Quantitative analysis of metabolism of hepatic triglyceride in ethanol-treated rats

Abrams, M A; Cooper, Cecil

doi:10.1042/bj1560033

Cited by 64 publications

(47 citation statements)

References 32 publications

(28 reference statements)

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“…Chronic alcohol consumption increases mobilization of fatty acids from adipose tissues (Feigelson et al ., 1961) or fatty acid synthesis in the liver. The presence of fatty acids in the liver facilitates the formation of TGs and phospholipids (Abrams and Cooper, 1976; Cairns and Peters, 1983). Moreover, alcohol feeding increases cholesterol synthesis (Lefevre et al ., 1972), decreases fatty acid oxidation in the liver, and attenuates lipid secretion into serum or bile (Blomstrand and Kager, 1973).…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Ecklonia stolonifera Extract on Ethanol-Induced Fatty Liver in Rats

Bang

Byun

Choi

et al. 2016

Biomolecules & Therapeutics

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Chronic alcohol consumption causes alcoholic liver disease, which is associated with the initiation of dysregulated lipid metabolism. Recent evidences suggest that dysregulated cholesterol metabolism plays an important role in the pathogenesis of alcoholic fatty liver disease. Ecklonia stolonifera (ES), a perennial brown marine alga that belongs to the family Laminariaceae, is rich in phlorotannins. Many studies have indicated that ES has extensive pharmacological effects, such as antioxidative, hepatoprotective, and antiinflammatory effects. However, only a few studies have investigated the protective effect of ES in alcoholic fatty liver. Male Sprague-Dawley rats were randomly divided into normal diet (ND) (fed a normal diet for 10 weeks) and ethanol diet (ED) groups. Rats in the ED group were fed a Lieber-DeCarli liquid diet (containing 5% ethanol) for 10 weeks and administered ES extract (50, 100, or 200 mg/kg/day), silymarin (100 mg/kg/day), or no treatment for 4 weeks. Each treatment group comprised of eight rats. The supplementation with ES resulted in decreased serum levels of triglycerides (TGs), total cholesterol, alanine aminotransferase, and aspartate aminotransferase. In addition, there were decreases in hepatic lipid and malondialdehyde levels. Changes in liver histology, as analyzed by Oil Red O staining, showed that the ES treatment suppressed adipogenesis. In addition, the ES treatment increased the expression of fatty acid oxidation-related genes (e.g., PPAR-α and CPT-1) but decreased the expression of SREBP 1, which is a TG synthesis-related gene. These results suggest that ES extract may be useful in preventing fatty acid oxidation and reducing lipogenesis in ethanol-induced fatty liver.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Ecklonia stolonifera Extract on Ethanol-Induced Fatty Liver in Rats

Bang

Byun

Choi

et al. 2016

Biomolecules & Therapeutics

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“…In the majority of cases the accumulating lipids are predominantly triglycerides (TG). Excessive consumption of alcohol or obesity are the major causes of a fatty liver [1]. When alcohol is metabolized, the generation of NADH in the cytosol by alcohol dehydrogenase (ADH) results in an increased NADH concentration in the mitochondrion and impairs β-oxidation and tricarboxylic acid cycle activity.…”

Section: Introductionmentioning

confidence: 99%

Traditional Chinese Medicine improves dysfunction of peroxisome proliferator-activated receptor α and microsomal triglyceride transfer protein on abnormalities in lipid metabolism in ethanol-fed rats

Kwon¹,

Hyun²,

Choung³

2005

BioFactors

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We report the effects of Traditional Chinese Medicine (TCM) on alcohol-induced fatty liver in rats. TCM consists of Astragalus membranaceus, Morus alba, Crataegus pinnatifida, Alisma oriental, Salvia miltiorrhiza and Pueraria lobata. The rats were separated randomly into five groups; the CD group (n=10), which was fed a control diet for 10 weeks, the ED group (n=10), which was fed an isocaloric liquid diet containing ethanol for 10 weeks and given daily oral doses of TCM (0.222 g/kg/day; TCM222, 0.667 g/kg/day; TCM667, and 2.000 g/kg/day; TCM2000, n=10, respectively) over the last four weeks of the study. The ED group developed fatty livers, as determined by their lipid profiles and liver histological findings. Compared with the control group, liver/body weight, plasma triglyceride (TG) and total cholesterol (TC), liver TG and TC, plasma alanine aminotransferase (ALT) and aspartic aminotransferase (AST) significantly increased in the ED group. Also, free fatty acids (FFA) levels increased in both plasma and liver during the administration of ethanol. On the other hand, when rats were administrated with TCM, their liver/body weight, plasma TG, TC and FFA, liver TG, TC and FFA, plasma ALT and AST decreased significantly and the degree of hepatic lipid droplets was markedly improved compared with those in the ED group. Proper function of the peroxisome proliferator-activated receptor alpha (PPARalpha) is essential for the regulation of hepatic fatty acid metabolism. Microsomal triglyceride transfer protein (MTP) is essential for the secretion of triglycerides from the liver. mRNAs for PPARalpha and MTP were reduced in the livers of ethanol-fed rats. TCM restored the mRNA levels of PPARalpha and MTP, and prevented development of fatty livers in ethanol-fed rats. Impairment of PPARalpha and MTP function during ethanol consumption contributes to the development of alcohol-induced fatty liver, which can be overcome by TCM.

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“…Triton WR1339, in contrast, inhibits lipoprotein lipase activity leading to an accumulation of VLDL at a rate reflecting net secretion from the liver. 12 We report here on studies using these techniques to test the above two possible origins of the VLDL hyperiipidemia in the JCR:LA-cp rat.…”

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confidence: 99%

Plasma lipid secretion and clearance in hyperlipidemic JCR:LA-corpulent rats.

et al. 1989

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The JCR: LA-corpulent rat Is an obese, hyperlipidemic, hyperinsullnemlc strain that Is atherosclerosis-prone and develops myocardlal lesions. The hyperllpldemla Is due to elevated plasma levels of a large relatively triglycerlde-rich very low density lipoprotein (VLDL). Both corpulent and lean male and female rats were studied. Postheparln llpid clearance and apparent hepatic secretion rate after Triton WR1339 Inhibition of lipoproteln llpase were determined. The concentrations of cholesterol and cholesteryl esters were not significantly altered by either treatment TrlglycerIdes showed rapid postheparln clearance In corpulent rats. The apparent hepatic secretion rate was markedly higher In corpulent male rats than In lean male rats, and the rate in corpulent females was again higher, reflecting the higher serum trlglyceride concentrations In corpulent female rats. The relative secretion rate of C 4 8 trlglycerlde molecular species was lower than that of the C: 50 to C: 56 species, while the postheparln clearance of C 4 8 trlglycerlde molecular species was impaired compared to the C: 50 species and those with higher carbon numbers. This effect was more marked In the male than In the female corpulent rats. The results Indicate that VLDL hyperllpldemia In the corpulent rat Is due to hepatic hypersecretlon of VLDL and not to a defect in lipoproteln llpase. Further, the atherogenesls that Is characteristic of the corpulent male rat may be related to the differential metabolism of fatty acids. (Arteriosclerosis 9:869-876, November/December 1989) T he JCR: L A-corpulent rat incorporates the corpulent (cp) gene isolated by Koletsky. 1^ The original strain was derived from a cross of the spontaneously hypertensive (SHR) and Sprague-Dawley rat strains and was hypertensive, hyperlipidemic, and prone to a fulminant atherosclerosis. Hansen 3 incorporated the cp gene into two inbred strains, the SHR/N and the LA/N. Repeated backcrosses (more than 12 times) were made to the parent strains to give two congenic strains. Rats that are homozygous for the cp gene (cp/cp) are obese, while rats that are heterozygous (cp/+) or homozygous normal (+/+) are lean and indistinguishable from the parent strain. The LA/N-cp strain has been described by Elwood et al. 4 and studied as a model for obesity and the effects of high sugar intake. The SHR/N-cp rat is highly sensitive to dietary sucrose and is regarded as a model for the study of obesity and insulin resistance. 5In the course of the development of the LA/N-cp congenic strain, breeding stock from the fifth backcross was used to establish a colony in our laboratories. This colony differs from the fully congenic LA/N-cp and has recently been designated JCR: LA-cp. We have described this strain in previous publications.6 ' 7 The cp/cp male rats spontaneously develop both atherosclerotic and myocarFrom the Departments of Surgery and Pathology, University of Alberta, Edmonton, Alberta, and the Department of Biochemistry, Dalhousie University, Halifax, Nova Scotia, Canada.This work was supp...

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Quantitative analysis of metabolism of hepatic triglyceride in ethanol-treated rats

Cited by 64 publications

References 32 publications

Protective Effects of Ecklonia stolonifera Extract on Ethanol-Induced Fatty Liver in Rats

Protective Effects of Ecklonia stolonifera Extract on Ethanol-Induced Fatty Liver in Rats

Traditional Chinese Medicine improves dysfunction of peroxisome proliferator-activated receptor α and microsomal triglyceride transfer protein on abnormalities in lipid metabolism in ethanol-fed rats

Plasma lipid secretion and clearance in hyperlipidemic JCR:LA-corpulent rats.

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