Dietary Regulation of Nuclear Receptors in Obesity-Related Metabolic Syndrome

In Western culture, excess visceral fat accumulation or obesity has reached epidemic proportions, resulting in metabolic syndrome. However, more than 10 years of research has shown that adipocytes also function as endocrine cells that release various bioactive substances, so called “adipocytokines or adipokines”, that play a major role in the regulation of food intake, insulin sensitivity, energy metabolism, and the vascular microenvironment. Adiponectin, an adipocytokine, is considered to improve insulin sensitivity. Recently, monocyte chemoattractant protein (MCP)-1 has been reported to be a novel adipocytokine involved in the development of obesity-associated insulin resistance and atherosclerosis. Nuclear receptors, especially peroxisome proliferator-activated receptor-α (PPARα) and PPARγ are ligand-activated transcription factors that regulate the metabolism of glucose and lipids. PPARγ is strongly expressed in adipocytes and plays a significant role in the transcriptional activation of adipocytokines including adiponectin. PPARα, another PPAR isoform, is involved in the control of lipid metabolism in the liver and skeletal muscle. PPARα activation causes lipid clearance via β-oxidation enhancement. We showed that various dietary terpenoids and other natural ingredients regulate the transcription of PPAR target genes, induces the expression and secretion of adiponectin, and inhibits those of MCP-1 in adipocytes and β-oxidation in liver. These findings indicate that dietary factor acts as an agonist of PPARs and is a valuable medical and food component for the gradual improvement of metabolic syndrome.

並列關鍵字

obesity ； nuclear receptors ； metabolic syndrome ； adipocytokine ； PPARs

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