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Decreased endogenous insulin production improves whole-body insulin sensitivity: is this a sympathetically mediated effect?

Pinto, R.

Decreased endogenous insulin production improves whole-body insulin sensitivity: is this a sympathetically mediated effect?, Proc International Society of Autonomic Neuroscience ISAN2015 ISAN2015, Stresa, Italy, Vol. Autonomic Neuroscience: Basic and Clinical 192 (2015) 1–55, pp. 27 - 28, September, 2015.

Digital Object Identifier: 10.1016/j.autneu.2015.07.336

Abstract
Insulin resistance is a core pathological feature of type 2 diabetes which runs with hyperinsulinemia and with sympathetic overactivity. Herein, we studied the effect of pharmacological blockade of insulin production on whole-body insulin sensitivity, investigating if this effect is mediated by the sympathetic nervous system.
Two groups of male Wistar rats were used: the high fat (HF, 60% lipid-rich diet, 4 weeks) and the control group. After 3 weeks of diet, steptozotocin (STZ) (25mg/kg, i.p.) was administered to half of the groups. Insulin sensitivity was evaluated at baseline and after 3 and 4 weeks of diet, through an insulin tolerance test. Glucose tolerance was also evaluated. . One week post-STZ, rats were anaesthetized with pentobarbitone (60mg/kg) and blood pressure and heart rate were recorded to evaluate autonomic nervous system using classical spectral analysis of heart rate variability.
HF diet significantly decreased insulin sensitivity to 3.16±0.22% glucose/min (KITT control=4.04±0.05%glucose/min).STZ did not alter insulin sensitivity in control animals, but restored the hypoglycemic response to exogenous insulin in HF (KITT HF+STZ=5.02±0.71%glucose/min). STZ did not modify plasma glucose a in control, but significantly increased it to 99.5±3.6 mg/dl in HF animals. STZ did not modify either glucose tolerance or mean arterial pressure. HF animals showed a higher sympathetic activity than control animals and STZ significantly decreased sympathetic activity exclusively in HF rats.
We conclude that prevention of compensatory hyperinsulinemic response by the pancreas through pharmacological blockade of insulin secretion restores peripheral insulin action and decreases sympathetic nervous system activation in prediabetes animal models.