Prevention mechanisms of glucose intolerance and obesity by cacao liquor procyanidin extract in high-fat diet-fed C57BL/6 mice
► Cacao liquor procyanidins (CLPrs) activate AMPKα in high-fat diet-fed mice. ► CLPr promotes GLUT4 translocation in skeletal muscle and brown adipose tissue. ► CLPr induces the expression of UCPs and PGC-1α in muscle, liver and adipose tissue. ► CLPr increases the secretion of adiponectin from whit...
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Veröffentlicht in: | Archives of biochemistry and biophysics 2012-11, Vol.527 (2), p.95-104 |
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Sprache: | eng |
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Zusammenfassung: | ► Cacao liquor procyanidins (CLPrs) activate AMPKα in high-fat diet-fed mice. ► CLPr promotes GLUT4 translocation in skeletal muscle and brown adipose tissue. ► CLPr induces the expression of UCPs and PGC-1α in muscle, liver and adipose tissue. ► CLPr increases the secretion of adiponectin from white adipose tissue. ► These effects of CLPr are involved in the prevention of hyperglycemia and obesity.
In this study, we investigated whether cacao liquor procyanidin (CLPr) extract, which consists of 4.3% catechin, 6.1% epicatechin, 39.4% procyanidins and others, ameliorated hyperglycemia and obesity in C57BL/6 mice fed a control or high-fat diet for 13weeks. CLPr suppressed high-fat diet-induced hyperglycemia, glucose intolerance and fat accumulation in white adipose tissue. CLPr also promoted translocation of glucose transporter 4 (GLUT4) and phosphorylation of AMP-activated protein kinase α (AMPKα) in the plasma membrane of skeletal muscle and brown adipose tissue. Phosphorylation of AMPKα was also enhanced in the liver and white adipose tissue. CLPr up-regulated the gene and protein expression levels of uncoupling protein (UCP)-1 in brown adipose tissue and UCP-3 in skeletal muscle. These results indicate that CLPr is a beneficial food material for the prevention of hyperglycemia and obesity. Activation of AMPKα, translocation of GLUT4 and up-regulation of UCP expression in skeletal muscle and adipose tissue are involved in the molecular mechanisms by which CLPr prevents hyperglycemia and obesity. |
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ISSN: | 0003-9861 1096-0384 |
DOI: | 10.1016/j.abb.2012.03.018 |