Hindsight: Does the Adipose Tissue Renin Angiotensin System



Gérard P. Ailhaud,  Professor of Biochemistry, Université de Nice, France

Gérard P. Ailhaud, Professor of Biochemistry, Université de Nice, France

Continuing our work on the role of the renin angiontensin system in fat tissue, in 2003, we published a review on its possible role in the metabolic syndrome in the International Journal of Biochemistry and Cell Biology.

Together with our French colleagues Gérard Ailhaud, Michèle Teboul, and Florence Massiéra, from the Centre de Biochimie (6543 CNRS), Faculté des Sciences, in Nice, we reviewed the available literature in the context of our findings.

It was clear that overfeeding of rodents lead to increased local formation of angiotensin II due to increased secretion of angiotensinogen from adipocytes.

It was also evident that while angiotensin II promotes adipocyte growth and preadipocyte recruitment, increased secretion of angiotensinogen from adipocytes also directly contributes to the close relationship between adipose-tissue mass and blood pressure in mice.

On the other hand, angiotensin II acts as an antiadipogenic substance in human adipose tissue, and the total increase in adipose-tissue mass may be more important in determining human plasma angiotensinogen levels than changes within the single adipocyte.

However, as increased local formation of angiotensin II in adipose tissue may be increased especially in obese hypertensive subjects, a contribution of the adipose-tissue renin-angiotensin system to the development of insulin resistance and hypertension is conceivable in humans, but not yet proven.

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.

Thus, although the mechanisms were still speculative, we proposed that the beneficial effects of ACE-inhibition and angiotensin-receptor blockade on the development of type 2 diabetes in large clinical trials may well suggest a pathophysiological role of the adipose-tissue renin-angiotensin system in the metabolic syndrome.

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