, H., additional
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- 1992
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33. Effects of hyperglycaemia on kidney function, atrial natriuretic factor and plasma renin in patients with insulin-dependent diabetes mellitus
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Skøtt, P., primary, Vaag, A., additional, Hother-Nielsen, O., additional, Andersen, P., additional, Bruun, N. E., additional, Giese, J., additional, Beck-Nielsen, H., additional, and Parving, H.-H., additional
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- 1991
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34. Assessment of hepatic insulin action in obese type 2 diabetic patients.
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Staehr, Peter, Hother-Nielsen, Ole, Levin, Klaus, Holst, Jens Juul, Beck-Nielsen, Henning, Staehr, P, Hother-Nielsen, O, Levin, K, Holst, J J, and Beck-Nielsen, H
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MECHANISM of action for insulin ,TYPE 2 diabetes - Abstract
Defects in hepatic insulin action in type 2 diabetes and its possible underlying mechanisms were assessed in euglycemic-hyperinsulinemic clamp studies, using improved tracer methods (constant specific activity technique). Ten obese diabetic patients (age 54 years, BMI 29 +/- 0.5 kg/m(2)) and ten matched control subjects were studied at baseline (after an overnight fast) and during insulin infusions of 20- and 40-mU. m(-2). min(-1). In the diabetic patients, plasma glucose levels were normalized overnight before the studies by low-dose insulin infusion. Hepatic sinusoidal insulin levels were estimated, and plasma levels of free fatty acids (FFAs) and glucagon were determined to assess the direct and indirect effects of insulin on hepatic glucose production (HGP) in type 2 diabetes. Baseline rates of HGP (86 +/- 3 vs. 76 +/- 3 mg. m(-2). min(-1), P < 0.05) were slightly elevated in the diabetic patients compared with control subjects, despite much higher hepatic sinusoidal insulin levels (26 +/- 3 vs. 12 +/- 2 mU/l, P < 0.001). Consequently, a marked defect in the direct (hepatic) effect of insulin on HGP appeared to be present at low insulin levels. However, in response to a small increase in baseline hepatic sinusoidal insulin levels of 11 mU/l (26 +/- 3 to 37 +/- 3 mU/l, P < 0.05) in the 20-mU clamp, a marked suppression of HGP was observed in the diabetic patients (86 +/- 3 to 32 +/- 5 mg. m(-2). min(-1), P < 0.001), despite only minimal changes in FFAs (0.33 +/- 0.05 to 0.25 +/- 0.05 mmol/l, NS) and glucagon (14 +/- 1 to 11 +/- 2 pmol/l, P < 0.05) levels, suggesting that the impairment in the direct effect of insulin can be overcome by a small increase in insulin levels. Compared with control subjects, suppression of HGP in the diabetic patients was slightly impaired in the 20-mU clamp (32 +/- 5 vs. 22 +/- 4 mg. m(-2). min(-1), P < 0.05) but not in the 40-mU clamp (25 +/- 2 vs. 21 +/- 3 mg. m(-2). min(-1), NS). In the 20-mU clamp, hepatic sinusoidal insulin levels in the diabetic patients were comparable with control subjects (37 +/- 3 vs. 36 +/- 3 mU/l, NS), whereas both FFA and glucagon levels were higher (i.e., less suppressed) and correlated with the rates of HGP (R = 0.71, P < 0.02; and R = 0.69, P < 0.05, respectively). Thus, at this insulin level impaired indirect (extrahepatic) effects of insulin seemed to prevail. In conclusion, hepatic insulin resistance is present in obese type 2 diabetic patients but is of quantitative significance only at low physiological insulin levels. Defects in both the direct and the indirect effects of insulin on HGP appear to contribute to this resistance. [ABSTRACT FROM AUTHOR]
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- 2001
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35. Impact of ubiquinone (coenzyme Q10) treatment on glycaemic control, insulin requirement and well-being in patients with Type 1 diabetes mellitus.
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Henriksen, J E, Andersen, C B, Hother-Nielsen, O, Vaag, A, Mortensen, S A, and Beck-Nielsen, H
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- 1999
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36. Impact of ubiquinone (coenzyme Q10) treatment on glycaemic control, insulin requirement and well-being in patients with Type 1 diabetes mellitus.
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Henriksen, J. E., Andersen, C. Bruun, Hother-Nielsen, O., Vaag, A., Mortensen, S. Aage, and Beck-Nielsen, H.
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UBIQUINONES ,HYPOGLYCEMIC agents ,TREATMENT of diabetes ,INSULIN pharmacokinetics ,PHYSIOLOGY ,DRUG side effects - Abstract
SummaryAim To investigate the effect of ubiquinone (coenzyme Q
10 ) on glycaemic control and insulin requirement in patients with Type 1 diabetes mellitus (DM). Methods We investigated 34 patients with Type 1 DM in a randomized, double-blind, placebo-controlled study. Patients received either 100 mg Q10 or placebo daily for 3 months. The insulin doses were adjusted according to patients’ home measurements of blood glucose concentrations and reported experience of hypoglycaemia. Results At randomization no differences existed between the Q10 and the placebo groups in age, body mass index (BMI), HbA1c , daily insulin dose or mean daily blood glucose concentration. Serum Q10 concentration increased in the Q10 group (mean ± sd: 0.9 ± 0.2 vs. 2.0 ± 1.0 μg/ml, P < 0.005), with no change in the placebo group (0.9 ± 0.3 vs. 0.9 ± 0.3 μg/ml, not significant (NS)). Following intervention no differences existed between the Q10 and the placebo groups regarding HbA1c (7.86 ± 0.88 vs. 7.84 ± 0.84%), mean daily blood glucose concentrations (8.06 ± 1.86 vs. 8.53 ± 1.88 mm), mean insulin dose (52.1 ± 13.2 vs. 52.6 ± 21.4 U), hypoglycaemic episodes (2.0 ± 1.8 vs. 2.5 ± 2.1 episodes/week), or cholesterol concentrations (4.81 ± 0.91 vs. 4.78 ± 1.07 mm). Furthermore, no differences existed in the well-being of the patients reported from a visual analogue scale (physical: 0.67 ± 0.21 vs. 0.71 ± 0.18, psychological: 0.70 ± 0.25 vs. 0.73 ± 0.24). Conclusion Q10 treatment does not improve glycaemic control, nor does it reduce insulin requirement, and it can therefore be taken by patients with Type 1 DM without any obvious risk of hypoglycaemia. No major beneficial or unfavourable effects on the investigated parameters could be demonstrated and no major changes in the sense of... [ABSTRACT FROM AUTHOR]- Published
- 1999
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37. On the determination of basal glucose production rate in patients with Type 2 (non-insulin-dependent) diabetes mellitus using primed-continuous 3-H-glucose infusion.
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Hother-Nielsen, O. and Beck-Nielsen, H.
- Abstract
Using primed-continuous 3-H-glucose infusion, basal glucose production rate has been reported to be 140% higher than normal or almost normal in hyperglycaemic patients with Type 2 (non-insulin-dependent) diabetes mellitus. To determine whether these markedly different results could be due to the mode of priming: fixed or adjusted, or the mode of calculation: steady state or non-steady state equations, we studied 11 patients with Type 2 diabetes (fasting plasma glucose 8-20 mmol/l). For 6 h 3-H-glucose (0.40 μCi/min) was infused preceded by a priming dose of 40 μCi (fixed priming), or 40 μCi · plasma glucose (mmol/l)·5 (adjusted priming). In diabetic patients the plasma glucose concentration was not constant but declined 0.52±0.07 mmol·l· h. Furthermore, the rate of fall was correlated to the fasting plasma glucose concentration ( r=0.90, p<0.01). Thus, the fasting state was not a steady state condition. Using adjusted priming a constant tracer steady state level was obtained within 60 min. In contrast, using fixed priming tracer steady state was not reached within 6 h. The initial tracer level was far below, and increased in time towards the steady state level observed after adjusted priming. Consequently, using Steele's equations after fixed priming, glucose production rates calculated after 90-120 min were overestimated in proportion to fasting hyperglycaemia. In conclusion: The fasting state in patients with Type 2 diabetes is not a steady state condition. Adjusted priming seems most appropriate in Type 2 diabetes. By estimating glucose production 2 h after fixed priming or assuming steady state conditions, most previous studies may have overestimated basal glucose production in Type 2 diabetes in proportion to fasting hyperglycaemia. [ABSTRACT FROM AUTHOR]
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- 1990
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38. Assessment of Glucose Turnover Rates in Euglycaemic Clamp Studies using Primed-constant [3-3H]-glucose Infusion and Labelled or Unlabelled Glucose Infusates.
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Hother-Nielsen, O., Møngel, A., Møller, J., Rasmussen, O., Schmitz, O., and Beck-Nielsen, H.
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- 1992
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39. Marked Impairment of the Effect of Hyperglycaemia on Glucose Uptake and Glucose Production in Insulin-dependent Diabetes.
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Arnfred, J., Schmitz, O., Hother-Nielsen, O., Ørskova, C., Beck-Nielsen, H., Hermansen, K., Christiansen, J. S., Alberti, K. G. M. M., and Ørskov, H.
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- 1988
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40. Mechanism of Action of Sulphonylureas with Special Reference to the Extrapancreatic Effect: An Overview.
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Beck-Nielsen, H., Hother-Nielsen, O., and Pedersen, O.
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- 1988
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41. Effect of short-term hyperglycemia per se on nociceptive and non-nociceptive thresholds.
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Thye-Rønn, P, Sindrup, S H, Arendt-Nielsen, L, Brennum, J, Hother-Nielsen, O, Beck-Nielsen, H, Thye-Rønn, Peter, Sindrup, Søren H, Arendt-Nielsen, Lars, Brennum, Jannick, Hother-Nielsen, Ole, and Beck-Nielsen, Henning
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- 1994
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42. Classification of newly diagnosed diabetic patients as insulin-requiring or non-insulin-requiring based on clinical and biochemical variables.
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Hother-Nielsen, Ole, Faber, Ole, Sørensen, Niels Schwartz, Beck-Nielsen, Henning, Hother-Nielsen, O, Faber, O, Sørensen, N S, and Beck-Nielsen, H
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- 1988
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43. Insulin action in insulin-dependent diabetics after short-term thiazide therapy.
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SCHMITZ, O., HERMANSEN, K., HOTHER NIELSEN, O., CHRISTENSEN, C. K., ARNFRED, J., HANSEN, H. E., MOGENSEN, C. E., ØRSKOV, H., BECK-NIELSEN, H., Nielsen, O H, and Orskov, H
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- 1986
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44. 35th Annual Meeting of the European Association for the Study of Diabetes
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Melander, A., Olsson, J., Lindberg, G., Salzman, A., Howard, T., Stang, P., Lydick, E., Emslie-Smith, A., Boyle, D. I. R., Evans, J. M. M., Macdonald, T. M., Bain, J., Sullivan, F., Juhl, C., Pørksen, N., Sturis, J., Hollingdal, M., Pincus, S., Veldhuis, J., Dejgaard, A., Schmitz, O., Kristensen, J. S., Frandsen, K. B., Bayer, Th., Müller, P., Dunning, B. E., Paladini, S., Gutierrez, C., Deacon, R., Valentin, M., Grunberger, G., Weston, W. M., Patwardhan, R., Rappaport, E. B., Sargeant, L. A., Wareham, N. J., Khaw, K. T., Zethelius, Björn, Lithell, Hans, Hales, C. Nicholas, Berne, Christian, Lakka, H.-M., Oksanen, L., Tuomainen, T.-P., Kontula, K., Salonen, J. T., Dekker, J. M., de Boks, P., de Vegt, F., Stehouwer, C. D. A., Nijpels, G., Bouter, L. M., Heine, R. J., Bruno, G., Cavallo-Perin, P., Bargero, G., D’Errico, N., Borra, M., Macchia, G., Pagano, G., Newton, R. W., Ruta, D. A., New, J. P., Wallace, C., Roxburgh, M. A., Young, R. J., Vaughan, N. J. A., Elliott, P., Brennan, G., Devers, M., MacAlpine, R., Steinke, D., Lawson, D. H., Decallonne, B., Casteels, K., Gysemans, C., Bouillon, R., Mathieu, C., Linn, Thomas, Strate, Christine, Schneider, Kerstin, Funda, D. P., Jirsa, M., Kozáková, H., Kaas, A., Kofronová, O., Tlaskalová-Hogenová, H., Buschard, K., Wanka, H., Hartmann, A., Kuttler, B., Rasmussen, S. B., Sørensen, T. S., Markholst, H., Petersen, J. S., Karounos, D., Dyrberg, T., Mabley, J. G., Haskó, G., Szabó, C., Seissler, J., Nguyen, T. B. T., Steinbrenner, H., Scherbaum, W. A., Cipriani, R., Gabriele, A., Sensi, M., Guidobaldi, L., Pantellini, F., Cerrito, M. G., Scarpa, S., Di Mario, U., Morano, S., Ceolotto, G., Iori, E., Baritono, E., Del Prato, S., Semplicini, A., Trevisan, R., Zerbini, G., Meregalli, G., Asnaghi, V., Tentori, F., Maestroni, A., Mangili, R., Marescotti, C., Vedovato, M., Tiengo, A., Tadjieva, J., Mankovsky, B. N., Van Aken, S., Raes, A., Vande Walle, J., Matthys, D., Craen, M., Hansen, H. P., Lund, S. S., Rossing, P., Jensen, T., Parving, H.-H., Andersen, S., Tarnow, L., Hansen, B. V., Trautner, C., Haastert, B., Ennenbach, N., Willich, S., Tabák, Á. Gy., Orchard, T. J., Spranger, J., Preissner, K. T., Schatz, H., Pfeiffer, A., Cantón, A., Burgos, R., Hernández, C., Lecube, A., Mesa, J., Segura, R. M., Mateo, C., Simó, R., Fathallah, L., Greene, D. A., Obrosova, I., Gilbert, R. E., Kelly, D. J., Cox, A. J., Berka-Wilkinson, J. L., Taylor, H. R., Panagiotopoulos, S., Lee, V., Jerums, G., Cooper, M. E., Hitman, G. A., Aganna, E., Ogunkolade, W. B., Rema, M., Deepa, R., Shanthi-Rani, C. S., Barakat, K., Kumarajeewa, T. R., Cassell, P. G., McDermott, M. F., Mohan, V., Ways, K., Bursell, S., Devries, T., Woodworth, J., Alatorre, C., King, G., Aiello, L. P., Karisen, A. E., Pavlovic, D., Nielsen, K., Jensen, J., Andersen, H. U., Pociot, F., Mandrup-Poulsen, T., Eizirik, D. L., Nerup, J., Lortz, S., Tiedge, M., Lenzen, S., Lally, F. J., Bone, A. J., Darville, M. I., Ho, Y.-S., Sternesjö, J., Sandler, S., Chen, M.-C., Schuit, F., Pipeleers, D. G., Merezak, S., Hardikar, A., Hoet, J. J., Remacle, C., Reusens, B., Bréant, B., Garofano, A., Czernichow, P., Kubota, N., Terauchi, Y., Miki, H., Tamemoto, H., Yamauchi, T., Nakano, R., Komeda, K., Eto, K., Tobe, K., Kimura, S., Kadowaki, T., Ide, T., Murakami, K., Tsunoda, M., Mochizuki, T., Ozanne, S. E., Nave, B. T., Wang, C. L., Dorling, M. W., Petry, C. J., Koopmans, S. J., van der Bent, C., Que, I., Radder, J. K., Sebokova, E., Sana, A. K., Klimes, I., Ruderman, N., Morviducci, L., Pastore, L., Morelli, S., Sagratella, E., Zorretta, D., Buongiomo, A., Tamburrano, G., Giaccari, A., Martinenghi, Sabina, De Angelis, Gabriella Cusella, Ravasi, Flavio, Bifari, Francesco, Bordignon, Claudio, Falqui, Luca, Kessler, A., Dransfeld, O., Sasson, S., Tomas, E., Zorzano, A., Eckel, J., Thorsby, P., Rosenfalck, A. M., Kjems, L., Hanssen, K. F., Madsbad, S., Birkeland, K. 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- 1999
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45. The importance of insulin resistance in skeletal muscles for development of NIDDM
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Beck-Nielsen, H., Damsbo, P., Vaag, A., Handberg, A., Hother-Nielsen, O., and Jan Erik Henriksen
46. Glucose medi-ated glucose disposal in insulin-resistant normoglycemic relatives of Type 2 diabetic patients
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Jan Erik Henriksen, Levin, K., Peter Thye-Rønn, Alford, F., Hother-Nielsen, O., Juul Holst, J., and Henning Beck-Nielsen
- Abstract
With the aim of investigating glucose-mediated glucose disposal (glucose effectiveness [GE]) in 15 (3 female and 12 male subjects) insulin-resistant normoglycemic relatives of patients with type 2 diabetes (DM2), and 15 age-, sex-, and BMI-matched control subjects without a family history of DM2, we performed 2 studies: 1) a 5-h euglycemic near-normoinsulinemic pancreatic clamp with somatostatin (360 microg/h), insulin (0.25 mU x kg(-1) x min(-1)), glucagon (0.5 ng x kg(-1) x min(-1)), growth hormone (6 ng x kg(-1) x min(-1)), and tritiated glucose infusion and indirect calorimetry; and 2) on a separate day, an identical 5-h clamp but at hyperglycemia (approximately 12 mmol/l) over the last 2 h. Fasting plasma insulin (PI) concentrations were elevated in the relatives compared with control subjects (49 +/- 6 vs. 32 +/- 5 pmol/l, P < 0.04), whereas plasma glucose (PG) was not (5.6 +/- 0.1 vs. 5.5 +/-0.1 mmol/l). At the end (i.e., 4.5-5.0 h) of the euglycemic clamp (PG, 6.1 +/- 0.4 vs. 5.6 +/- 0.1 mmol/l; PI, 78 +/- 5 vs. 73 +/-6 pmol/l), peripheral glucose uptake (Rd(euglycemia)) was decreased in the relatives (2.93 +/- 0.08 vs. 3.70 +/-0.23 mg x min(-1) x kg(-1) fat free mass [FFM], P < 0.005), due to a decreased nonoxidative glucose disposal (0.83 +/-0.21 vs. 1.62 +/- 0.19 mg x min(-1) x kg(-1) FFM, P < 0.01), but hepatic glucose production (HGP) was increased (1.97 +/-0.19 vs. 1.50 +/- 0.13 mg x min(-1) x kg(-1) FFM, P < 0.05). At the matched end of the hyperglycemic clamp (PG, 12.7 +/-0.2 vs. 12.6 +/- 0.2 mmol/l; PI, 87 +/- 5 vs. 78 +/- 7 pmol/l), peripheral glucose disposal (Rd(hyperglycemia)) (5.52 +/- 0.22 vs. 5.92 +/- 0.29 mg x min(-1) x kg(-1) FFM, NS), nonoxidative glucose disposal (2.93 +/- 0.18 vs. 2.78 +/- 0.25 mg x min(-1) x kg(-1) FFM, NS), and HGP(hyperglycemia) (1.20 +/- 0.09 vs. 1.37 +/-0.23 mg x min(-1) x kg(-1) FFM, NS) were all identical. When the effectiveness of glucose itself on glucose uptake and production [(Rd(hyperglycemia) - Rd(euglycemia))/deltaPG and (HGP(euglycemia)- HGP(hyperglycemia))/deltaPG] was calculated, the relatives had a 22% increase in peripheral uptake (0.022 +/- 0.002 vs. 0.018 +/- 0.002 mg x min(-1) x kg(-1) FFM per mg/dl), due to a significantly increased nonoxidative glucose metabolism and enhanced suppression of HGP (0.0076 +/- 0.0021 vs. 0.0011 +/- 0.0022 mg x min(-1) x kg(-1) FFM per mg/dl, P < 0.05). In conclusion, in insulin-resistant relatives of DM2 patients, whole-body glucose-mediated glucose disposal is increased by GE enhancement of the muscle nonoxidative glucose pathway and by GE enhancement of the suppression of HGP. These mechanisms may represent a compensatory mechanism to the ongoing insulin resistance of these relatives.
47. 35th Annual Meeting of the European Association for the Study of Diabetes : Brussels, Belgium, 28 September-2 October 1999
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Melander, A., Olsson, J., Lindberg, G., Salzman, A., Howard, T., Stang, P., Lydick, E., Emslie-Smith, A., Boyle, D. I. R., Evans, J. M. M., Macdonald, T. M., Bain, J., Sullivan, F., Ad Darts Memo, Morris For The Collaboration, Juhl, C., Porksen, N., Sturis, J., Hollingdal, M., Pincus, S., Veldhuis, J., Dejgaard, A., Schmitz, O., Kristensen, J. S., Frandsen, K. B., Bayer, Th, Muller, P., Dunning, B. E., Paladini, S., Gutierrez, C., Deacon, R., Valentin, M., Grunberger, G., Weston, W. M., Patwardhan, R., Rappaport, E. B., Sargeant, L. A., Wareham, N. J., Khaw, K. T., Zethelius, Bjorn, Lithell, Hans, Hales, C. Nicholas, Berne, Christian, Lakka, H-M, Oksanen, L., Tuomainen, T-P, Kontula, K., Salonen, J. T., Dekker, J. M., Boks, P., Vegt, F., Stehouwer, C. D. A., Nijpels, G., Bouter, L. M., Heine, R. J., Bruno, G., Cavallo-Perin, P., Bargero, G., D Errico, N., Borra, M., Macchia, G., Pagano, G., Newton, R. W., Ruta, D. A., New, J. P., Wallace, C., Roxburgh, M. A., Young, R. J., Vaughan, N. 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J., Quinones Galvan, A., Simeoni, M., Basu, A., Uosukainen, A., Makimattila, S., Schlenzka, A., Adler, A. I., Levy, J., Stevens, R., Matthews, D., Holman, R., Boland, B. J., Jeanjean, M., Hermans, M. P., Maudoigt, C., Tonglet, R., Robert, A., Cini, G., Galetta, F., Sanna, G., Gernone, F., Janssen, M. J., Gonera, R. K., Wolffenbuttel, B. H. R., Leeuw, P. W., Schaper, N. C., Moleda, P., Kuczerowski, R., Czech, A., Taton, J., Taddei, S., Patiag, D., Qu, X., Wilkes, M., Gray, S., Seale, J. P., Donnelly, R., Campion, J., Maestro, B., Davila, N., Carranza, M. C., Calle, C., Hales, C. N., Fernandez-Real, J. M., Grasa, M., Pugeat, M., Barret, C., Ricart, W., Lindmark, S., Olsson, T., Tufvesson, M., Loeblein, K., Mehnert, B., Haering, H. 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S., Murphy, L., Rodger, N. W., Ross, S. A., Ryan, E., Yale, J-F, Wolever, T. M. S., Haller, T., Elias, I., Segal, P., Standi, E., Rybka, J., Sencer, E., Schlcnzka, A., Vakkilainen, J., Tsaglis, H., Ioannidis, I., Giakoumaki, A., Amantou, A., Komitopoulos, N., Georgiou, S., Varsamis, E., Katsilambros, N., El Gayar, M., Shereba, N., Botros, R., Fikry, R., Jackson, D., Balme, M., Silva-Nunes, J., Alves, J., Bogalho, P., Gardete-Correia, L., Nunes-Correa, J., Kot Atkova, A., Nemcova, D., Vrbikova, J., Zamrazil, V., Meyer, L., Delbachian, I., Lehert, P., Cugnardey, N., Drouin, P., Guerci, B., Wagner, O. F., Jones, N. P., Vallance, S. E., Thompson, K. A., Miller, A. K., Inglis, A. M. L., Patterson, S., Jorkasky, D., Freed, M. I., Mathisen, A. L., Schneider, R., Rubin, C., Houser, V., Beebe, K. L., Kortboyer, J. M., Eckland, D. J. 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E., Niekerk, N., Rosenkranz, B., Schoenle, E., Hoe, Study Group, Witthaus, Elke, Bradley, Clare, Stewart, John, Barbeau, M., Myers, S., Flora, D., Dimarchi, R., Chance, R., Plum, A., Larsen, P. S., Larsen, U. D., Kristensen, J. B., Jansen, J. A., Olsen, B., Mortensen, H., Hylleberg, B., Jacobsen, L. V., Gall, M-A, Sogaard, B., Ewing, F. M., Ireland, R. H., Hoogwerf, B., Raskin, P., Jovanovic, L., Leiter, L., Boss, A. H., Bott, U., Ebrahim, S., Hirschberger, S., Leukel, P., Sieber, H. J., Mcgill, J., Kilo, C., Kamp, N. M., Wutte, A., Le Thai, F., Balarac, N., Allicar, M. P., Cazeneuve, B., Augendre, B., Wise, S. D., Seah, E. S., Koivisto, V., Torlone, E., Del Sindaco, P., Ciofetta, M., Hedman, C., Orre Pettersson, A-C, Lindstrom, T., Cernigoi, A. M., Kong, N., Kitchen, M. M., Ryder, R. E. 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48. Effects of insulin on kidney function and sodium excretion in healthy subjects
- Author
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Sk�tt, P., primary, Hother-Nielsen, O., additional, Bruun, N.E., additional, Giese, J., additional, Nielsen, M.D., additional, Beck-Nielsen, H., additional, and Parving, H.-H., additional
- Published
- 1989
- Full Text
- View/download PDF
49. The effect of coenzyme Q 10 on blood glucose and insulin requirement in patients with insulin dependent dlabetes mellitus
- Author
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Andersen, C.B., Henriksen, J.E., Hother-Nielsen, O., Vaag, A., Mortensen, S.A., and Beck-Nielsen, H.
- Published
- 1997
- Full Text
- View/download PDF
50. Effects of sulfonylureas on adipocyte and skeletal muscle insulin action in patients with non-insulin-dependent diabetes mellitus.
- Author
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Pedersen, Oluf, Hother-Nielsen, Ole, Bak, Jens, Hjollund, Elisabeth, Beck-Nielsen, Henning, Pedersen, O, Hother-Nielsen, O, Bak, J, Hjollund, E, and Beck-Nielsen, H
- Subjects
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GLIBENCLAMIDE , *INSULIN , *FAT cells , *TYPE 2 diabetes , *GLUCOSE metabolism , *ADIPOSE tissues , *CELL receptors , *GENETIC disorders , *HYPOGLYCEMIC sulfonylureas , *LIPID metabolism disorders , *MUSCLES , *PHARMACODYNAMICS - Abstract
The effect of glibenclamide treatment on insulin action in isolated fat cells was studied in eight moderately obese patients with non-insulin-dependent diabetes mellitus (NIDDM). Insulin receptor binding and the effect of insulin on glucose transport and lipogenesis were determined before and after 3 months of glibenclamide therapy. At the end of the treatment period, mean daytime plasma glucose concentrations were reduced (10.8 +/- 0.4 versus 7.0 +/- 0.3 mmol/L, p less than 0.001) whereas mean daytime plasma insulin level was increased (40 +/- 12 versus 71 +/- 9 mU/L, p less than 0.001). Adipocyte insulin receptor binding as well as basal glucose transport and metabolism were unaffected by drug treatment. In contrast, insulin-stimulated glucose transport and lipogenesis were both significantly enhanced (p less than 0.05). These findings are comparable to those of another study involving seven moderately obese subjects with NIDDM who had biopsies of the lateral vastus muscle taken for measurement of insulin receptor function and glycogen synthase activity before and during 2 months of gliclazide treatment. In that study insulin receptors purified with wheatgerm agglutinin showed unchanged insulin binding and receptor kinase activity. Moreover, gliclazide had no impact on maximal glycogen synthase activity. However, under physiologic hyperinsulinemic conditions gliclazide therapy was associated with an increased sensitivity of glycogen synthase for its allosteric activation by glucose-6-phosphatase (p less than 0.04). In conclusion, sulfonylurea treatment of NIDDM enhances insulin-stimulated peripheral glucose utilization in part through a potentiation of insulin action on adipose tissue glucose transport and lipogenesis and skeletal muscle glycogen synthase. [ABSTRACT FROM AUTHOR]
- Published
- 1991
- Full Text
- View/download PDF
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