Barley sprout extracts reduce hepatic lipid accumulation in ethanol-fed mice by activating hepatic AMP-activated protein kinase

Kim, Yeon Ji; Hwang, Su Hyeon; Jia, Yongyi; Seo, Woo Duck; Lee, Sung Joon

doi:10.1016/j.foodres.2017.08.068

Cited by 17 publications

(14 citation statements)

References 34 publications

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“…The AMPK pathway is important for lipid metabolism. A number of studies have confirmed that inhibition of the AMPK pathway can cause fat accumulation in the liver (Boudaba et al, 2018;Esquejo et al, 2018;Fentz et al, 2015;Kim et al, 2017;Woods et al, 2017;Xi et al, 2015;York et al, 2017;Zadra et al, 2014). Moreover, activation of the AMPK pathway can also inhibit the growth of prostate cancer by inhibiting lipid synthesis (Zadra et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

S100A16, a novel lipogenesis promoting factor in livers of mice and hepatocytes in vitro

Kan

Zhao

Lü

et al. 2019

Journal Cellular Physiology

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To investigate the role of S100 calcium-binding protein A16 (S100A16) in hepatic lipid metabolism, S100a16 transgenic, S100a16 knockdown, and wildtype C57BL/6 mice were fed either a high-fat diet (HFD) or normal-fat diet (NFD) for 16 weeks. The results showed that for HFD-fed mice, S100a16 transgenic mice showed significantly more severe fatty liver than other HFD-fed mice, with a significant increase in serum triglyceride (TG) concentration, with more and larger lipid droplets in the liver, whereas S100a16 knockdown mice were completely opposite, with liver fat lesions and TG serological changes being the mildest; for NFD-fed mice, liver fat accumulation and serum TG concentrations were significantly lower than those fed HFD, and no significant lipid droplets were found in the liver. Further, we found that calmodulin (CaM) interacts with S100A16, a member of the AMP-activated protein kinase (AMPK) pathway. Our research found that S100A16 regulates the AMPK pathway-associated protein by interacting with CaM to regulate liver lipid synthesis. S100A16 regulates liver lipid metabolism through the CaM/CAMKK2/AMPK pathway. Overexpression of S100A16 promotes the deterioration of fatty liver induced by HFD, and low expression of S100A16 can attenuate fatty liver. K E Y W O R D Scalmodulin, fatty liver, S100 calcium-binding protein A16

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Section: Discussionmentioning

confidence: 99%

S100A16, a novel lipogenesis promoting factor in livers of mice and hepatocytes in vitro

Kan

Zhao

Lü

et al. 2019

Journal Cellular Physiology

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“…Liver is the central organ of lipid metabolism that maintains balance between lipid availability and lipid disposal [19]. Long-term ethanol consumption, infection or other specific etiologies might induce hepatic lipid accumulation [20-22]. Chen et al reported that intraperitoneal injections of LPS for 24h was able to increase the liver weight and hepatic TG contents in CD-1 mice [23].…”

Section: Discussionmentioning

confidence: 99%

AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection

Fang

Wang

Song

et al. 2018

Aging

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To investigate the different effects of acute pulmonary infection induced by Escherichia coli (E. coli) on lipid metabolism between diet-induced obesity (DIO, fed with high-fat diet) mice and lean mice. A total of 180 ICR mice were selected to be challenged intranasally with phosphate-buffered saline or 109 CFUs/mL of E. coli, and the body character indexes, biochemical indexes and expressions of genes and proteins involved in lipid metabolism were examined pre- and post-infection. Results revealed that, before infection, DIO mice had significantly higher body weight, adipose and liver indexes, free fatty acid and triglyceride contents than lean mice. After infection, increased free fatty acid and triglyceride contents, increased expressions of resistin, SREBP-1c, ACC1, FAS and SCD-1, and declined PPARα, CPT-1α expressions and AMPKα phosphorylation were detected in the infected group, while the change rates were more serious in the lean mice than the DIO mice. The above-mentioned findings verified that, after being infected with E. coli, hepatic lipid metabolism disorder was aggravated by activating SREBP-1c related lipid synthesis pathway and inhibiting PPARα related fatty acid oxidation pathway. However, infection-induced lipid metabolic disorders was slighter in the DIO mice than the lean mice through AMPKα pathway.

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“…In the in vitro experiment of hepatocytes exposed to ethanol, dihydroquercetin was found to significantly increase the activity and phosphorylation of LKB1 and AMPK to inhibit the expression of ACC and SREBP-1c, thereby inhibiting lipid production, promoting fatty acid oxidation and finally reducing fat accumulation ( Zhang et al, 2018 ). In the in vivo experiment of mice exposed to ethanol, Kim et al (2017) found that saponin, an active compound in barley malt extract, could significantly enhance AMPK activity in mice, which in turn regulated target proteins related to lipid metabolism through phosphorylation, and directly inhibit fatty acid synthesis and promote fatty acid oxidation ( Kim et al, 2017 ). It could also degrade the lipid droplets accumulated in hepatocytes by enhancing autophagy, and finally reduce hepatic qualitative change and improve ALFD.…”

Section: Research Status Of Fatty Liver Disease Treatment Drugsmentioning

confidence: 99%

The AMPK pathway in fatty liver disease

et al. 2022

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Lipid metabolism disorders are the primary causes for the occurrence and progression of various liver diseases, including non-alcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease (AFLD) caused by a high-fat diet and ethanol. AMPK signaling pathway plays an important role in ameliorating lipid metabolism disorders. Progressive research has clarified that AMPK signal axes are involved in the prevention and reduction of liver injury. Upregulation of AMK can alleviate FLD in mice induced by alcohol or insulin resistance, type 2 diabetes, and obesity, and most natural AMPK agonists can regulate lipid metabolism, inflammation, and oxidative stress in hepatocytes, consequently regulating FLD in mice. In NAFLD and AFLD, increasing the activity of AMPK can inhibit the synthesis of fatty acids and cholesterol by down-regulating the expression of adipogenesis gene (FAS, SREBP-1c, ACC and HMGCR); Simultaneously, by increasing the expression of fatty acid oxidation and lipid decomposition genes (CPT1, PGC1, and HSL, ATGL) involved in fatty acid oxidation and lipid decomposition, the body’s natural lipid balance can be maintained. At present, some AMPK activators are thought to be beneficial during therapeutic treatment. Therefore, activation of AMPK signaling pathway is a potential therapeutic target for disorders of the liver. We summarized the most recent research on the role of the AMPK pathway in FLD in this review. Simultaneously, we performed a detailed description of each signaling axis of the AMPK pathway, as well as a discussion of its mechanism of action and therapeutic significance.

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Barley sprout extracts reduce hepatic lipid accumulation in ethanol-fed mice by activating hepatic AMP-activated protein kinase

Cited by 17 publications

References 34 publications

S100A16, a novel lipogenesis promoting factor in livers of mice and hepatocytes in vitro

S100A16, a novel lipogenesis promoting factor in livers of mice and hepatocytes in vitro

AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection

The AMPK pathway in fatty liver disease

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