Effects of Yeast Hydrolysate on Hepatic Lipid Metabolism in High-Fat-Diet-Induced Obese Mice: Yeast Hydrolysate Suppresses Body Fat Accumulation by Attenuating Fatty Acid Synthesis

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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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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Carbenoxolone ameliorates hepatic lipid metabolism and inflammation in obese mice induced by high fat diet via regulating the JAK2/STAT3 signaling pathway

International Immunopharmacology ◽

10.1016/j.intimp.2019.03.011 ◽

2019 ◽

Vol 74 ◽

pp. 105498 ◽

Cited By ~ 3

Author(s):

Yuning Chen ◽

Wen Lu ◽

Zhengyu Jin ◽

Jian Yu ◽

Bimin Shi

Keyword(s):

Lipid Metabolism ◽

Signaling Pathway ◽

High Fat Diet ◽

Obese Mice ◽

High Fat ◽

Hepatic Lipid Metabolism ◽

Hepatic Lipid ◽

Stat3 Signaling ◽

Stat3 Signaling Pathway

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Maternal high-fat diet consumption modulates hepatic lipid metabolism and microRNA-122 (miR-122) and microRNA-370 (miR-370) expression in offspring

British Journal Of Nutrition ◽

10.1017/s0007114514000579 ◽

2014 ◽

Vol 111 (12) ◽

pp. 2112-2122 ◽

Cited By ~ 79

Author(s):

R. O. Benatti ◽

A. M. Melo ◽

F. O. Borges ◽

L. M. Ignacio-Souza ◽

L. A. P. Simino ◽

...

Keyword(s):

Fatty Acid ◽

Lipid Metabolism ◽

High Fat Diet ◽

Fatty Acid Synthase ◽

High Fat ◽

Hepatic Lipid Metabolism ◽

Expression Levels ◽

Hepatic Lipid ◽

Pregnancy And Lactation ◽

Maternal Consumption

Maternal consumption of a high-fat diet (HFD) during pregnancy and lactation is closely related to hepatic lipid accumulation, insulin resistance and increased serum cytokine levels in offspring and into their adulthood. MicroRNA (miRNA) have been implicated in cholesterol biosynthesis and fatty acid metabolism. We evaluated the modulation of hepatic fatty acid synthesis (de novo), β-oxidation pathways, and miRNA-122 (miR-122) and miRNA-370 (miR-370) expression in recently weaned offspring (day 28) of mouse dams fed a HFD (HFD-O) or a standard chow (SC-O) during pregnancy and lactation. Compared with SC-O mice, HFD-O mice weighed more, had a larger adipose tissue mass and were more intolerant to glucose and insulin (P< 0·05). HFD-O mice also presented more levels of serum cholesterol, TAG, NEFA and hepatic IκB kinase and c-Jun N-terminal kinase phosphorylation compared with SC-O mice (P< 0·05). Protein levels of fatty acid synthase, acetyl-CoA carboxylase and 3-hydroxy-3-methylglutaryl-CoA reductase were similar in HFD-O and SC-O mice, whereas expression levels of SCD1 mRNA and protein were more abundant in HFD-O mice than in SC-O mice (P< 0·05). Interestingly, mRNA expression levels of the β-oxidation-related genes ACADVL and CPT1 were decreased in HFD-O mice (P< 0·05). Furthermore, the expression of miR-122 was reduced but that of miR-370 was increased in HFD-O mice compared with that in SC-O mice (P< 0·05). Changes in hepatic lipid metabolism were accompanied by increased mRNA content of AGPAT1 and TAG deposition in HFD-O mice (P< 0·05). Taken together, the present results strongly suggest that maternal consumption of a HFD affects the early lipid metabolism of offspring by modulating the expression of hepatic β-oxidation-related genes and miRNA that can contribute to metabolic disturbances in adult life.

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Deepure Tea Improves High Fat Diet-Induced Insulin Resistance and Nonalcoholic Fatty Liver Disease

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2015/980345 ◽

2015 ◽

Vol 2015 ◽

pp. 1-8 ◽

Cited By ~ 5

Author(s):

Jing-Na Deng ◽

Juan Li ◽

Hong-Na Mu ◽

Yu-Ying Liu ◽

Ming-Xia Wang ◽

...

Keyword(s):

Insulin Resistance ◽

Fatty Acid ◽

Hepatic Steatosis ◽

Fatty Acid Synthesis ◽

High Fat Diet ◽

Molecular Mechanisms ◽

Regulatory Element ◽

Acid Synthesis ◽

High Fat ◽

The Metabolic Syndrome

This study was to explore the protective effects of Deepure tea against insulin resistance and hepatic steatosis and elucidate the potential underlying molecular mechanisms. C57BL/6 mice were fed with a high fat diet (HFD) for 8 weeks to induce the metabolic syndrome. In the Deepure tea group, HFD mice were administrated with Deepure tea at 160 mg/kg/day by gavage for 14 days. The mice in HFD group received water in the same way over the same period. The age-matched C57BL/6 mice fed with standard chow were used as normal control. Compared to the mice in HFD group, mice that received Deepure tea showed significantly reduced plasma insulin and improved insulin sensitivity. Deepure tea increased the expression of insulin receptor substrate 2 (IRS-2), which plays an important role in hepatic insulin signaling pathway. Deepure tea also led to a decrease in hepatic fatty acid synthesis and lipid accumulation, which were mediated by the downregulation of sterol regulatory element binding protein 1c (SREBP-1c), fatty acid synthesis (FAS), and acetyl-CoA carboxylase (ACC) proteins that are involved in liver lipogenesis. These results suggest that Deepure tea may be effective for protecting against insulin resistance and hepatic steatosis via modulating IRS-2 and downstream signaling SREBP-1c, FAS, and ACC.

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Dietary Supplementation with α-Amylase Inhibitor Wheat Albumin to High-Fat Diet-Induced Insulin-Resistant Rats Is Associated with Increased Expression of Genes Related to Fatty Acid Synthesis in Adipose Tissue

Journal of Agricultural and Food Chemistry ◽

10.1021/jf901484t ◽

2009 ◽

Vol 57 (19) ◽

pp. 9332-9338 ◽

Cited By ~ 1

Author(s):

Yuki Murayama ◽

Kazuki Mochizuki ◽

Masaya Shimada ◽

Saki Fujimoto ◽

Kazuki Nukui ◽

...

Keyword(s):

Adipose Tissue ◽

Fatty Acid ◽

Fatty Acid Synthesis ◽

High Fat Diet ◽

Dietary Supplementation ◽

Acid Synthesis ◽

High Fat ◽

Insulin Resistant ◽

Amylase Inhibitor ◽

Expression Of Genes

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The effect of dietary fat on lipogenesis in mammary gland and liver from lactating and virgin mice

Biochemical Journal ◽

10.1042/bj1150807 ◽

1969 ◽

Vol 115 (4) ◽

pp. 807-815 ◽

Cited By ~ 54

Author(s):

Stuart Smith ◽

Harriet T. Gagné ◽

Dorothy R. Pitelka ◽

S. Abraham

Keyword(s):

Mammary Gland ◽

Fatty Acid ◽

Fatty Acid Synthesis ◽

Dietary Fat ◽

High Fat Diet ◽

Corn Oil ◽

Acid Synthesis ◽

High Fat ◽

C3h Mice ◽

Parenchymal Cells

1. Virgin and lactating C3H mice maintained on laboratory chow were transferred to a high-fat (15% corn oil) or a fat-free diet 3 days before being killed. 2. The linoleate content of liver, mammary gland and milk was decreased in lactating mice given the fat-free diet but was increased in those fed on the high-fat diet. Changes in linoleate content and mammary gland followed a similar but much less marked trend in virgin animals. 3. Hepatic fatty acid synthesis in lactating and virgin mice fed on the fat-free diet was higher than in corresponding animals fed on either the chow or the high-fat diet. The lipogenic capacity of livers from mice fed on either the chow or the high-fat diet was greater in lactating than in virgin animals. These changes in hepatic lipogenic capacity were accompanied by alterations in the specific activities of certain enzymes involved in fat synthesis. 4. Mammary gland from virgin and lactating animals showed no such adaptation to dietary fat. Results indicate that fatty acid synthesis in neither mammary-gland parenchymal cells nor mammary-gland adipose cells can be influenced by dietary fat in the same way as in the hepatocyte.

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