4.7 Article

(-)-Hydroxycitric acid regulates energy metabolism by activation of AMPK-PGC1α-NRF1 signal pathway in primary chicken hepatocytes

期刊

LIFE SCIENCES
卷 254, 期 -, 页码 -

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2020.117785

关键词

(-)-Hydroxycitric acid; AMPK signaling pathway; Glucose and lipid metabolism; Chicken hepatocytes

资金

  1. National Natural Science Foundation of China [31572483]
  2. Fundamental Research Funds for the Central Universities [KYDZ201901]
  3. Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
  4. Postgraduate Research and Practice Innovation Program of Jiangsu Province [KYCX18_0715]

向作者/读者索取更多资源

As the most important bioactive substance in Garcinia cambogia, (-)-hydroxycitric acid (HCA) is widely used in food additives to regulate obesity and diabetes in animals or humans, while the mechanism is poorly understood. The purpose of this study was to elucidate the regulatory effect and mechanism of (-)-HCA in regulating glucose and lipid metabolism in chicken primary hepatocytes. The results showed that (-)-HCA obviously decreased triglyceride content through inhibiting the fatty acid synthase protein level, and enhancing the protein level of phosphorylated acetyl CoA carboxylase, enoyl coenzyme A hydratase short chain 1 and carnitine palmitoyltransferase 1A in hepatocytes. Moreover, (-)-HCA markedly enhanced the protein level of phosphofructokinase-1, pyruvate dehydrogenase, succinate dehydrogenase A and complex IV, and which led to the enhancing of glucose uptake and catabolism in hepatocytes. Importantly, the regulation of (-)-HCA on these key factors associated with lipid and glucose metabolism in hepatocytes was mainly achieved through activation of AMP-activated protein kinase/peroxisome proliferator-activated receptor gamma coactivator 1 alpha-nuclear respiratory factor 1 signaling pathway. These results convincingly demonstrated the mechanism of (-)-HCA's regulating on glucose and lipid metabolism, and provided a strategy in prevention of diseases associated with glycolipid metabolic abnormalities in animals, even in humans.

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