Insulin resistance is defined as a preliminary step of type 2 diabetes mellitus with decreased insulin action
evoked by continuous postprandial hyperglycemia, which is provoked by high fat and calories dieting, a lack of physical
activity and obesity. In the early phase of type 2 diabetes mellitus, patients have a hyperinsulinemia to compensate deficient
insulin action by increased secretion from the pancreas to maintain euglycemia. Then, pancreatic β cells progressively
decrease secretion function, resulting in the development of diabetes mellitus with decreased serum insulin levels.
Accumulating evidences show that insulin resistance is associated with hypertension. However, the mechanisms underlying
hypertension associated with type 2 diabetes mellitus have still unknown. Therefore, to elucidate the mechanisms of
insulin resistance-induced hypertension, we investigated that the effects of hyperinsulinemia or hyperglycemia on vascular
responses mediated by perivascular nerves including sympathetic adrenergic nerves and calcitonin gene-related peptide
(CGRP)-containing nerves (CGRPergic nerves). In this article, we show evidence that insulin resistance-induced hypertension
could be resulted from increased density and function of sympathetic nerve, and decreased density and function of
CGRPergic nerves. Furthermore, our findings provide a new insight into the research of therapeutic drugs for insulin resistance-
Keywords: Insulin resistance, hypertension, hyperinsulinemia, hyperglycemia, perivascular CGRPergic nerves, perivascular
sympathetic adrenergic nerves.
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