Green tomato extract attenuates high-fat-diet-induced obesity through activation of the AMPK pathway in C57BL/6 mice

Choi, Kunhee; younsun, Lee; Shin, Dong‐Mi; Lee, Seung–Hyun; Yoo, Kyo Sang; Lee, Mi Kyeong; Lee, Jae-Hak; Kim, Sun Yeou; Lee, Young Moo; Jiang, Hong; Yun, Young Won; Yoo, Hwan‐Soo

doi:10.1016/j.jnutbio.2012.06.018

Cited by 50 publications

(42 citation statements)

References 35 publications

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“…It was surprising that ginkgolide B could not reduce the TC levels of serum in obese mice [39]. Recent studies demonstrated that more HDL would be able to clear blood cholesterol to decrease the incidence of cardiovascular disease [40].…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

Wang¹,

Liou²,

Wu³

et al. 2018

Oncotarget

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Ginkgolide B is isolated from Ginkgo biloba leaves. It has multiple biological functions, including alleviating lung injury and ischemic stroke in mice and protecting pancreatic beta cells and improving endothelial dysfunction in diabetic mice. Here we sought to determine whether ginkgolide B ameliorates nonalcoholic fatty liver disease (NALFD) in high-fat diet (HFD)-induced obese mice. We also evaluated whether or not ginkgolide B reduces lipid accumulation of hepatocytes in vitro. C57BL/6 mice were fed with HFD and treated with ginkgolide B by intraperitoneal injection twice a week for last 10 weeks of the 14-week HFD feeding period. In addition, HepG2 cells were treated with oleic acid to establish a fatty liver cell model and exposed to various concentrations of ginkgolide B. Ginkgolide B significantly decreased hepatic lipid accumulation and alleviated steatosis in HFD-induced obese mice. It also reduced body weight and epididymal adipose tissue weight. Serum assay results showed that ginkgolide B inhibited leptin, alanine aminotransferase, and aspartate aminotransferase levels and increased HDL levels compared to obese mice. It also decreased fatty acid synthase expression and increased Sirt-1 and phosphorylation of AMP-activated protein kinase α in liver tissue. Furthermore, ginkgolide B significantly inhibited lipid accumulation and expression of adipogenesis-related proteins and increased adipolysis-associated protein expression in hepatocytes in vitro. These results suggest that ginkgolide B is an effective natural compound for alleviating hepatic lipid accumulation and reducing body weight in obese mice. It also ameliorated NALFD in HFD-induced obese mice. www.impactjournals.com/oncotarget/

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Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

Wang¹,

Liou²,

Wu³

et al. 2018

Oncotarget

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“…Lipids were extracted from liver as described by Choi et al [21]. Mouse liver (100 mg) was homogenized in 0.5 ml of 1 M NaCl and then extracted with 3 ml of chloroform/methanol (2:1) plus 0.5 ml of 1 M NaCl.…”

Section: Hepatic Lipid Extraction and Measurementmentioning

confidence: 99%

Sulforaphane attenuates obesity by inhibiting adipogenesis and activating the AMPK pathway in obese mice

Choi

younsun

Kim

et al. 2014

The Journal of Nutritional Biochemistry

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146

107

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“…Green tea extract attenuated hepatic stetosis by inhibiting adipose lipogenesis, restoring hepatic antioxidant defenses, as well as decreasing hepatic lipid peroxidation and inflammatory responses in ob/ob mice [8]. Niacin has also been demonstrated to effectively prevent and reverse experimental hepatic steatosis through decreasing hepatic triglyceride synthesis and lipid peroxidation [9].…”

Section: Introductionmentioning

confidence: 99%

Regressive Effect of Myricetin on Hepatic Steatosis in Mice Fed a High-Fat Diet

Xia

Wang³

et al. 2016

Nutrients

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Myricetin is an effective antioxidant in the treatment of obesity and obesity-related metabolic disorders. The objective of this study was to explore the regressive effect of myricetin on pre-existing hepatic steatosis induced by high-fat diet (HFD). C57BL/6 mice were fed either a standard diet or a HFD for 12 weeks and then half of the mice were treated with myricetin (0.12% in the diet, w/w) while on their respective diets for further 12 weeks. Myricetin treatment significantly alleviated HFD-induced steatosis, decreased hepatic lipid accumulation and thiobarbituric acid reactive substance (TBARS) levels, and increased antioxidative enzyme activities, including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities. Microarray analysis of hepatic gene expression profiles showed that myricetin significantly altered the expression profiles of 177 genes which were involved in 12 biological pathways, including the peroxisome proliferator activated receptor (PPAR) signaling pathway and peroxisome. Further research indicated that myricetin elevated hepatic nuclear Nrf2 translocation, increased the protein expression of heme oxygenase-1 (HO-1) and NAD(P)H quinone dehydrogenase 1 (NQO1), reduced the protein expression of PPARγ, and normalized the expressions of genes that were involved in peroxisome and the PPAR signaling pathway. Our data indicated that myricetin might represent an effective therapeutic agent to treat HFD-induced hepatic steatosis via activating the Nrf2 pathway and the PPAR signaling pathway.

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Green tomato extract attenuates high-fat-diet-induced obesity through activation of the AMPK pathway in C57BL/6 mice

Cited by 50 publications

References 35 publications

WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

Sulforaphane attenuates obesity by inhibiting adipogenesis and activating the AMPK pathway in obese mice

Regressive Effect of Myricetin on Hepatic Steatosis in Mice Fed a High-Fat Diet

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