Clove extract functions as a natural fatty acid synthesis inhibitor and prevents obesity in a mouse model

2017 ◽  
Vol 8 (8) ◽  
pp. 2847-2856 ◽  
Author(s):  
Yiran Ding ◽  
Zhennan Gu ◽  
Yihe Wang ◽  
Shunhe Wang ◽  
Haiqin Chen ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Medicinal Plants ◽  
Mouse Model ◽  
Chronic Diseases ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Synthesis Inhibitor ◽  
Clove Extract ◽  
Natural Fatty Acid

Numerous medicinal plants have been reported to prevent various chronic diseases.

scholarly journals Ganoderma Lucidum Polysaccharide Peptide Alleviates Hepatoteatosis via Modulating Bile Acid Metabolism Dependent on FXR-SHP/FGF

2018 ◽  
Vol 49 (3) ◽  
pp. 1204-1220 ◽  
Author(s):  
Dandan Zhong ◽  
Zhengwei Xie ◽  
Boyue Huang ◽  
Shuai Zhu ◽  
Guoqian Wang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Bile Acid ◽  
Mouse Model ◽  
Therapeutic Effect ◽  
Fatty Acid Synthesis ◽  
Hepg2 Cells ◽  
Ganoderma Lucidum ◽  
Acid Metabolism ◽  
Acid Synthesis ◽  
Primary Hepatocytes

Background/Aims: Non-alcoholic fatty liver disease (NAFLD) encompasses a series of pathologic changes ranging from steatosis to steatohepatitis, which may progress to cirrhosis and hepatocellular carcinoma. The purpose of this study was to determine whether ganoderma lucidum polysaccharide peptide (GLPP) has therapeutic effect on NAFLD. Methods: Ob/ ob mouse model and ApoC3 transgenic mouse model were used for exploring the effect of GLPP on NAFLD. Key metabolic pathways and enzymes were identified by metabolomics combining with KEGG and PIUmet analyses and key enzymes were detected by Western blot. Hepatosteatosis models of HepG2 cells and primary hepatocytes were used to further confirm the therapeutic effect of GLPP on NAFLD. Results: GLPP administrated for a month alleviated hepatosteatosis, dyslipidemia, liver dysfunction and liver insulin resistance. Pathways of glycerophospholipid metabolism, fatty acid metabolism and primary bile acid biosynthesis were involved in the therapeutic effect of GLPP on NAFLD. Detection of key enzymes revealed that GLPP reversed low expression of CYP7A1, CYP8B1, FXR, SHP and high expression of FGFR4 in ob/ob mice and ApoC3 mice. Besides, GLPP inhibited fatty acid synthesis by reducing the expression of SREBP1c, FAS and ACC via a FXR-SHP dependent mechanism. Additionally, GLPP reduced the accumulation of lipid droplets and the content of TG in HepG2 cells and primary hepatocytes induced by oleic acid and palmitic acid. Conclusion: GLPP significantly improves NAFLD via regulating bile acid synthesis dependent on FXR-SHP/FGF pathway, which finally inhibits fatty acid synthesis, indicating that GLPP might be developed as a therapeutic drug for NAFLD.

scholarly journals Inhibitors of Fatty Acid Synthesis Induce PPARα-Regulated Fatty Acidβ-Oxidative Genes: Synergistic Roles of L-FABP and Glucose

PPAR Research ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-22 ◽  
Author(s):  
Huan Huang ◽  
Avery L. McIntosh ◽  
Gregory G. Martin ◽  
Anca D. Petrescu ◽  
Kerstin K. Landrock ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
High Glucose ◽  
Fatty Acid Synthase ◽  
Binding Protein ◽  
Acid Synthesis ◽  
Oxidative Enzymes ◽  
Peroxisome Proliferator ◽  
Synthesis Inhibitor ◽  
Fatty Acid Binding

While TOFA (acetyl CoA carboxylase inhibitor) and C75 (fatty acid synthase inhibitor) prevent lipid accumulation by inhibiting fatty acid synthesis, the mechanism of action is not simply accounted for by inhibition of the enzymes alone. Liver fatty acid binding protein (L-FABP), a mediator of long chain fatty acid signaling to peroxisome proliferator-activated receptor-α(PPARα) in the nucleus, was found to bind TOFA and its activated CoA thioester, TOFyl-CoA, with high affinity while binding C75 and C75-CoA with lower affinity. Binding of TOFA and C75-CoA significantly altered L-FABP secondary structure. High (20 mM) but not physiological (6 mM) glucose conferred on both TOFA and C75 the ability to induce PPARαtranscription of the fatty acidβ-oxidative enzymes CPT1A, CPT2, and ACOX1 in cultured primary hepatocytes from wild-type (WT) mice. However, L-FABP gene ablation abolished the effects of TOFA and C75 in the context of high glucose. These effects were not associated with an increased cellular level of unesterified fatty acids but rather by increased intracellular glucose. These findings suggested that L-FABP may function as an intracellular fatty acid synthesis inhibitor binding protein facilitating TOFA and C75-mediated induction of PPARαin the context of high glucose at levels similar to those in uncontrolled diabetes.

In silico Mapping and Structure Analysis of Key Enzyme Genes in Fatty Acid Synthesis of Soybean

2009 ◽  
Vol 35 (10) ◽  
pp. 1942-1947
Author(s):  
Wan-Kun SONG ◽  
Ming-Xi ZHU ◽  
Yang-Lin ZHAO ◽  
Jing WANG ◽  
Wen-Fu LI ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Structure Analysis ◽  
Fatty Acid Synthesis ◽  
In Silico ◽  
Acid Synthesis ◽  
In Silico Mapping ◽  
Key Enzyme
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