Influence of short-term submaximal exercise on parameters of glucose assimilation analyzed with the minimal model.

After exercise, glucose uptake in tissues increases by insulin-dependent and -independent mechanisms. We evaluated whether these two effects of exercise on glucose disposal can be detected with the minimal model technique. Seven healthy volunteers were submitted at random order to two frequently sampled intravenous glucose tolerance test (FSIVGTTs), one at rest and the other 25 minutes after a 15-minute exercise test. This exercise included 5 minutes of increasing workload on a cycloergometer followed by 10 minutes at 85% of the maximal theoretic heart rate. Bergman's minimal model of insulin action was used to analyze the two FSIVGTTs and produced the following parameters: coefficient of glucose tolerance (Kg), ie, the slope of the exponential decrease in glycemia between 4 and 19 minutes after intravenous glucose; insulin sensitivity (Sl); and glucose effectiveness at basal insulin (Sg). Sg was divided into its two components: basal insulin effectiveness ([BIE] Sl x basal insulin) and glucose effectiveness at zero insulin ([GEZI] Sg-BIE). After the exercise bout, subjects had an increased Kg (3.44 +/- 0.44 v 2.06 +/- 0.28 x 10(-2).min-1, P < .02), Sl (11.43 +/- 1.27 v 6.23 +/- 0.97 x 10(-4) microU/mL.min-1, P < .01), and Sg (4.40 +/- 0.55 v 2.81 +/- 0.36 x 10(-2).min-1, P < .02). The increase in Sg was mainly explained by a 60% increase in GEZI (3.6 +/- 0.57 v 2.25 +/- 0.36 x 10(-2).min-1, P < .02), but also by an increase in BIE (0.80 +/- 0.12 v 0.47 +/- 0.08 x 10(-2).min-1, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Protective effect of gamma-hydroxybutyrate and nicotinamide on low-dose streptozotocin-induced diabetes in mice.

The purpose of this study was to investigate the effect of a treatment by gamma-hydroxybutyrate (GHB) and nicotinamide (NA) on low-dose streptozotocin (STZ)-induced diabetes in mice. Mean plasma glucose level was significantly elevated in mice given STZ by day 12 after the first STZ injection compared to controls (15.0 +/- 4.7 vs 8.0 +/- 1.6 mmol/l, p < 0.001) and 100% of the animals were severely diabetic by day 18. Plasma glucose levels remained in the normal range and no diabetic values were found in mice treated with combined treatment by GHB and NA for 25 days. However, hyperglycemia and glycosuria appeared within one week after discontinuation of the treatment. Treatment by either GHB or NA alone had only a slight and transient effect in preventing hyperglycemia. In vitro experiment on isolated pancreatic islets demonstrated that STZ-induced loss of insulin response to glucose was also counteracted by incubation with GHB and NA (Peak insulin response to 16.4 mM glucose: 0.69 +/- 0.31 vs 3.03 +/- 0.67 microU/islet/min), but not by GHB or NA alone. These results indicate that GHB and NA have complementary effects in preventing STZ-induced beta cell damage both in vivo and in vitro. This should be taken into account for future preventive strategies in human insulin-dependent diabetes mellitus.

Effects of oral zinc gluconate on glucose effectiveness and insulin sensitivity in humans.

Zinc improves both insulin secretion and insulin sensitivity, and exerts insulin-like effects. We investigated its acute effects on the parameters of glucose assimilation determined with the minimal model technique from frequent sampling intravenous glucose tolerance test (FSIVGTT) in seven healthy volunteers. FSIVGTTs (0.5 g/kg of glucose, followed by 2 U insulin i.v. injection at 19 min) were performed after the subjects had taken 20 mg zinc gluconate twice (the evening before and 30 min before the beginning of the test) or placebo pills (simple blind randomized protocol). Glucose assimilation was analyzed by calculating Kg (slope of the exponential decrease in glycemia), glucose effectiveness Sg (i.e., ability of glucose itself to increase its own disposal independent of insulin response), and SI (insulin sensitivity, i.e. the effect of increases in insulinemia on glucose disposal). The two latter parameters were calculated by fitting the experimental data with the two equations of Bergman's "minimal model." Zinc increased Kg (p < 0.05) and Sg (p < 0.05), whereas SI and insulin first-phase secretion did not significantly increase. This study suggests that zinc improves glucose assimilation, as evidenced by the increase in Kg, and that this improvement results mainly from an increase in glucose effectiveness (insulin-like effect), rather than an action on insulin response or insulin sensitivity.