Short-chain fatty acids in diet stimulate fat utilization
Gijs den Besten, Ph.D., of the University of Groningen in the Netherlands, and colleagues compared a high-fat semisynthetic diet, the SCFA diet, and a normal-fat diet (control group) in mice.
The researchers found that, in mice, dietary supplementation with SCFAs prevented and reversed metabolic abnormalities induced by a high-fat diet by decreasing PPARγ expression and activity. As a result, expression of mitochondrial uncoupling protein 2 was increased and the AMP/ATP ratio was raised, stimulating oxidative metabolism in liver and adipose tissue via AMP-activated protein kinase. In mice with adipose-specific disruption of PPARγ, SCFA-induced reduction in body weight and stimulation of insulin sensitivity were absent. In mice lacking hepatic PPARγ, SCFA-induced reduction of hepatic steatosis was absent.
"These results demonstrate that adipose and hepatic PPARγ are critical mediators of the beneficial effects of SCFA on the metabolic syndrome, with clearly distinct and complementary roles," the authors write. "Our findings indicate that SCFAs may be used therapeutically as cheap and selective PPARγ modulators."
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