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Beta Cell Function (beta + cell_function)
Selected AbstractsThe different mechanisms of insulin sensitizers to prevent type 2 diabetes in OLETF ratsDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 5 2007Sung Hee Choi Abstract Objective To investigate the effects of pioglitazone and metformin treatment during pre-diabetic period for the prevention of diabetes in a rat model. Methods OLETF rats aged 18-weeks, were treated with pioglitazone (10 mg/kg/day) and metformin (300 mg/kg/day) for 10 weeks from their pre-diabetic period. We measured weight, lipid profiles, fat distribution, glucose tolerance, and pancreatic insulin content. Results Prominent weight gain (mostly subcutaneous fat area) was observed in the pioglitazone-treated OLETF (O-P) rats versus significant weight loss was observed in the metformin-treated OLETF (O-M) rats. Pioglitazone reversed the serum triglyceride (TG) and FFAs levels to normal (TG 0.46 ± 0.04 vs 0.88 ± 0.05 mmol/l in LETO). At the age of 28 weeks, the O-P rats showed completely normal glucose tolerance, and the glucose disposal rate (GDR) was markedly improved (25.6 ± 0.4 vs 20.6 ± 0.5 mg/min/kg in O-C, p < 0.05). The O-M rats also showed an improved fasting glucose and GDR level, but not as much as those with O-P rats. The pancreas insulin contents were much improved in the O-P rats (22.9 ± 1.2 vs 18.8 ± 1.3 nmol/pancreas in O-M rats, p < 0.05) with histological improvement. Conclusion The pre-diabetic treatment with pioglitazone, despite significant weight gain, completely prevents to develop diabetes and enhances beta cell function with preservation of islet cell changes. Metformin treatment was also effective, but mainly by ameliorating the insulin resistance with marked reduction in body weight. The reversal of dyslipidaemia and the fat redistribution might contribute to the greater improvement of pioglitazone treatment compared to metformin in OLETF rats. Copyright © 2007 John Wiley & Sons, Ltd. [source] The OGTT as test for beta cell function?EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 5 2001M. Stumvoll [source] Preservation of beta cell functionPEDIATRIC DIABETES, Issue 3 2010Mark A Sperling M.D. Editor-in-Chief No abstract is available for this article. [source] CLINICAL QUESTION: What is the best management strategy for patients with severe insulin resistance?CLINICAL ENDOCRINOLOGY, Issue 3 2010Robert K. Semple Summary Management of severe insulin resistance (IR) is a major clinical challenge in many patients with obesity or lipodystrophy, and also in rarer patients with proven or suspected genetic defects in the insulin receptor or downstream signalling. The latter group can present at any time between birth and early adult life, with a variable clinical course broadly correlated with the severity of IR. Primary insulin signalling defects are usually associated with poor weight gain rather than obesity. Initially, extreme hyperinsulinaemia produces ovarian enlargement and hyperandrogenism in women, and often fasting or postprandial hypoglycaemia. However, any hypoglycaemia gradually evolves into insulin-resistant hyperglycaemia when beta cell function declines. Optimal management of these complex disorders depends on early diagnosis and appropriate targeting of both high and low glucose levels. In newborns, continuous nasogastric feeding may reduce harmful glycaemic fluctuations, and in older patients, acarbose may mitigate postprandial hypoglycaemia. Insulin sensitization, initially with metformin but later with trials of additional agents such as thiazolidinediones, is the mainstay of early therapy, but insulin replacement, eventually with very high doses, is required once diabetes has supervened. Preliminary data suggest that rhIGF-1 can improve survival in infants with the most severe insulin receptor defects and also improve beta cell function in older patients with milder receptoropathies. The utility of newer therapies such as glucagon-like peptide-1 agonists and dipeptidyl peptidase-IV inhibitors remains untested in this condition. Thus, management of these patients remains largely empirical, and there is a pressing need to collate data centrally to optimize treatment algorithms. [source] Interactions between TCF7L2 genotype and growth hormone-induced changes in glucose homeostasis in small for gestational age childrenCLINICAL ENDOCRINOLOGY, Issue 1 2010Sandra W. K. De Kort Summary Context, The Transcription factor 7-like 2 (TCF7L2) rs7903146 gene polymorphism has been associated with risk of developing type 2 diabetes mellitus (DM), possibly by decreasing insulin secretion. Small for gestational age (SGA) birth has been associated with type 2 DM in later life. Growth hormone (GH) treatment reduces insulin sensitivity and increases insulin secretion. Therefore, GH-treated SGA children are an ideal group to investigate whether the TCF7L2 rs7903146 genotype is associated with changes in glucose homeostasis. Objective, To determine the impact of the TCF7L2 rs7903146 polymorphism on changes in insulin secretion and insulin sensitivity during 4 years of GH treatment in children born SGA. Subjects, A total of 246 Caucasian short children born SGA, with a median age of 7·8 years. Outcome measures, Insulin sensitivity and insulin secretion were measured by the frequently sampled intravenous glucose tolerance test (FSIGT) (n = 68) and homeostasis model assessment (HOMA) calculations (all). Results, There was no association between rs7903146 genotype and insulin sensitivity or insulin secretion at baseline but after adjustment for possible confounders, insulin secretion was higher in the CT/TT group than in the CC group. During GH treatment, carriers of the rs7903146 T allele had an increase in insulin secretion similar to that of carriers of the CC genotype. The decrease in insulin sensitivity was only significant in the CT/TT group, but the difference in decrease between genotype groups did not reach significance (P = 0·06). The disposition index (insulin secretion × insulin sensitivity), which is an estimate of beta cell function, was not associated with genotype and did not change during GH treatment. Conclusion, The TCF7L2 rs7903146 polymorphism is not associated with the change in insulin secretion during GH treatment in short SGA children. [source] Cigarette smoking is an independent risk factor for type 2 diabetes: a four-year community-based prospective studyCLINICAL ENDOCRINOLOGY, Issue 5 2009Nam H. Cho Summary Objectives, We investigated the association between smoking and its additive effects with insulin resistance and ,-cell function on the incidence of type 2 diabetes in a prospective population-based cohort study. Design and method, A total of 10 038 subjects were recruited from rural and urban areas. All subjects underwent 75 g oral glucose tolerance tests and full biochemical assessments at baseline and during 4-year follow-up period. The final analysis was limited to 4041 men due to the low smoking rates in women. Results, The ex- and heavy current smokers had the highest incidence of diabetes of 12·5% and 11·1% respectively, compared with never-smokers (7·9%) during 4 years. After multivariate adjustment by Cox-proportional hazard model, ex- and current smokers reveal a relative risk of 1·60 (95% CI: 1·07,2·39), 2·06 (1·35,3·16, for <20 cigarettes/day) and 2·41 (1·48,3·93, for ,20 cigarettes/day) respectively compared with never smokers. The risk of new onset diabetes was the highest in those with low homeostasis model assessment for beta cell function (HOMA-,) and high homeostasis model assessment for insulin resistance (HOMA-IR) group in both smokers and never smokers. Conclusions, Smoking is an independent risk factor for type 2 diabetes mellitus and showed synergistic interaction with the status of low insulin secretion and high insulin resistance for developing diabetes. Given the high rates of smoking and growing burden of diabetes in the world, cessation of smoking should be considered as one of the key factors for diabetes prevention and treatment programmes. [source] | ||||||||||