Nordihydroguaiaretic acid protects against high-fat diet-induced fatty liver by activating AMP-activated protein kinase in obese mice

Lee, Myoung Su; Kim, Dae-Young; Jo, Keunae; Hwang, Jae Kwan

doi:10.1016/j.bbrc.2010.09.016

Cited by 41 publications

(20 citation statements)

References 18 publications

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“…HMGCR is phosphorylated by AMPK as a precursor of cholesterol biosynthesis. Recent studies have demonstrated that SREBP‐1c regulates lipid metabolism (Kim and Spiegelman, ) by upregulation of FAS, SREBP‐2 inhibits HMGCR in the liver (Engelking et al ., ), and PPARα plays a critical role in hepatic lipid metabolism (Lee et al ., ; Zhou et al ., ) through upregulation of lipid oxidation gene CPT‐1 (Tailleux et al ., ).…”

Section: Discussionmentioning

confidence: 97%

Hovenia Dulcis Extract Reduces Lipid Accumulation in Oleic Acid‐Induced Steatosis of Hep G2 Cells via Activation of AMPK and PPARα/CPT‐1 Pathway and in Acute Hyperlipidemia Mouse Model

Kim

Woo

Park

et al. 2016

Phytotherapy Research

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Hovenia dulcis Thunb. (HDT) was known to have anti-fatigue, anti-diabetes, neuroprotective, and hepatoprotective effects. In the present study, the anti-fatty liver mechanism of HDT was elucidated in oleic acid (OA)-treated Hep G2 cells and acute hyperlipidemia mouse model using Triton WR-1339. Here, HDT activated p-AMP-activated protein kinase (p-AMPK), proliferator activated receptor-α, carnitine palmitoyltransferase and also inhibited the expression of lipogenesis and cholesterol synthesis proteins, such as 3-hydroxy-3-methylglutaryl-CoA reductase, sterol regulatory element binding protein-1c, SREBP-2, and fatty acid synthase in OA-treated Hep G2 cells. Conversely, AMPK inhibitor compound C blocked the anti-fatty liver effect of HDT to induce AMPK phosphorylation and decrease 3-hydroxy-3-methylglutaryl-CoA reductase and lipid accumulation by oil red O staining in OA-treated Hep G2 cells. Additionally, HDT pretreatment protected against the increase of serum total cholesterol, triglyceride, low-density lipoprotein cholesterol and phospholipid in an acute hyperlipidemia mouse model with enhancement of glutathione reductase, glutathione peroxidase, superoxide dismutase, and catalase activities. Taken together, HDT inhibits OA-induced hepatic lipid accumulation via activation of AMPK and proliferator activated receptor-α/carnitine palmitoyltransferase signaling and enhancement of antioxidant activity as a potent candidate for nonalcoholic fatty liver disease and hyperlipidemia. Copyright © 2016 John Wiley & Sons, Ltd.

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Section: Discussionmentioning

confidence: 97%

Hovenia Dulcis Extract Reduces Lipid Accumulation in Oleic Acid‐Induced Steatosis of Hep G2 Cells via Activation of AMPK and PPARα/CPT‐1 Pathway and in Acute Hyperlipidemia Mouse Model

Kim

Woo

Park

et al. 2016

Phytotherapy Research

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“…AMPK can indirectly regulate PPARα, but the mechanism of correlation is not clear. Studies have shown that pretreatment with AMPK inhibitor Compound C attenuates the effects of lipid accumulation and expression of PPARa proteins, 42 which suggest that PPARα is a downstream gene of AMPK. Inhibition of AMPK activity leads to reduced expression of PPARα.…”

Section: Discussionmentioning

confidence: 99%

<p>Radix Polygoni Multiflori and Its Main Component Emodin Attenuate Non-Alcoholic Fatty Liver Disease in Zebrafish by Regulation of AMPK Signaling Pathway</p>

Gong²,

Wang³

et al. 2020

DDDT

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Purpose: Nonalcoholic fatty liver disease (NAFLD) has become a predictor of death in many diseases. This study was carried out to investigate the therapeutic effect of Radix Polygoni Multiflori Preparata (RPMP) and its main component emodin on egg yolk powderinduced NAFLD in zebrafish. Further investigation was performed to explore whether emodin was the main component of RPMP for the treatment of NAFLD as well as the underlying therapeutic mechanism of RPMP and emodin. Methods: Zebrafish were divided into control group, egg yolk powder group, RPMP group and emodin group. The obesity of zebrafish was evaluated by body weight, body length and BMI. The content of lipid was detected by triglyceride (TG), total cholesterol (TC) reagent kit and the fatty acid was detected by nonesterified free fatty acids (NEFA) reagent kit. HE staining was used to detect the histological structure of liver. Whole-mount Oil red O staining and Frozen oil red O staining were carried out to investigate the lipid accumulation in liver. KEGG and STRING databases were performed to analyze the potential role of AMPK between insulin resistance (IR) and fatty acid oxidation. Western blot and RT-qPCR were carried out for mechanism research. Results: RPMP and emodin significantly reduced zebrafish weight, body length and BMI. Both RPMP and emodin treatment could reduce the lipid deposition in zebrafish liver. RPMP significantly reduced the content of TG. However, emodin significantly reduced the contents of TG, TC and NEFA in zebrafish with NAFLD. The protein interaction network indicated that AMPK participated in both IR and fatty acid oxidation. Further investigation indicated that RPMP and emodin reduced hepatic lipogenesis via up-regulating the expressions of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT2), amp-activated protein kinase alpha (AMPKα), proliferator-activated receptor alpha (PPARα), carnitine palmitoyl transferase 1a (CPT-1a) and acyl-coenzyme A oxidase 1 (ACOX1). Conclusion: These findings suggest that emodin is the main component of RPMP for the treatment of NAFLD, which is closely related to the regulation of AMPK signaling pathway which increases IR and fatty acid oxidation.

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“…Many animal studies (Tandy et al, 2010;Lee, Kim, Jo, & Hwang, 2010;Liu, Hung, & Huang, 1995) have demonstrated that prolonged administration of a HF and high-cholesterol diet accelerates the synthesis of TGs, inhibits the metabolism of fatty acids, and diminishes the secretion of TGs from the liver into blood by decreasing the β-oxidation of fatty acids. This leads to the accumulation of excess TGs within the liver.…”

Section: Discussionmentioning

confidence: 99%

Anti-fat deposition and antioxidant effects of haw pectic oligosaccharide in the liver of high-fat-fed mice

Liu

Dong

et al. 2013

CyTA - Journal of Food

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(2014) Antifat deposition and antioxidant effects of haw pectic oligosaccharide in the liver of high-fat-fed mice, CyTA -Journal of Food, 12:1, 27-31, DOI: 10.1080/19476337.2013 To link to this article: https://doi.org/10. 1080/19476337.2013 Pectin and its acidic oligosaccharide derivatives are believed to have many potential applications in the food and pharmaceutical industries.In this article, we have investigated the effects of haw pectic oligosaccharide (HPOS) on hyperlipidemia (HL) and oxidative stress in mice induced by a high-fat diet. The results showed that HPOS significantly suppressed the fat deposition in the liver of HL mice. In addition, it significantly increased superoxide dismutase activity and suppressed the production and accumulation of malondialdehyde in liver. It may also be helpful in normalizing fatty acid metabolism in the liver of mice by altering the proportions of saturated fatty acid and monounsaturated fatty acid. These results reveal that HPOS has potentially beneficial effects against HL and oxidative stress in mice.Keywords: hyperlipidemia; lipid metabolism; fatty liver; fatty acid composition; malondialdehyde Se cree que la pectina y sus derivados oligosacáridos ácidos tienen muchas aplicaciones potenciales en la industria alimentaria y farmacéutica. En este trabajo, investigamos los efectos del oligosacárido péctico de espino chino (HPOS) en la hiperlipidemia (HL) y el estrés oxidativo de ratones inducida por una dieta alta en grasas. Los resultados mostraron que HPOS suprimió de forma significativa la deposición de grasa en el hígado de HL ratones. Además, los HPOS aumentaron significativamente la actividad de la superóxido dismutasa (SOD) y suprimió la producción y acumulación de malondialdehído (MDA) en el hígado. HPOS también pueden ser útiles para normalizar el metabolismo de ácidos grasos en el hígado de los ratones mediante la alteración de las proporciones de ácidos grasos saturados (SFA) y ácidos grasos monoinsaturados (MUFA). Estos resultados revelaron que HPOS tiene efectos potencialmente beneficiosos contra HL y el estrés oxidativo en ratones.

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Nordihydroguaiaretic acid protects against high-fat diet-induced fatty liver by activating AMP-activated protein kinase in obese mice

Cited by 41 publications

References 18 publications

Hovenia Dulcis Extract Reduces Lipid Accumulation in Oleic Acid‐Induced Steatosis of Hep G2 Cells via Activation of AMPK and PPARα/CPT‐1 Pathway and in Acute Hyperlipidemia Mouse Model

Hovenia Dulcis Extract Reduces Lipid Accumulation in Oleic Acid‐Induced Steatosis of Hep G2 Cells via Activation of AMPK and PPARα/CPT‐1 Pathway and in Acute Hyperlipidemia Mouse Model

<p>Radix Polygoni Multiflori and Its Main Component Emodin Attenuate Non-Alcoholic Fatty Liver Disease in Zebrafish by Regulation of AMPK Signaling Pathway</p>

Anti-fat deposition and antioxidant effects of haw pectic oligosaccharide in the liver of high-fat-fed mice

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