There is growing evidence that inhibition of the RAS system by either ACE inhibition or ATI receptor antagonism can increase insulin sensitivity and glucose utilization. Studies using euglycemic hyperinsulinemic clamps have shown that ACE inhibitor treatment improves insulin sensitivity in most (136-140), but not all (141,142) individuals with hypertension, obesity, and/or type 2 diabetes. Similarly, although ATI antagonism has been reported to improve muscle sympathetic nerve activity and insulin sensitivity in obese hypertensive subjects (143) and increase basal and insulin-stimulated glucose oxidation in normotensive individuals with type 1 diabetes (144), other clinical studies have not observed improvement on insulin sensitivity and glucose homeostasis following treatment with ATI receptor antagonists (139,145,146).
In experimental rodent models, ACE inhibition has been shown to enhance glucose transport skeletal muscle and adipose tissue in insulin-resistant obese Zucker rats and spontaneously hypertensive rats (147-150). Angiotensin ATI receptor antagonism has been shown to improve insulin sensitivity and glucose uptake in skeletal muscle of normotensive diabetic KK-Ay mice (151), partially reduce insulin resistance in Wistar fatty rats (114), and increase 2DG uptake and GLUT-4 expression in skeletal muscle in obese Zucker rats (152). Because insulin resistance and the metabolic syndrome accelerate CVD (153) inhibition of the RAS may improve cardiovascular outcomes, in part, by increasing insulin sensitivity and improving metabolic control.
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Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...