scholarly journals Prevention of free fatty acids/high fat diet‐induced hepatic lipotoxicity by 18 β glycyrrhetinic acid

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Xudong Wu ◽  
Luyong Zhang ◽  
Jiang Shang ◽  
Emily Gurley ◽  
Elaine Studer ◽  
...  
2008 ◽  
Vol 134 (4) ◽  
pp. A-754-A-755
Author(s):  
Xudong Wu ◽  
Luyong Zhang ◽  
Jing Shang ◽  
Emily C. Gurley ◽  
Elaine Studer ◽  
...  

2011 ◽  
Vol 49 (5) ◽  
pp. 1129-1140 ◽  
Author(s):  
Mohamed A. El-Moselhy ◽  
Ashraf Taye ◽  
Sara Shaaban Sharkawi ◽  
Suzan F.I. El-Sisi ◽  
Ahmed Fahmy Ahmed

2012 ◽  
Vol 51 (3) ◽  
pp. 163-169 ◽  
Author(s):  
Wataru Motomura ◽  
Takayuki Yoshizaki ◽  
Nobuhiko Takahashi ◽  
Shima Kumei ◽  
Yusuke Mizukami ◽  
...  

2021 ◽  
Author(s):  
Lujing Wang ◽  
Min Liu ◽  
Xigan Li ◽  
Yucui Wu ◽  
Fei Yin ◽  
...  

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...


Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2507 ◽  
Author(s):  
Wenyu Zhao ◽  
Fanfen Song ◽  
Diangeng Hu ◽  
Haiqin Chen ◽  
Qixiao Zhai ◽  
...  

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.


2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Linghuan Li ◽  
Wanfang Zheng ◽  
Can Wang ◽  
Jiameng Qi ◽  
Hanbing Li

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.


Endocrinology ◽  
2013 ◽  
Vol 154 (6) ◽  
pp. 2188-2199 ◽  
Author(s):  
Shweta Sharma ◽  
Hidetaka Morinaga ◽  
Vicky Hwang ◽  
WuQiang Fan ◽  
Marina O. Fernandez ◽  
...  

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.


2018 ◽  
Vol 96 (8) ◽  
pp. 765-771 ◽  
Author(s):  
Yuanfa Yao ◽  
Xuqin Zhao ◽  
Jinxia Xin ◽  
Yingqi Wu ◽  
Hanbing Li

Coumarins extensively exist in plants and are utilized against diabetes in some folk medicines. Recent studies have demonstrated that oxidative stress plays a crucial role in the etiology and pathogenesis of diabetes mellitus. We investigated the antioxidant ability of 3 coumarins (osthole, esculin, and fraxetin) in type 2 diabetes. After being fed a high-fat diet, ICR mice were exposed to low doses of streptozotocin and then treated with experimental coumarins for 5 weeks. We found osthole, esculin, and metformin significantly lowered fasting blood glucose, HOMA-IR, and 3 blood lipids (total cholesterol, total triglyceride, free fatty acids), and increased insulin levels, while fraxetin only enhanced insulin levels and lessened free fatty acids. Both osthole and esculin had antioxidative effects in pancreas through elevating the activities of glutathione peroxidase, catalase, and superoxide dismutase; fraxetin, however, merely heightened catalase activity. By contrast, 3 coumarins significantly increased those antioxidase activities in liver. Hematoxylin and eosin staining revealed 3 coumarins, especially osthole, attenuated cellular derangement, blurry fringes of hepatic sinusoid and extensive vacuolization due to hepatocellular lipid accumulation, and lessened inflammatory infiltration in pancreas. The glomerular and islet structure of diabetic mice were improved, with reduced mesangial matrix and glomerular basement membrane thickening. Therefore, our study supports that coumarins could be promising candidates against type 2 diabetes through antioxidative mechanisms.


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