SRAS overactivated in animal, human obesity; RAS blockade improves insulin sensitivity
FRIDAY, Nov. 4 (HealthDay News) -- Both the systemic and adipose tissue renin-angiotensin systems (RASs) are associated with obesity and insulin resistance, according to research published online Oct. 31 in Obesity Reviews.
Nishan S. Kalupahana, and Naima Moustaid-Moussa, Ph.D., from the University of Tennessee in Knoxville, reviewed available human and animal studies to summarize the evidence and mechanistic insights on the associations between RAS, obesity, and insulin resistance. Special emphasis was given to the role of adipose tissue RAS in the pathogenesis of obesity-related metabolic derangements.
The investigators found evidence that supported overactivation of both systemic and adipose RAS in animal and human obesity. RAS blockade through angiotensin II (Ang II) type 1 (AT1) blockers (ARB), and AT1 converting enzyme inhibitors (ACE1) improves insulin sensitivity and glycemic control. Adipose tissue renin, ACE, and AT1 expression increased in human obesity models, but there were discrepancies in regulation of these RAS components in animal models. Adipose RAS overactivation led to adiposity and overweight, but RAS blockade by ARB or ACE1 decreased adiposity in animals only. Skeletal muscle insulin resistance was induced by AngII in a reduced nicotinamide adenine dinucleotide phosphate oxidase-, AT1-, and NF-κB-dependent manner. Ang II increased glucose production, and induced insulin resistance in the liver. In adipose tissue, Ang II increased pro-inflammatory cytokine secretion, and promoted lipid deposition by promoting lipogenesis and inhibiting lipolysis. Evidence suggested a role for Ang II in adipogenesis inhibition.
"Overall, both systemic and adipose tissue RAS are associated with obesity and insulin resistance and could be a potential causal link for the metabolic derangements in obesity," the authors write.
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