Mode of action of choline. IV. Activity of the enzymes related to fatty acid synthesis and the levels of metabolic intermediates in choline-deficient rats

1969 ◽  
Vol 47 (10) ◽  
pp. 917-926 ◽  
Author(s):  
A. Chalvardjian
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Adenine Nucleotides ◽  
Acid Synthesis ◽  
Acid Oxidation ◽  
High Fat ◽  
Metabolic Intermediates ◽  
Fatty Livers ◽  
The Mean ◽  
Fat Diets

Three groups of choline-deficient (c.d.) and choline-supplemented (c.s.) rats were fed, respectively, a fat-free, a moderate (7%), or a high-fat (31.5%) diet for 3 days. Further groups of c.d. and c.s. rats on the 7% fat diet were killed at intervals of 2, 3, 4, 5, 8, 11, and 15 days. (1) The c.d. rats on the 7% and 31.5% fat diets developed fatty livers. (2) The activities in the liver of the enzymes related to lipogenesis were increased slightly in the initial stages in c.d. rats fed the 7% fat diet over their c.s. controls; but, by the end of 15 days the mean activities of the enyzmes were greater in the c.s. controls, indicating a diminished response of the c.d. livers to dietary challenges. (3) The hepatic levels of total adenine nucleotides and ATP were lower in the c.d. than in the c.s. rats fed the 7% and 31.5% fat diets. Increasing the levels of adenine nucleotides and ATP by feeding adenine sulfate did not prevent fatty liver in the c.d. rats fed a 7% fat diet. (4) Fatty acid oxidation, as assessed indirectly by the cytoplasmic NADH/NAD ratios and levels of β-hydroxybutyrate, was not impaired in the c.d. rats compared to the c.s. controls on diets containing 7% and 31.5% fat.

scholarly journals Proteomics study of the effect of high-fat diet on rat liver

2019 ◽  
Vol 122 (9) ◽  
pp. 1062-1072 ◽  
Author(s):  
Jian Sang ◽  
Hengxian Qu ◽  
Ruixia Gu ◽  
Dawei Chen ◽  
Xia Chen ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Rat Liver ◽  
High Fat Diet ◽  
Acid Synthesis ◽  
High Energy ◽  
The Body ◽  
Acid Oxidation ◽  
High Fat ◽  
Bioinformatics Analyses ◽  
Fat Diets

AbstractExcessive intake of high-energy diets is an important cause of most obesity. The intervention of rats with high-fat diet can replicate the ideal animal model for studying the occurrence of human nutritional obesity. Proteomics and bioinformatics analyses can help us to systematically and comprehensively study the effect of high-fat diet on rat liver. In the present study, 4056 proteins were identified in rat liver by using tandem mass tag. A total of 198 proteins were significantly changed, of which 103 were significantly up-regulated and ninety-five were significantly down-regulated. These significant differentially expressed proteins are primarily involved in lipid metabolism and glucose metabolism processes. The intake of a high-fat diet forces the body to maintain physiological balance by regulating these key protein spots to inhibit fatty acid synthesis, promote fatty acid oxidation and accelerate fatty acid degradation. The present study enriches our understanding of metabolic disorders induced by high-fat diets at the protein level.

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.

Effect of Diets Low in Organic Sulfur on Metabolism of Cholesterol-C14 in the Rat

1956 ◽  
Vol 186 (3) ◽  
pp. 403-405 ◽  
Author(s):  
Oscar W Portman
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Test Dose ◽  
Acid Synthesis ◽  
Organic Sulfur ◽  
Aminobenzoic Acid ◽  
The Mean ◽  
Deficient Group

Mechanisms involved in the hypercholesteremia of rats fed diets relatively deficient in organic sulfur were investigated. Acetate-C14 was injected into rats fed diets including alpha-protein and into methionine-supplemented rats. The rates of synthesis and elimination of cholesterol-C14 from tissues were studied. The biological half lives of cholesterol-C14 in all tissues were similar for both diet groups. The rate of incorporation of acetate into cholesterol was somewhat less in the livers of rats from the deficient group at 40 minutes after injection of the acetate. The ratio of cholesterol to fatty acid synthesis was similar for the two groups. The mean acetylation of a test dose of p-aminobenzoic acid was almost identical for the two groups.

Haw pectin pentaglaracturonide inhibits fatty acid synthesis and improves insulin sensitivity in high-fat-fed mice

2017 ◽  
Vol 34 ◽  
pp. 440-446 ◽  
Author(s):  
Suhong Li ◽  
Zhu Huang ◽  
Yinping Dong ◽  
Rugang Zhu ◽  
Tuoping Li
Keyword(s):  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
High Fat

scholarly journals Acetate Affects the Process of Lipid Metabolism in Rabbit Liver, Skeletal Muscle and Adipose Tissue

Animals ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 799 ◽  
Author(s):  
Lei Liu ◽  
Chunyan Fu ◽  
Fuchang Li
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Synthesis ◽  
Lipid Accumulation ◽  
Acid Synthesis ◽  
Control Group ◽  
Acid Oxidation ◽  
Signal Pathways ◽  
Peroxisome Proliferator ◽  
Acid Uptake

Short-chain fatty acids (SCFAs) (a microbial fermentation production in the rabbit gut) have an important role in many physiological processes, which may be related to the reduced body fat of rabbits. In the present experiment, we study the function of acetate (a major SCFA in the rabbit gut) on fat metabolism. Ninety rabbits (40 days of age) were randomly divided into three groups: a sham control group (injection of saline for four days); a group experiencing subcutaneous injection of acetate for four days (2 g/kg BM per day, one injection each day, acetate); and a pair-fed sham treatment group. The results show that acetate-inhibited lipid accumulation by promoting lipolysis and fatty acid oxidation and inhibiting fatty acid synthesis. Activated G protein-coupled receptor 41/43, adenosine monophosphate activated protein kinase (AMPK) and extracellular-signal-regulated kinase (ERK) 1/2 signal pathways were likely to participate in the regulation in lipid accumulation of acetate. Acetate reduced hepatic triglyceride content by inhibiting fatty acid synthesis, enhancing fatty acid oxidation and lipid output. Inhibited peroxisome proliferator-activated receptor α (PPARα) and activated AMPK and ERK1/2 signal pathways were related to the process in liver. Acetate reduced intramuscular triglyceride level via increasing fatty acid uptake and fatty acid oxidation. PPARα was associated with the acetate-reduced intracellular fat content.

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