Abstract
BackgroundHepatic metabolic derangements are key components in the development of fatty liver disease. AMP-activated protein kinase (AMPK) plays a central role in controlling hepatic lipid metabolism through modulating the downstream acetyl CoA carboxylase (ACC) and carnitine palmitoyl transferase 1 (CPT-1) pathway. In this study, cyanidin-3-O-β-glucoside (Cy-3-g), a typical anthocyanin pigment was used to examine its effects on AMPK activation and fatty acid metabolism in human HepG2 hepatocytes.ResultsAnthocyanin Cy-3-g increased cellular AMPK activity in a calmodulin kinase kinase dependent manner. Furthermore, Cy-3-g substantially induced AMPK downstream target ACC phosphorylation and inactivation, and then decreased malonyl CoA contents, leading to stimulation of CPT-1 expression and significant increase of fatty acid oxidation in HepG2 cells. These effects of Cy-3-g are largely abolished by pharmacological and genetic inhibition of AMPK.ConclusionThis study demonstrates that Cy-3-g regulates hepatic lipid homeostasis via an AMPK-dependent signaling pathway. Targeting AMPK activation by anthocyanin may represent a promising approach for the prevention and treatment of obesity-related nonalcoholic fatty liver disease.
Highlights
Hepatic metabolic derangements are key components in the development of fatty liver disease
Anthocyanin induces AMP-activated protein kinase (AMPK) activation in HepG2 cells To assess the impact of anthocyanin on AMPK activation, the human HepG2 cells were treated with Cy-3-g of 1~100 μM or with an AMPK activator-aminoimidazole-4-carboxamide 1-ribofuranoside (AICAR) (1 mM) for 1 h, respectively
Anthocyanin suppresses acetyl CoA carboxylase (ACC) activity, decreases malonyl CoA contents and stimulates carnitine palmitoyl transferase 1 (CPT-1) expression in HepG2 cells To determine whether AMPK activation affects its downstream target proteins, we examined the activity of ACC, a key enzyme in the regulation of fatty acid metabolism [5]
Summary
Hepatic metabolic derangements are key components in the development of fatty liver disease. AMP-activated protein kinase (AMPK) plays a central role in controlling hepatic lipid metabolism through modulating the downstream acetyl CoA carboxylase (ACC) and carnitine palmitoyl transferase 1 (CPT-1) pathway. Nonalcoholic fatty liver disease (NAFLD) is a serious consequence of obesity, increasing the risk of liver cancer or cirrhosis [1]. The origin of this disease is unknown and probably multifactorial. AMP-activated protein kinase (AMPK) is a key sensor of cellular energy status and it is recognized as a Anthocyanins are naturally occurring polyphenolic compounds in the plant foods and widely distributed in fruits, vegetables, and pigmented cereals, suggesting that we can ingest significant amounts of anthocyanins from plant-based daily diets [6]. The molecular mechanism under this action remains unknown and needs further investigation in cells
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