THE ADIPOSE-TISSUE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
Overfeeding of rodents leads to increased local formation of angiotensin II due to increased secretion of angiotensinogen form adipocyted. Angiotensin II acts as an antiadipogenic substance in human plasma angiotensinogen levels than changes within the single adipocyte. However, as increased local formation of angiotensin II in adipose tissue may be increasedespecially inobse hypertensive subjects, a contribution of the adipose-tissue renin-angiotensin system to the development of insulin resistance and hypertension is conceivable in humans. Insulin resistance may be aggravated by the inhibition of preadipocyte recruitment, which results in the redistribution of triglycerides to the liver and skeletal muscle, and blood pressure may be influenced by local formation of angiotensin II in perivascular adipose tissue. Although the mechanisms are still speculative, the beneficial effecs of ACE-inhibition and angiotensin-receptor blockade on the development of type 2 diabetes. Suggest a pathophysiological role of the adipose-tissue renin-angiotensin system in the metabolic syndrome.
Overfeeding of rodents leads to increased local formation of angiotensin II due to increased secretion of angiotensinogen form adipocyted. Angiotensin II acts as an antiadipogenic substance in human plasma angiotensinogen levels than changes within the single adipocyte. However, as increased local formation of angiotensin II in adipose tissue may be increasedespecially inobse hypertensive subjects, a contribution of the adipose-tissue renin-angiotensin system to the development of insulin resistance and hypertension is conceivable in humans. Insulin resistance may be aggravated by the inhibition of preadipocyte recruitment, which results in the redistribution of triglycerides to the liver and skeletal muscle, and blood pressure may be influenced by local formation of angiotensin II in perivascular adipose tissue. Although the mechanisms are still speculative, the beneficial effecs of ACE-inhibition and angiotensin-receptor blockade on the development of type 2 diabetes. Suggest a pathophysiological role of the adipose-tissue renin-angiotensin system in the metabolic syndrome.
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