AMPK: Central Regulator of Glucose and Lipid Metabolism

Mihaylova, Maria M.; Shaw, Reuben J.

doi:10.1002/9780470747919.ch35

Cited by 1 publication

(2 citation statements)

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“…AMPK is a metabolic energy sensor that plays a major role in regulating glucose and lipid metabolism (Mihaylova & Shaw, 2009). Moreover, AMPK activation decreases expression of SREBP‐1c and its downstream lipogenic enzymes resulting in decreased synthesis of cholesterol and TG, and lower lipid accumulation in the liver (Yang, Alkayed, Hurn, & Kirsch, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…In mammals, AMP‐activated protein kinase (AMPK) is a sensor of intracellular energy state that restores energy balance during metabolic stress both at the cellular and physiological levels (Mihaylova & Shaw, 2009). AMPK activation induces ATP production and fatty acid oxidation and inhibits ATP‐consuming pathways such as lipogenesis and gluconeogenesis (Carling, Thornton, Woods, & Sanders, 2012; Kim et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

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Puerarin attenuates hepatic steatosis via G‐protein‐coupled estrogen receptor‐mediated calcium and SIRT1 signaling pathways

Pham

Lee

Jin

et al. 2022

Phytotherapy Research

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Puerarin, the major bioactive ingredient isolated from the root of Pueraria lobata (Willd.), attenuates body weight gain and reduces lipid levels in high‐fat diet‐induced obese mice; however, the underlying mechanism responsible for regulating lipid metabolism remains unclear. This study investigated the molecular mechanism(s) underlying the role of puerarin in regulating lipogenesis and lipolysis in human HepG2 cells. In this study, puerarin strongly inhibited the expression of fatty acid synthase (FASN) and sterol regulatory element binding protein 1c (SREBP‐1c). Moreover, puerarin significantly induced the expression of adipose triglyceride lipase (ATGL), which is responsible for triacylglycerol hydrolase activity in cells. Puerarin enhanced 5′ AMP‐activated protein kinase (AMPK) activity, which is a central regulator of hepatic lipid metabolism. Furthermore, this AMPK activation could be mediated by sirtuin 1 (SIRT1) and calcium signaling pathways involved in G protein‐coupled estrogen receptor (GPER) signaling. GPER blockage significantly reversed the effect of puerarin on lipid accumulation and the related signaling pathways. Docking studies showed that puerarin could bind in the GPER in a similar manner as GPER agonist G1. Our results suggest that puerarin can improve hepatic steatosis by activating GPER; it’s signaling cascade sequentially induced calcium and SIRT1 signaling pathways. Thus, puerarin may be a potential therapeutic agent for the treatment of non‐alcoholic fatty liver disease.

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Section: Discussionmentioning

confidence: 99%