The antihyperglycemic effect of curcumin in high fat diet fed rats. Role of TNF-α and free fatty acids

Cognitive dysfunction is linked to chronic low-grade inflammatory stress that contributes to cell-mediated immunity in creating an oxidative environment. Food is a vitally important energy source; it affects brain function and provides direct energy. Several studies have indicated that high-fat consumption causes overproduction of circulating free fatty acids and systemic inflammation. Immune cells, free fatty acids, and circulating cytokines reach the hypothalamus and initiate local inflammation through processes such as microglial proliferation. Therefore, the role of high-fat diet (HFD) in promoting oxidative stress and neurodegeneration is worthy of further discussion. Of particular interest in this article, we highlight the associations and molecular mechanisms of HFD in the modulation of inflammation and cognitive deficits. Taken together, a better understanding of the role of oxidative stress in cognitive impairment following HFD consumption would provide a useful approach for the prevention of cognitive dysfunction.

Download Full-text

112 18β-Glycyrrhetinic Acid Prevents Free Fatty Acids/High Fat Diet-Induced Hepatic Toxicity By Inhibiting Cathepsin B Expression and Enzyme Activities

Gastroenterology ◽

10.1016/s0016-5085(08)63524-6 ◽

2008 ◽

Vol 134 (4) ◽

pp. A-754-A-755

Author(s):

Xudong Wu ◽

Luyong Zhang ◽

Jing Shang ◽

Emily C. Gurley ◽

Elaine Studer ◽

...

Keyword(s):

Fatty Acids ◽

Free Fatty Acids ◽

Enzyme Activities ◽

High Fat Diet ◽

Cathepsin B ◽

Glycyrrhetinic Acid ◽

Hepatic Toxicity ◽

High Fat

Download Full-text

Free fatty acids induce the demethylation of fructose 1,6-biphosphatase 2 gene promoter and potentiate its expression in hepatocytes

Food & Function ◽

10.1039/d0fo02654a ◽

2021 ◽

Author(s):

Lujing Wang ◽

Min Liu ◽

Xigan Li ◽

Yucui Wu ◽

Fei Yin ◽

...

Keyword(s):

Fatty Acids ◽

Risk Factor ◽

Free Fatty Acids ◽

High Fat Diet ◽

Metabolic Diseases ◽

Gene Promoter ◽

Health Issue ◽

High Fat ◽

Social Burden ◽

The Social

Obesity is a serious health issue due to the social burden and the most risk factor of other metabolic diseases. Increasing evidence indicates that high-fat diet (HFD) is the key...

Download Full-text

The Protective Effect of Myristica fragrans Houtt. Extracts Against Obesity and Inflammation by Regulating Free Fatty Acids Metabolism in Nonalcoholic Fatty Liver Disease

Nutrients ◽

10.3390/nu12092507 ◽

2020 ◽

Vol 12 (9) ◽

pp. 2507 ◽

Cited By ~ 1

Author(s):

Wenyu Zhao ◽

Fanfen Song ◽

Diangeng Hu ◽

Haiqin Chen ◽

Qixiao Zhai ◽

...

Keyword(s):

Fatty Acids ◽

Liver Disease ◽

Fatty Liver ◽

Free Fatty Acids ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Lipid Synthesis ◽

High Fat ◽

Nonalcoholic Fatty Liver ◽

Myristica Fragrans Houtt

Nonalcoholic fatty liver disease (NAFLD) is a disorder characterized by the excess accumulation of fat in the hepatocytes. It is commonly associated with severe obesity and inflammation. Free fatty acids (FFAs) are the key to regulate lipid metabolism and immune response in hepatocyte cells. This study examined the effects of AEN (alcohol extract of nutmeg, the seed of Myristica fragrans Houtt.) on the inhibition of lipid synthesis and inflammation in vitro and in vivo and on high-fat diet-induced obesity in NAFLD mice. Our results showed that AEN treatment could downregulate the expression of lipid synthesis-related genes fatty acid synthase (FASN) and sterol regulatory element-binding protein 1c (SREBP-1c) and lower the lipid content of cells. AEN also inhibited FFAs-mediated inflammation-related cytokines interleukin-6 (IL-6) and tumor necrosis factor α (TNFα) expression in cells. In a mouse model, AEN reduced the bodyweight of obese mice and improved NAFLD without affecting food intake. Further analysis revealed that AEN significantly reduced inflammation level, cholesterol and lipid accumulation, blood glucose, and other liver function indexes in mice fed with a high-fat diet. In conclusion, AEN inhibited the aggravation of obesity and inflammation by downregulating lipid-gene expression in the liver to ameliorate NAFLD.

Download Full-text

Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK Activation

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2020/7826874 ◽

2020 ◽

Vol 2020 ◽

pp. 1-11

Author(s):

Linghuan Li ◽

Wanfang Zheng ◽

Can Wang ◽

Jiameng Qi ◽

Hanbing Li

Keyword(s):

Fatty Acids ◽

Fatty Acid ◽

Lipid Metabolism ◽

Free Fatty Acids ◽

Mrna Expression ◽

Hepatic Steatosis ◽

High Fat Diet ◽

De Novo ◽

Acid Oxidation ◽

High Fat

Previous studies presented various beneficial effects of mogrosides extract from Siraitia grosvenorii, which has been included in the list of Medicine Food Homology Species in China. Mogroside V (MV) is one of the main ingredients in mogrosides extract; however, whether and how MV improves impaired lipid metabolism in the liver remains to be elucidated. Herein, we investigated the therapeutic effects of mogroside V upon hepatic steatosis in vivo and in vitro and explored the underlying mechanisms. The results showed that MV significantly ameliorated hepatic steatosis in high-fat diet- (HFD-) fed mice. Furthermore, the increased protein expression of PPAR-γ, SREBP-1, and FASN and mRNA expression of pparg, srebp1, scd1, and fasn in the liver in HFD-fed mice, which contribute to de novo lipogenesis, were dose-dependently reversed by MV treatment. Meanwhile, MV counteracted the suppressed expression of PPAR-α and CPT-1A and mRNA expression of atgl, hsl, ppara, and cpt1a, thus increasing lipolysis and fatty acid oxidation. In addition, in free fatty acids- (FFAs-) incubated LO2 cells MV downregulated de novo lipogenesis and upregulated lipolysis and fatty acid oxidation, thereby attenuating lipid accumulation, which was significantly abrogated by treatment with Compound C, an inhibitor of AMP-activated protein kinase (AMPK). Taken together, these results suggested that MV exerted a pronounced effect upon improving hepatic steatosis through regulating the disequilibrium of lipid metabolism in the liver via an AMPK-dependent pathway, providing a potential lead compound candidate for preventing nonalcoholic fatty liver disease.

Download Full-text

Role of exercise training on insulin resistance and TNF-α in high-fat diet rats

Frontiers of Medicine in China ◽

10.1007/s11684-009-0071-0 ◽

2009 ◽

Vol 3 (4) ◽

pp. 403-407

Author(s):

Hui Sun ◽

Xiuling Deng ◽

Fangxi Xiao ◽

Lulu Chen ◽

Huiqing Li

Keyword(s):

Insulin Resistance ◽

Exercise Training ◽

High Fat Diet ◽

High Fat ◽

Tnf Α

Download Full-text

Free Fatty Acids Induce Lhb mRNA but Suppress Fshb mRNA in Pituitary LβT2 Gonadotropes and Diet-Induced Obesity Reduces FSH Levels in Male Mice and Disrupts the Proestrous LH/FSH Surge in Female Mice

Endocrinology ◽

10.1210/en.2012-2218 ◽

2013 ◽

Vol 154 (6) ◽

pp. 2188-2199 ◽

Cited By ~ 26

Author(s):

Shweta Sharma ◽

Hidetaka Morinaga ◽

Vicky Hwang ◽

WuQiang Fan ◽

Marina O. Fernandez ◽

...

Keyword(s):

Fatty Acids ◽

Free Fatty Acids ◽

Mrna Expression ◽

High Fat Diet ◽

Mapk Signaling ◽

Seminiferous Tubules ◽

Corpora Lutea ◽

Toll Like Receptor ◽

High Fat ◽

Female Mice

Abstract Female obesity is associated with insulin resistance, hyperandrogenemia, and reproductive dysfunction. We hypothesized that elevated free fatty acids (FFAs) might directly modulate pituitary gonadotropin production. FFAs caused a time- and dose-dependent increase in phosphorylation of the MAPKs p38MAPK, c-Jun N-terminal kinase (JNK)-1/2, and ERK1/2 in LβT2 gonadotrope cells. Furthermore, FFAs up-regulated Lhb mRNA expression acutely, an effect that was blocked by JNK inhibition, but suppressed Fshb mRNA expression, an effect that was independent of MAPK signaling. FFAs enhanced the activation of the MAPKs in the presence of GnRH, although the cotreatment did not alter Lhb induction but did eliminate the GnRH induction of Fshb. FFAs also suppressed activin-induced Fshb expression. Knockdown experiments showed that the FFA effect on the inflammatory kinases p38MAPK and JNK and on Lhb, but not Fshb, mRNA expression is mediated via toll-like receptor-2 and toll-like receptor-4 and was mimicked by lipopolysaccharide stimulation. In vivo, male C57BL/6 mice on a high-fat diet showed reduced FSH levels consistent with the suppression of Fshb seen in vitro. Histological analysis of the testes showed an increased number of abnormal seminiferous tubules. Female mice on a high-fat diet lacked the expected proestrus LH and FSH surge and exhibited an increase in the number of days at estrus and a reduced number of days at proestrus, and ovaries had significantly fewer corpora lutea. Taken together, our findings suggest that lipid excess can lead to reproductive defects in both male and female mice.

Download Full-text