Elevated hepatic fatty acid elongase‐5 (Elovl5) attenuates fatty liver in high fat diet induced obese mice

Licochalcone A is a chalcone isolated from Glycyrrhiza uralensis. It showed anti-tumor and anti-inflammatory properties in mice with acute lung injuries and regulated lipid metabolism through the activation of AMP-activated protein kinase (AMPK) in hepatocytes. However, the effects of licochalcone A on reducing weight gain and improving nonalcoholic fatty liver disease (NAFLD) are unclear. Thus, the present study investigated whether licochalcone A ameliorated weight loss and lipid metabolism in the liver of high-fat diet (HFD)-induced obese mice. Male C57BL/6 mice were fed an HFD to induce obesity and NAFLD, and then were injected intraperitoneally with licochalcone A. In another experiment, a fatty liver cell model was established by incubating HepG2 hepatocytes with oleic acid and treating the cells with licochalcone A to evaluate lipid metabolism. Our results demonstrated that HFD-induced obese mice treated with licochalcone A had decreased body weight as well as inguinal and epididymal adipose tissue weights compared with HFD-treated mice. Licochalcone A also ameliorated hepatocyte steatosis and decreased liver tissue weight and lipid droplet accumulation in liver tissue. We also found that licochalcone A significantly regulated serum triglycerides, low-density lipoprotein, and free fatty acids, and decreased the fasting blood glucose value. Furthermore, in vivo and in vitro, licochalcone A significantly decreased expression of the transcription factor of lipogenesis and fatty acid synthase. Licochalcone A activated the sirt-1/AMPK pathway to reduce fatty acid chain synthesis and increased lipolysis and β-oxidation in hepatocytes. Licochalcone A can potentially ameliorate obesity and NAFLD in mice via activation of the sirt1/AMPK pathway.

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

10.20944/preprints201907.0180.v1 ◽

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’s lipid signalling pathways.

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Psoralea corylifolia L. Seed Extract Attenuates Nonalcoholic Fatty Liver Disease in High-Fat Diet-Induced Obese Mice

Nutrients ◽

10.3390/nu8020083 ◽

2016 ◽

Vol 8 (2) ◽

pp. 83 ◽

Cited By ~ 12

Author(s):

Eunhui Seo ◽

Yoon Sin Oh ◽

Hee-Sook Jun

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Nonalcoholic Fatty Liver Disease ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Seed Extract ◽

Obese Mice ◽

Psoralea Corylifolia ◽

High Fat ◽

Nonalcoholic Fatty Liver

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A lupine (Lupinus angustifolious L.) peptide prevents non-alcoholic fatty liver disease in high-fat-diet-induced obese mice

Food & Function ◽

10.1039/d0fo00206b ◽

2020 ◽

Vol 11 (4) ◽

pp. 2943-2952 ◽

Cited By ~ 1

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 ◽

Obese Mice ◽

High Fat ◽

Alcoholic Fatty Liver ◽

Alcoholic Fatty Liver Disease

A lupine (Lupinus angustifolious L.) peptide prevents non-alcoholic fatty liver disease in high-fat-diet-induced obese mice.

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Omega-3 Phospholipids from Krill Oil Enhance Intestinal Fatty Acid Oxidation More Effectively than Omega-3 Triacylglycerols in High-Fat Diet-Fed Obese Mice

Nutrients ◽

10.3390/nu12072037 ◽

2020 ◽

Vol 12 (7) ◽

pp. 2037 ◽

Cited By ~ 1

Author(s):

Petra Kroupova ◽

Evert M. van Schothorst ◽

Jaap Keijer ◽

Annelies Bunschoten ◽

Martin Vodicka ◽

...

Keyword(s):

Gene Expression ◽

Fatty Acid ◽

High Fat Diet ◽

Body Weight Gain ◽

Acid Oxidation ◽

Obese Mice ◽

Krill Oil ◽

Omega 3 ◽

High Fat ◽

Lower Body Weight

Antisteatotic effects of omega-3 fatty acids (Omega-3) in obese rodents seem to vary depending on the lipid form of their administration. Whether these effects could reflect changes in intestinal metabolism is unknown. Here, we compare Omega-3-containing phospholipids (krill oil; ω3PL-H) and triacylglycerols (ω3TG) in terms of their effects on morphology, gene expression and fatty acid (FA) oxidation in the small intestine. Male C57BL/6N mice were fed for 8 weeks with a high-fat diet (HFD) alone or supplemented with 30 mg/g diet of ω3TG or ω3PL-H. Omega-3 index, reflecting the bioavailability of Omega-3, reached 12.5% and 7.5% in the ω3PL-H and ω3TG groups, respectively. Compared to HFD mice, ω3PL-H but not ω3TG animals had lower body weight gain (−40%), mesenteric adipose tissue (−43%), and hepatic lipid content (−64%). The highest number and expression level of regulated intestinal genes was observed in ω3PL-H mice. The expression of FA ω-oxidation genes was enhanced in both Omega-3-supplemented groups, but gene expression within the FA β-oxidation pathway and functional palmitate oxidation in the proximal ileum was significantly increased only in ω3PL-H mice. In conclusion, enhanced intestinal FA oxidation could contribute to the strong antisteatotic effects of Omega-3 when administered as phospholipids to dietary obese mice.

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RS4-type resistant starch prevents high-fat diet-induced obesity via increased hepatic fatty acid oxidation and decreased postprandial GIP in C57BL/6J mice

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00468.2009 ◽

2010 ◽

Vol 298 (3) ◽

pp. E652-E662 ◽

Cited By ~ 41

Author(s):

Akira Shimotoyodome ◽

Junko Suzuki ◽

Daisuke Fukuoka ◽

Ichiro Tokimitsu ◽

Tadashi Hase

Keyword(s):

Fatty Acid ◽

Fatty Acid Oxidation ◽

Resistant Starch ◽

High Fat Diet ◽

Acid Oxidation ◽

High Fat ◽

Fat Utilization ◽

Hepatic Fatty Acid ◽

Diet Induced Obesity ◽

Hepatic Fatty Acid Oxidation

Chemically modified starches (CMS) are RS4-type resistant starch, which shows a reduced availability, as well as high-amylose corn starch (HACS, RS2 type), compared with the corresponding unmodified starch. Previous studies have shown that RS4 increases fecal excretion of bile acids and reduces zinc and iron absorption in rats. The aim of this study was to investigate the effects of dietary RS4 supplementation on the development of diet-induced obesity in mice. Weight- and age-matched male C57BL/6J mice were fed for 24 wk on a high-fat diet containing unmodified starch, hydroxypropylated distarch phosphate (RS4), or HACS (RS2). Those fed the RS4 diet had significantly lower body weight and visceral fat weight than those fed either unmodified starch or the RS2 diet. Those fed the RS4 diet for 4 wk had a significantly higher hepatic fatty acid oxidation capacity and related gene expression and lower blood insulin than those fed either unmodified starch or the RS2 diet. Indirect calorimetry showed that the RS4 group exhibited higher energy expenditure and fat utilization compared with the RS2 group. When gavaged with fat (trioleate), RS4 stimulated a lower postprandial glucose-dependent insulinotropic polypeptide (GIP; incretin) response than RS2. Higher blood GIP levels induced by chronic GIP administration reduced fat utilization in high-fat diet-fed mice. In conclusion, dietary supplementation with RS4-type resistant starch attenuates high-fat diet-induced obesity more effectively than RS2 in C57BL/6J mice, which may be attributable to lower postprandial GIP and increased fat catabolism in the liver.

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Terminalia paniculata bark extract attenuates non-alcoholic fatty liver via down regulation of fatty acid synthase in high fat diet-fed obese rats

Lipids in Health and Disease ◽

10.1186/1476-511x-13-58 ◽

2014 ◽

Vol 13 (1) ◽

pp. 58 ◽

Cited By ~ 4

Author(s):

Mopuri Ramgopal ◽

Banavathy S Kruthika ◽

Damineni Surekha ◽

Balaji Meriga

Keyword(s):

Fatty Acid ◽

Fatty Liver ◽

High Fat Diet ◽

Fatty Acid Synthase ◽

Bark Extract ◽

High Fat ◽

Down Regulation ◽

Alcoholic Fatty Liver ◽

Obese Rats ◽

Terminalia Paniculata

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Fisetin Protects Against Hepatic Steatosis Through Regulation of the Sirt1/AMPK and Fatty Acid β-Oxidation Signaling Pathway in High-Fat Diet-Induced Obese Mice

Cellular Physiology and Biochemistry ◽

10.1159/000493650 ◽

2018 ◽

Vol 49 (5) ◽

pp. 1870-1884 ◽

Cited By ~ 25

Author(s):

Chian-Jiun Liou ◽

Ciao-Han Wei ◽

Ya-Ling Chen ◽

Ching-Yi Cheng ◽

Chia-Ling Wang ◽

...

Keyword(s):

Fatty Acid ◽

Lipid Metabolism ◽

Hepatic Steatosis ◽

Lipid Accumulation ◽

High Fat Diet ◽

Fatty Acid Synthase ◽

Epididymal Adipose Tissue ◽

Obese Mice ◽

High Fat

Background/Aims: Fisetin is a naturally abundant flavonoid isolated from various fruits and vegetables that was recently identified to have potential biological functions in improving allergic airway inflammation, as well as anti-oxidative and anti-tumor properties. Fisetin has also been demonstrated to have anti-obesity properties in mice. However, the effect of fisetin on nonalcoholic fatty liver disease (NAFLD) is still elusive. Thus, the present study evaluated whether fisetin improves hepatic steatosis in high-fat diet (HFD)-induced obese mice and regulates lipid metabolism of FL83B hepatocytes in vitro. Methods: NAFLD was induced by HFD in male C57BL/6 mice. The mice were then injected intraperitoneally with fisetin for 10 weeks. In another experiment, FL83B cells were challenged with oleic acid to induce lipid accumulation and treated with various concentrations of fisetin. Results: NAFLD mice treated with fisetin had decreased body weight and epididymal adipose tissue weight compared to NAFLD mice. Fisetin treatment also reduced liver lipid droplet and hepatocyte steatosis, alleviated serum free fatty acid, and leptin concentrations, significantly decreased fatty acid synthase, and significantly increased phosphorylation of AMPKα and the production of sirt-1 and carnitine palmitoyltransferase I in the liver tissue. In vitro, fisetin decreased lipid accumulation and increased lipolysis and β-oxidation in hepatocytes. Conclusion: This study suggests that fisetin is a potential novel treatment for alleviating hepatic lipid metabolism and improving NAFLD in mice via activation of the sirt1/AMPK and β-oxidation pathway.

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