THE EFFECT OF ETHANOL ON FATTY ACID METABOLISM; STIMULATION OF HEPATIC FATTY ACID SYNTHESIS IN VITRO*

1. A single glucose meal stimulated the incorporation of acetate into fatty acids in liver slices. If the glucose was added in vitro, it had no effect. Fructose and glycerol in vitro markedly stimulated fatty acid synthesis from acetate. Fructose and glycerol probably by-passed a rate-controlling reaction between glucose and triose phosphate. This reaction may have been stimulated by glucose administered in vivo. 2. The stimulation of fatty acid synthesis caused by fructose did not require the synthesis of enzyme, thus indicating that fatty acid-synthesizing enzymes were present in a latent form in the livers from unfed chicks.

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Fatty acid synthesis and triacylglycerol accumulation in rat liver after chronic ethanol consumption

Clinical Science ◽

10.1042/cs0730159 ◽

1987 ◽

Vol 73 (2) ◽

pp. 159-163 ◽

Cited By ~ 18

Author(s):

S. Venkatesan ◽

R. J. Ward ◽

T. J. Peters

Keyword(s):

Fatty Acid ◽

Fatty Acid Synthesis ◽

Time Course ◽

Fatty Acid Synthase ◽

Acid Synthesis ◽

Hepatic Fatty Acid ◽

Chronic Ethanol Consumption ◽

Triacylglycerol Content ◽

Triacylglycerol Accumulation

1. Liver slices from chronically alcohol-fed rats incubated with 3H2O showed less than half the fatty acid synthesis rates of pair-fed controls. Addition of 50 mmol/l ethanol or of 10 mmol/l lactate and 1 mmol/l pyruvate to the incubation medium did not alter the fatty acid synthesis rates in either groups. Hepatic fatty acid synthesis rates measured in vivo with 3H2O were also significantly reduced in alcohol-fed rats. 2. Time-course experiments showed that after 1 week on the ethanol diet hepatic fatty acid synthesis rates in vitro were similar to control rats, although the liver triacylglycerol content was significantly increased. From the second week of feeding, fatty acid synthesis rates were significantly lower in alcohol-fed rats and the liver triacylglycerol content progressively increased compared with controls. 3. Fatty acid synthase activity in liver cytosolic fractions were similar to controls in the alcohol-fed group after 1 week of feeding but were significantly lower in alcohol-fed rats from the second week onwards. 4. These results indicate that hepatic triacylglycerol accumulation after alcohol feeding is not due to increased fatty acid synthesis. The reduced fatty acid synthesis observed is a consequence of triacylglycerol accumulation.

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Maternal Supplementation of Clofibrate Stimulates Hepatic Fatty Acid Oxidation in Newborn Suckling Piglets

Current Developments in Nutrition ◽

10.1093/cdn/nzaa050_026 ◽

2020 ◽

Vol 4 (Supplement_2) ◽

pp. 703-703

Author(s):

Jinan Zhao ◽

Brandon Pike ◽

Jack Odle ◽

Lin Xi

Keyword(s):

Fatty Acid ◽

Fatty Acid Oxidation ◽

Fatty Acid Metabolism ◽

Acid Metabolism ◽

Acid Oxidation ◽

Standard Diet ◽

Hepatic Fatty Acid ◽

Food And Agriculture ◽

Hepatic Fatty Acid Oxidation

Abstract Objectives To evaluate effects of maternal feeding of clofibrate, a PPARα agonist, on development of hepatic fatty acid metabolism in offspring using pig as a model. Methods Pregnant sows (N = 27) were randomly assigned into three treatment groups. Each group was fed a standard diet (3265 kcal ME/kg) supplemented with either 0, 0.25% or 5% clofibrate (w/w) from d 107 of gestation to d 7 of lactation. Liver tissue was collected from piglets at birth, d1, 7, 14 and 19. Fatty acid oxidation was examined in fresh homogenates using 1 mM [1–14C] oleic acid (9.9 mBq/mmol) as substrate. Oxidation was measured in the absence or presence of in vitro supplemented L-carnitine (1 mM) and/or malonate (5 mM). Results Clofibrate was not detected in piglet liver or sow milk. Interactions between clofibrate and postnatal age (P < 0.001) on the 14C accumulation in 14CO2, acid soluble products (14C-ASP) and esterified products (14C-ESP) were observed. Accumulation in 14CO2 was not altered by piglet age in control sows; however, accumulation in 14C-ASP was higher at d14 and lower at d19 compared to d1. In contrast, maternal clofibrate increased 14CO2 by 100% and 14C-ASP by 80% in pigs at d1, and the increase was higher in pigs from sows given 0.5% versus 0.25% clofibrate. Accumulation in 14C-ESP in pigs from control sows increased from d1 to d14, but there was no difference detected between d14 and 19. Assessment of pigs from sows fed the 0.25% clofibrate dose revealed no impact on 14C-ESP, but the 0.5% dose increased 14C-ESP by 31%. No interaction was observed between clofibrate and the in vitro treatments (carnitine and malonate; P = 0.5). In vitro supplementation of carnitine increased radiolabel accumulation in CO2 by 60% and in ASP by 120%, but reduced 14C-ESP by 39% compared to control incubations. Supplementation of malonate reduced 14CO2 by 95% and 14C-ESP by 44%, but had no impact on 14C-ASP. Conclusions Maternal clofibrate enhances hepatic fatty acid metabolism in offspring, but the effect fades with postpartum age. The availability of carnitine in the milk could be a key element to support fatty acid oxidation in postnatal pigs. Funding Sources USDA National Institute of Food and Agriculture.

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Oleiferasaponin A2, a Novel Saponin from Camellia oleifera Abel. Seeds, Inhibits Lipid Accumulation of HepG2 Cells Through Regulating Fatty Acid Metabolism

Molecules ◽

10.3390/molecules23123296 ◽

2018 ◽

Vol 23 (12) ◽

pp. 3296 ◽

Cited By ~ 4

Author(s):

Tai-Mei Di ◽

Shao-Lan Yang ◽

Feng-Yu Du ◽

Lei Zhao ◽

Xiao-Han Li ◽

...

Keyword(s):

Fatty Acid ◽

Fatty Acid Metabolism ◽

Fatty Acid Synthesis ◽

Lipid Accumulation ◽

Acid Metabolism ◽

Acid Synthesis ◽

Triterpenoid Saponin ◽

Camellia Oleifera ◽

Medicinal Value ◽

Hepg2 Cell Lines

A new triterpenoid saponin, named oleiferasaponin A2, was isolated and identified from Camellia oleifera defatted seeds. Oleiferasaponin A2 exhibited anti-hyperlipidemic activity on HepG2 cell lines. Further study of the hypolipidemic mechanism showed that oleiferasaponin A2 inhibited fatty acid synthesis by significantly down-regulating the expression of SREBP-1c, FAS and FAS protein, while dramatically promoting fatty acid β-oxidation by up-regulating the expression of ACOX-1, CPT-1 and ACOX-1 protein. Our results demonstrate that the oleiferasaponin A2 possesses potential medicinal value for hyperlipidemia treatment.

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Stimulation of fatty acid synthesis in vitro by gonadotrophin-induced testicular ribonucleic acid

Biochemical Journal ◽

10.1042/bj1080147 ◽

1968 ◽

Vol 108 (1) ◽

pp. 147-152 ◽

Cited By ~ 9

Author(s):

Ajit Goswami ◽

James K. Skipper ◽

William L. Williams

Keyword(s):

Fatty Acids ◽

Fatty Acid ◽

Luteinizing Hormone ◽

Polyunsaturated Fatty Acids ◽

Fatty Acid Synthesis ◽

Follicle Stimulating Hormone ◽

Acid Synthesis ◽

Stimulation Of ◽

Stimulating Hormone

RNA from testes of hypophysectomized rats treated with follicle-stimulating hormone and luteinizing hormone markedly stimulates in vitro the incorporation of acetate and malonate (as CoA derivatives) into polyunsaturated fatty acids. The system in vitro contains the components necessary for both protein and fatty acid synthesis. That the RNA is a hormone-induced messenger type that causes enzyme synthesis that then causes fatty acid synthesis is supported by the following observations: (1) the stimulation of RNA synthesis by follicle-stimulating hormone and luteinizing hormone is decreased by injection of the animals with actinomycin D; (2) puromycin in the system in vitro decreases the synthesis of polyunsaturated fatty acids; (3) the activity of the RNA preparation is destroyed by digestion with ribonuclease; in fact, the digest is inhibitory, which is a characteristic of messenger-RNA-mediated protein synthesis; (4) protein that might be denatured enzyme is virtually absent from the effective RNA preparations.

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