Ingested cocoa can prevent high-fat diet-induced obesity by regulating the expression of genes for fatty acid metabolism.

According to recent research from Japan, "We previously found that ingested cocoa decreased visceral adipose tissue weight in rats. To elucidate the molecular mechanisms of that effect, we carried out experiments aimed at analyzing biochemical parameters and gene expression profiles. Rats were fed either of two high-fat diets, differing only in supplementation with real or mimetic cocoa. On day 21, body weights, mesenteric, white adipose tissue weights, and concentrations of serum triacylglycerol were measured.

"To investigate the molecular mechanisms underlying the effects of cocoa on lipid metabolism and triacylglycerol accumulation, we examined gene expression profiles in the liver and mesenteric white adipose tissues using the GeneChip microarray system."

"Final body weights and mesenteric white adipose tissue weights were significantly lower in rats fed the real cocoa diet than in those fed the mimetic cocoa diet (p<0.05), and serum triacylglycerol concentrations tended to be lower in rats fed the real cocoa diet (p=0.072)," stated Naoko Matsui and collaborators at Morinaga and Company Ltd. and University of Tokyo.

"DNA microarray analysis showed that cocoa ingestion suppressed the expression of genes for enzymes involved in fatty acid synthesis in liver and white adipose tissues. In white adipose tissue, cocoa ingestion also decreased the expression of genes for fatty acid transport-relating molecules, whereas it up-regulated the expression of genes for uncoupling protein-2 as a thermogenesis factor."

The researchers concluded, "Ingested cocoa can prevent high-fat diet-induced obesity by modulating lipid metabolism, especially by decreasing fatty acid synthesis and transport systems, and enhancement of part of the thermogenesis mechanism in liver and white adipose tissue."

Matsui and associates published their study in Nutrition (“Ingested Cocoa Can Prevent High-fat Diet-induced Obesity by Regulating the Expression of Genes for Fatty Acid Metabolism.” Nutrition, 2005;21(5):594-601).

For additional information, contact Naoko Matsui, Research Institute, Morinaga and Company, Ltd., Kanagawa, Japan. E-mail: n-matsui-jj@morinaga.co.jp.