Insulin

About: Insulin is a research topic. Over the lifetime, 124295 publications have been published within this topic receiving 5129734 citations. The topic is also known as: human insulin.

TCF7L2 polymorphisms and progression to diabetes in the Diabetes Prevention Program.

Abstract: Background Common polymorphisms of the transcription factor 7–like 2 gene (TCF7L2) have recently been associated with type 2 diabetes. We examined whether the two most strongly associated variants (rs12255372 and rs7903146) predict the progression to diabetes in persons with impaired glucose tolerance who were enrolled in the Diabetes Prevention Program, in which lifestyle intervention or treatment with metformin was compared with placebo. Methods We genotyped these variants in 3548 participants and performed Cox regression analysis using genotype, intervention, and their interactions as predictors. We assessed the effect of genotype on measures of insulin secretion and insulin sensitivity at baseline and at one year. Results Over an average period of three years, participants with the risk-conferring TT genotype at rs7903146 were more likely to have progression from impaired glucose tolerance to diabetes than were CC homozygotes (hazard ratio, 1.55; 95 percent confidence interval, 1.20 to 2.01; P<0.001)....

Plasma insulin response to oral and intravenous glucose administration.

Abstract: This paper describes a new method for evaluating glucose metabolism in man using an oral glucose load. The procedure permits the calculation of a blood glucose disappearance rate constant (K) and thereby makes it possible to compare quantitatively the response to oral and intravenous glucose administration in a given individual. Ten metabolically normal adult humans were studied under carefully controlled conditions. Each received similar amounts (20 g) of glucose both orally and intravenously (2–7 days apart) by constant infusion for 1 hr. The effects on blood glucose disappearance rate constants (K) and plasma insulin concentrations (immunoassay) during and for 1 hr following the infusion were compared. Blood glucose concentrations and K values with the 2 routes of glucose administration were similar. In contrast, plasma insulin responses showed a significant difference: oral glucose resulted in a significant and sustained rise, whereas intravenous glucose was associated with a smaller and transient inc...

Insulin Degradation: Progress and Potential

Abstract: I. Introduction II. Insulin Clearance A. Liver B. Kidney C. Other tissues D. Extracellular insulin degradation III. Cellular Insulin Uptake IV. Cellular Insulin Degradation A. Degradation products B. Assay for insulin degradation C. Insulin-degrading enzymes V. Biological Role of Insulin Degradation VI. Insulin-IDE-Proteasome Interactions and Control of Protein Degradation VII. Summary and Conclusions

Insulin Secretion in Response to Glycemic Stimulus: Relation of Delayed Initial Release to Carbohydrate intolerance in Mild Diabetes Mellitus*

Abstract: Insulin secretory responses to paired intravenous and oral glucose loads were determined in 38 nonobese individuals classified as normal (nondiabetic) subjects, "mild" diabetics (fasting blood glucose below 105 mg per 100 ml), or "moderate" diabetics (fasting glucose below 192 mg per 100 ml). Studies were also performed in 29 obese persons who were similarly grouped. The intravenous load was given to assess the alacrity of hormonal release after glycemic stimulus, and the oral glucose to determine how the speed of initial insulinogenesis modifies the disposition of ingested carbohydrate. In the nonobese group, normal subjects responded to massive hyperglycemia after rapid injection of glucose with immediate and maximal outpouring of insulin, in contrast to a desultory insulinogenic response in patients with mild diabetes, and no initial response at all in moderate diabetics. During oral glucose tolerance tests, the much faster clearance of blood sugar in nondiabetic subjects was actually associated with lower absolute insulin output than was found in mildly diabetic patients, since the latter exhibited delayed hyperinsulinemia in concert with prolonged hyperglycemia. Moderate diabetics never showed excessive insulin release despite even greater hyperglycemia. An empirical "insulinogenic index," the ratio relating enhancement of circulating insulin to magnitude of corresponding glycemic stimulus, was used to compare the secretory capacities of respective groups. Despite the higher absolute hormonal output after oral glucose in mild diabetics, the index revealed that insulin release in normal subjects was proportionally more than twice as great. This relatively greater normal secretory response declared itself shortly after the administration of glucose by either route, and was maintained throughout both tests. In the 29 obese individuals, differences among groups were essentially the same as in persons of normal weight. Obese nondiabetics did show much larger absolute insulinogenic responses during both tests than did nonobese controls. Since corresponding glucose tolerance curves were also higher, the mean insulinogenic indexes for obese subjects were not statistically greater. Moreover, when comparable glucose curves of obese and nonobese controls