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

2010 ◽  
Vol 401 (1) ◽  
pp. 92-97 ◽  
Author(s):  
Myoung-Su Lee ◽  
Daeyoung Kim ◽  
Keunae Jo ◽  
Jae-Kwan Hwang
Keyword(s):  
Protein Kinase ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Nordihydroguaiaretic Acid ◽  
Obese Mice ◽  
High Fat ◽  
Amp Activated Protein Kinase

scholarly journals A High-Fat Diet Attenuates Amp-Activated Protein Kinase α1 in Adipocytes to Induce Exosome Shedding and Nonalcoholic Fatty Liver Development in Vivo

2020 ◽  
Author(s):  
Ada Admin ◽  
Chenghui Yan ◽  
Xiaoxiang Tian ◽  
Jiayin Li ◽  
Dan Liu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Kinase ◽  
Fatty Liver ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Liver Development ◽  
High Fat ◽  
Tissue Specific ◽  
Nonalcoholic Fatty Liver ◽  
Amp Activated Protein Kinase

Exosomes are important for intercellular communication, but the role of exosomes in the communication between adipose tissue (<a>AT</a>) and the liver remains unknown. The aim of this study is to determine the contribution of AT-derived exosomes in nonalcoholic fatty liver disease (<a>NAFLD</a>). Exosome components, liver fat content, and liver function were monitored in AT in mice fed a <a>high-fat diet </a>(<a>HFD</a>) or treated with metformin- or GW4869 and with AMP-activated protein kinase (AMPKα1)<i> </i>floxed<i> (Prkaα1</i><sup>fl/fl</sup>/WT), <a><i>Prkaα1</i><sup>-/-</sup></a>, liver tissue-specific <i>Prkaα1</i><sup>-/-</sup>, or AT-specific <i>Prkaα1</i><sup>-/-</sup> modification. In cultured adipocytes and white adipose tissue (WAT), the absence of <a><i>AMPKα1</i></a> increased exosome release and exosomal proteins by elevating <a>tumor susceptibility gene 101 (<i>TSG101</i></a>)-mediated exosome biogenesis. In adipocytes treated with palmitic acid, TSG101 facilitated scavenger receptor class B (CD36) sorting into exosomes. CD36-containing exosomes were then endocytosed by hepatocytes to induce lipid accumulation and inflammation. Consistently, an HFD induced more severe lipid accumulation and cell death in <a><i>Prkaα1</i><sup>-/-</sup> </a>and adipose tissue-specific <i>Prkaα1</i><sup>-/-</sup> mice than in WT and liver-specific <i>Prkaα1</i><sup>-/-</sup> mice. AMPK activation by metformin reduced adipocyte-mediated exosome release and mitigated fatty liver development in WT and liver specific <i>Prkaα1</i><sup>-/-</sup> mice. Moreover, administration of the exosome inhibitor GW4869 blocked exosome secretion and alleviated HFD-induced fatty livers in <i>Prkaα1</i><sup>-/-</sup> and adipocyte-specific <i>Prkaα1</i><sup>-/-</sup> mice. We conclude that HFD-mediated AMPKα1 inhibition promotes NAFLD by increasing numbers of AT C<a>D36</a>-containing exosomes.

scholarly journals Antiobesity Effect ofAstilbe chinensisFranch. et Savet. Extract through Regulation of Adipogenesis and AMP-Activated Protein Kinase Pathways in 3T3-L1 Adipocyte and High-Fat Diet-Induced C57BL/6N Obese Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Xian Hua Zhang ◽  
Zhiqiang Wang ◽  
Bueom-Goo Kang ◽  
Seung Hwan Hwang ◽  
Jae-Young Lee ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Lipid Content ◽  
High Fat Diet ◽  
Binding Protein ◽  
Resistance Index ◽  
Nonesterified Fatty Acid ◽  
Dependent Manner ◽  
Obese Mice ◽  
High Fat ◽  
Amp Activated Protein Kinase

Astilbe chinensisFranch. et Savat. (AC) has been used in traditional medicine for the treatment of chronic bronchitis, arthralgia, and gastralgia. In this study, we investigated the antiobesity effect of AC extract on 3T3-L1 preadipocytes and high-fat-diet-fed C57BL/6N obese mice. We found that AC extracts dramatically decreased the lipid content of 3T3-L1 cells in a concentration-dependent manner without cytotoxicity. The action mechanism of AC extract was demonstrated to be the inhibition of lipid accumulation and dose-dependent decrease in the expression of CCAAT/enhancer-binding proteinα(C/EBPα), peroxisome proliferator-activated receptor-γ(PPAR-γ), and sterol regulatory element-binding protein 1 (SREBP1). Furthermore, AC extract increased the mitochondrial phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC), mitochondrial biogenesis, and lipolysis-related factors. In amice model of high-fat-diet-induced obesity, the mice administered AC extract experienced significant decrease of 64% in weight gain, 55% in insulin resistance index, 22% in plasma triglycerides (TG), 56% in total cholesterol (TC), and 21% in nonesterified fatty acid (NEFA) levels compared with those in the high-fat diet-fed control mice. Collectively, these results indicated that AC extract exerted antiobesogenic activity through the modulation of the AMPK signaling pathway, inhibition of adipogenesis, decreased lipid content, and reduced adipocyte size.

Protective effect of resveratrol derivatives on high-fat diet induced fatty liver by activating AMP-activated protein kinase

2014 ◽  
Vol 37 (9) ◽  
pp. 1169-1176 ◽  
Author(s):  
You-Jin Choi ◽  
Hyo-Ryung Suh ◽  
Yujin Yoon ◽  
Kyung-Jin Lee ◽  
Dong Gwang Kim ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Fatty Liver ◽  
Protective Effect ◽  
High Fat Diet ◽  
High Fat ◽  
Resveratrol Derivatives ◽  
Amp Activated Protein Kinase

scholarly journals A High-Fat Diet Attenuates Amp-Activated Protein Kinase α1 in Adipocytes to Induce Exosome Shedding and Nonalcoholic Fatty Liver Development in Vivo

2020 ◽  
Author(s):  
Ada Admin ◽  
Chenghui Yan ◽  
Xiaoxiang Tian ◽  
Jiayin Li ◽  
Dan Liu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Kinase ◽  
Fatty Liver ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Liver Development ◽  
High Fat ◽  
Tissue Specific ◽  
Nonalcoholic Fatty Liver ◽  
Amp Activated Protein Kinase

Exosomes are important for intercellular communication, but the role of exosomes in the communication between adipose tissue (<a>AT</a>) and the liver remains unknown. The aim of this study is to determine the contribution of AT-derived exosomes in nonalcoholic fatty liver disease (<a>NAFLD</a>). Exosome components, liver fat content, and liver function were monitored in AT in mice fed a <a>high-fat diet </a>(<a>HFD</a>) or treated with metformin- or GW4869 and with AMP-activated protein kinase (AMPKα1)<i> </i>floxed<i> (Prkaα1</i><sup>fl/fl</sup>/WT), <a><i>Prkaα1</i><sup>-/-</sup></a>, liver tissue-specific <i>Prkaα1</i><sup>-/-</sup>, or AT-specific <i>Prkaα1</i><sup>-/-</sup> modification. In cultured adipocytes and white adipose tissue (WAT), the absence of <a><i>AMPKα1</i></a> increased exosome release and exosomal proteins by elevating <a>tumor susceptibility gene 101 (<i>TSG101</i></a>)-mediated exosome biogenesis. In adipocytes treated with palmitic acid, TSG101 facilitated scavenger receptor class B (CD36) sorting into exosomes. CD36-containing exosomes were then endocytosed by hepatocytes to induce lipid accumulation and inflammation. Consistently, an HFD induced more severe lipid accumulation and cell death in <a><i>Prkaα1</i><sup>-/-</sup> </a>and adipose tissue-specific <i>Prkaα1</i><sup>-/-</sup> mice than in WT and liver-specific <i>Prkaα1</i><sup>-/-</sup> mice. AMPK activation by metformin reduced adipocyte-mediated exosome release and mitigated fatty liver development in WT and liver specific <i>Prkaα1</i><sup>-/-</sup> mice. Moreover, administration of the exosome inhibitor GW4869 blocked exosome secretion and alleviated HFD-induced fatty livers in <i>Prkaα1</i><sup>-/-</sup> and adipocyte-specific <i>Prkaα1</i><sup>-/-</sup> mice. We conclude that HFD-mediated AMPKα1 inhibition promotes NAFLD by increasing numbers of AT C<a>D36</a>-containing exosomes.

Rheum palmatum L. Attenuates High Fat Diet-Induced Hepatosteatosis by Activating AMP-Activated Protein Kinase

2016 ◽  
Vol 44 (03) ◽  
pp. 551-564 ◽  
Author(s):  
Mingxing Yang ◽  
Xiumin Li ◽  
Xin Zeng ◽  
Zhimin Ou ◽  
Mei Xue ◽  
...  
Keyword(s):  
Liver Disease ◽  
Protein Kinase ◽  
Glucose Tolerance ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Low Dose ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Amp Activated Protein Kinase

Nonalcoholic fatty liver disease (NAFLD) is a common metabolic disorder characterized by the accumulation of excess fat in the liver. Rheum palmatumL. (RP) decoctions have been reported to ameliorate NAFLD. The aim of the present study was to investigate the effects and underlying mechanisms of RP in fatty liver disease induced by a high-fat diet (HFD) in rats. Low and high doses of aqueous RP extraction were orally administered to HFD-fed rats for six weeks. Body weight, tissue weight, glucose tolerance, insulin tolerance, hepatic morphology, and liver triglyceride (TG) content were assessed. The effects of RP on the expressions of lipogenic and lipolysis genes were measured by quantitative real-time PCR. The phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) was determined by Western blotting. Treatment with low-dose RP significantly reduced liver weight, liver TG content, and improved glucose tolerance in HFD-fed rats. Consistently, RP attenuated excess fat accumulation and downregulated the expression of lipogenic genes in the liver. Further, an increased phosphorylation of AMPK and ACC was observed. These findings suggest that low-dose RP alleviates hepatosteatosis, at least in part, by stimulating AMPK activity.

scholarly journals Baicalin Attenuates High Fat Diet-Induced Obesity and Liver Dysfunction: Dose-Response and Potential Role of CaMKKβ/AMPK/ACC Pathway

2015 ◽  
Vol 35 (6) ◽  
pp. 2349-2359 ◽  
Author(s):  
Youli Xi ◽  
Miaozong Wu ◽  
Hongxia Li ◽  
Siqi Dong ◽  
Erfei Luo ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Molecular Mechanisms ◽  
Liver Steatosis ◽  
Serum Levels ◽  
Whole Body ◽  
Therapeutic Effects ◽  
High Fat ◽  
Dependent Protein

Background/Aims: Obesity-associated fatty liver disease affects millions of individuals. This study aimed to evaluate the therapeutic effects of baicalin to treat obesity and fatty liver in high fat diet-induced obese mice, and to study the potential molecular mechanisms. Methods: High fat diet-induced obese animals were treated with different doses of baicalin (100, 200 and 400 mg/kg/d). Whole body, fat pad and liver were weighed. Hyperlipidemia, liver steatosis, liver function, and hepatic Ca2+/CaM-dependent protein kinase kinase β (CaMKKβ) / AMP-activated protein kinase (AMPK) / acetyl-CoA carboxylase (ACC) were further evaluated. Results: Baicalin significantly decreased liver, epididymal fat and body weights in high fat diet-fed mice, which were associated with decreased serum levels of triglycerides, total cholesterol, LDL, alanine transaminase and aspartate transaminase, but increased serum HDL level. Pathological analysis revealed baicalin dose-dependently decreased the degree of hepatic steatosis, with predominantly diminished macrovesicular steatosis at lower dose but both macrovesicular and microvesicular steatoses at higher dose of baicalin. Baicalin dose-dependently inhibited hepatic CaMKKβ/AMPK/ACC pathway. Conclusion: These data suggest that baicalin up to 400 mg/kg/d is safe and able to decrease the degree of obesity and fatty liver diseases. Hepatic CaMKKβ/AMPK/ACC pathway may mediate the therapeutic effects of baicalin in high fat diet animal model.

scholarly journals Lupine (Lupinus angustifolius L.) Peptide Prevents Non-Alcoholic Fatty Liver Disease in High-Fat Diet-Induced Obese Mice

2019 ◽  
Author(s):  
Ana Lemus-Conejo ◽  
Elena Grao-Cruces ◽  
Rocio Toscano ◽  
Lourdes M Varela ◽  
Carmen Claro ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Lupinus Angustifolius ◽  
Standard Diet ◽  
Obese Mice ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Bioactive peptides are related to the prevention and treatment of many diseases. GPETAFLR is an octapeptide which was isolated from lupine (Lupinus angustifolius L.) and showed anti-inflammatory properties. The aim of this study was to evaluate the potential activity of GPETAFLR to prevent non-alcoholic fatty liver disease (NAFLD) in high-fat diet (HFD)-induced obese mice. C57BL/6J mice were fed a standard diet or an HFD. Two of the groups fed the HFD diet were treated with GPETAFLR in their drinking water at 0,5 mg/kg/d or 1 mg/kg/d. To determine the ability of GPETAFLR to improve the onset and progression of NAFLD, histological studies, hepatic enzyme profile, inflammatory cytokine and lipid metabolism-related genes and proteins were analyzed. Our results suggest that HFD-induced inflammatory metabolic disorders were alleviated by treatment with GPETAFLR. In conclusion, dietary lupine consumption could repair HFD-induced hepatic damage, possibly via modifications in the liver&rsquo;s lipid signalling pathways.

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