Changes in some Enzyme Activities Associated with Fatty Acid Synthesis in Ethanol-Induced Fatty Liver in the Rat

1973 ◽  
Vol 1 (4) ◽  
pp. 947-949 ◽  
Author(s):  
TREVOR J. BAINES ◽  
ANTHONY K. CAMPBELL
Keyword(s):  
Fatty Acid ◽  
Fatty Liver ◽  
Fatty Acid Synthesis ◽  
Enzyme Activities ◽  
Acid Synthesis

scholarly journals Acetyl-CoA carboxylase inhibition by ND-630 reduces hepatic steatosis, improves insulin sensitivity, and modulates dyslipidemia in rats

2016 ◽  
Vol 113 (13) ◽  
pp. E1796-E1805 ◽  
Author(s):  
Geraldine Harriman ◽  
Jeremy Greenwood ◽  
Sathesh Bhat ◽  
Xinyi Huang ◽  
Ruiying Wang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Insulin Sensitivity ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Fatty Acid Synthesis ◽  
Fatty Liver Disease ◽  
Acid Synthesis ◽  
Acid Oxidation ◽  
Acetyl Coa Carboxylase

Simultaneous inhibition of the acetyl-CoA carboxylase (ACC) isozymes ACC1 and ACC2 results in concomitant inhibition of fatty acid synthesis and stimulation of fatty acid oxidation and may favorably affect the morbidity and mortality associated with obesity, diabetes, and fatty liver disease. Using structure-based drug design, we have identified a series of potent allosteric protein–protein interaction inhibitors, exemplified by ND-630, that interact within the ACC phosphopeptide acceptor and dimerization site to prevent dimerization and inhibit the enzymatic activity of both ACC isozymes, reduce fatty acid synthesis and stimulate fatty acid oxidation in cultured cells and in animals, and exhibit favorable drug-like properties. When administered chronically to rats with diet-induced obesity, ND-630 reduces hepatic steatosis, improves insulin sensitivity, reduces weight gain without affecting food intake, and favorably affects dyslipidemia. When administered chronically to Zucker diabetic fatty rats, ND-630 reduces hepatic steatosis, improves glucose-stimulated insulin secretion, and reduces hemoglobin A1c (0.9% reduction). Together, these data suggest that ACC inhibition by representatives of this series may be useful in treating a variety of metabolic disorders, including metabolic syndrome, type 2 diabetes mellitus, and fatty liver disease.

scholarly journals Red Quinoa Bran Extract Prevented Alcoholic Fatty Liver Disease via Increasing Antioxidative System and Repressing Fatty Acid Synthesis Factors in Mice Fed Alcohol Liquid Diet

Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 6973
Author(s):  
Ting-An Lin ◽  
Bo-Jun Ke ◽  
Shih-Cheng Cheng ◽  
Chun-Lin Lee
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Liver Injury ◽  
Fatty Liver ◽  
Fatty Acid Synthesis ◽  
Fatty Liver Disease ◽  
Acid Synthesis ◽  
Alcoholic Fatty Liver ◽  
Ethanol Extraction ◽  
Alcoholic Fatty Liver Disease

Alcohol is metabolized in liver. Chronic alcohol abuse results in alcohol-induced fatty liver and liver injury. Red quinoa (Chenopodium formosanum) was a traditional staple food for Taiwanese aborigines. Red quinoa bran (RQB) included strong anti-oxidative and anti-inflammatory polyphenolic compounds, but it was usually regarded as the agricultural waste. Therefore, this study is to investigate the effect of water and ethanol extraction products of RQB on the prevention of liquid alcoholic diet-induced acute liver injury in mice. The mice were given whole grain powder of red quinoa (RQ-P), RQB ethanol extract (RQB-E), RQB water extract (RQB-W), and rutin orally for 6 weeks, respectively. The results indicated that RQB-E, RQB-W, and rutin decreased alcoholic diet-induced activities of aspartate aminotransferase and alanine aminotransferase, and the levels of serum triglyceride, total cholesterol, and hepatic triglyceride. Hematoxylin and eosin staining of liver tissues showed that RQB-E and RQB-W reduced lipid droplet accumulation and liver injury. However, ethanol extraction process can gain high rutin and antioxidative agents contents from red quinoa, that showed strong effects in preventing alcoholic fatty liver disease and liver injury via increasing superoxide dismutase/catalase antioxidative system and repressing the expressions of fatty acid synthesis enzyme acetyl-CoA carboxylase.

scholarly journals BHLHE40, a third transcription factor required for insulin induction of SREBP-1c mRNA in rodent liver

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Jing Tian ◽  
Jiaxi Wu ◽  
Xiang Chen ◽  
Tong Guo ◽  
Zhijian J Chen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Fatty Acid ◽  
Fatty Liver ◽  
Fatty Acid Synthesis ◽  
Gene Knockout ◽  
Rat Hepatocytes ◽  
Acid Synthesis ◽  
Gene Encoding ◽  
Fasted Rats

In obesity, elevated insulin causes fatty liver by activating the gene encoding SREBP-1c, a transcription factor that enhances fatty acid synthesis. Two transcription factors, LXRα and C/EBPβ, are necessary but not sufficient for insulin induction of hepatic SREBP-1c mRNA. Here, we show that a third transcription factor, BHLHE40, is required. Immunoprecipitation revealed that BHLHE40 binds to C/EBPβ and LXRα in livers of rats that had fasted and then refed. Hepatic BHLHE40 mRNA rises rapidly when fasted rats are refed and when rat hepatocytes are incubated with insulin. Preventing this rise by gene knockout in mice or siRNAs in hepatocytes reduces the insulin-induced rise in SREBP-1c mRNA. Although BHLHE40 is necessary for insulin induction of SREBP-1c, it is not sufficient as demonstrated by failure of lentiviral BHLHE40 overexpression to increase hepatocyte SREBP-1c mRNA in the absence of insulin. Thus, an additional event is required for insulin to increase SREBP-1c mRNA.

Nano Biotechnology Investigation of the Fatty Acid Synthesis (FAS): Preventing the Fatty Liver Disease

2017 ◽  
Vol 14 (1) ◽  
pp. 659-669
Author(s):  
Arina Rahimi ◽  
Majid Monajjemi
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Liver Disease ◽  
Electrical Properties ◽  
Potential Energy ◽  
Fatty Liver ◽  
Computational Chemistry ◽  
Fatty Acid Synthesis ◽  
Fatty Liver Disease ◽  
Acid Synthesis

Fatty acids in liver are subject to different patterns of regulation and the importance of fat deposition began to be realized with the evolution of vertebrates and the liver was the initial site of deposition. Modern sharks frequently have massive livers containing cells loaded with triglycerides. Based on our previous works we have modeled and simulated various molecules of those fatty acids. A number of computational chemistry studies carried out to understand the of the fatty acid synthesis (FAS) for preventing the fatty liver disease. In this work the electrical properties such as electron densities, energy densities, potential energy densities, ELF, LOL, ellipticity of electron density, eta index and ECP for some of the fatty acids have been calculated.

scholarly journals Gleevec (STI571) Influences Metabolic Enzyme Activities and Glucose Carbon Flow toward Nucleic Acid and Fatty Acid Synthesis in Myeloid Tumor Cells

2001 ◽  
Vol 276 (41) ◽  
pp. 37747-37753 ◽  
Author(s):  
Joan Boren ◽  
Marta Cascante ◽  
Silvia Marin ◽  
Begoña Comı́n-Anduix ◽  
Josep J. Centelles ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Nucleic Acid ◽  
Tumor Cells ◽  
Fatty Acid Synthesis ◽  
Enzyme Activities ◽  
Acid Synthesis ◽  
Carbon Flow ◽  
Metabolic Enzyme ◽  
Glucose Carbon
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