Paradoxical effect of ethanol on liver lipogenesis in the genetically-obese Zucker rat

Karsenty, C.; Ulmer, M.; Chanussot, F.; Ratanasavanh, R.; Debry, G

doi:10.1079/bjn19850087

Cited by 6 publications

(3 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Possibly, we missed a rise in circulating lipids on an earlier time point. On the other hand, obesity has been shown to influence the turnover rate of circulating fatty acids and glycerol, and thus increased metabolization of these substrates by the liver could have decreased their serum concentrations . In our mouse study we indeed observed such signs of an elevated fatty acid and glycerol turnover rate in all obese mice, unaffected by nutrition or illness.…”

Section: Discussionmentioning

confidence: 53%

Premorbid obesity, but not nutrition, prevents critical illness‐induced muscle wasting and weakness

Goossens

Marques

Derde

et al. 2016

J cachexia sarcopenia muscle

View full text Add to dashboard Cite

BackgroundThe ‘obesity paradox’ of critical illness refers to better survival with a higher body mass index. We hypothesized that fat mobilized from excess adipose tissue during critical illness provides energy more efficiently than exogenous macronutrients and could prevent lean tissue wasting.MethodsIn lean and premorbidly obese mice, the effect of 5 days of sepsis‐induced critical illness on body weight and composition, muscle wasting, and weakness was assessed, each with fasting and parenteral feeding. Also, in lean and overweight/obese prolonged critically ill patients, markers of muscle wasting and weakness were compared.ResultsIn mice, sepsis reduced body weight similarly in the lean and obese, but in the obese with more fat loss and less loss of muscle mass, better preservation of myofibre size and muscle force, and less loss of ectopic lipids, irrespective of administered feeding. These differences between lean and obese septic mice coincided with signs of more effective hepatic fatty acid and glycerol metabolism, and ketogenesis in the obese. Also in humans, better preservation of myofibre size and muscle strength was observed in overweight/obese compared with lean prolonged critically ill patients.ConclusionsDuring critical illness premorbid obesity, but not nutrition, optimized utilization of stored lipids and attenuated muscle wasting and weakness.

show abstract

Section: Discussionmentioning

confidence: 53%

Premorbid obesity, but not nutrition, prevents critical illness‐induced muscle wasting and weakness

Goossens

Marques

Derde

et al. 2016

J cachexia sarcopenia muscle

View full text Add to dashboard Cite

show abstract

“…These include the role of Free Fatty Acids, FFA oxidation, reactive oxygen species, endoplasmic reticulum stress, genetics/epigenetics, the innate immune system, gut derived endotoxins, endogenous alcohol, intestinal dysbiosis and small intestinal bacterial overgrowth (SIBO). [193] Hepatic lipogenesis and fatty degeneration reduced in obese (fa/fa) rats given an ethanol diet showing a paradoxical effect of ethanol on liver lipogenesis in the genetically-obese Zucker rat Carmiel-Haggai et al, 2003 [194] Binge ethanol exposure increases liver injury in obese rats Olleros et al, 2008 [195] Moderately FAT diet and low-dose EtOH generate steatohepatitis and TNF liver expression. Changes in regulation of TNF associated with increased IL-6, IFN-gamma and iNOS expression.…”

Section: Nutritional Support In the Setting Of Alcohol Or Nicotine Usmentioning

confidence: 99%

The bidirectional impacts of alcohol consumption and the metabolic syndrome: Cofactors for progressive fatty liver disease

Boyle

Masson

Anstee

2018

Journal of Hepatology

129

109

View full text Add to dashboard Cite

Current medical practice artificially dichotomises a diagnosis of fatty liver disease into one of two common forms: alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD). Together, these account for the majority of chronic liver diseases worldwide. In recent years, there has been a dramatic increase in the prevalence of obesity and metabolic syndrome within the general population. These factors now coexist with alcohol consumption in a substantial proportion of the population. Each exposure sensitises the liver to the injurious effects of the other; an interaction that drives and potentially accelerates the genesis of liver disease. We review the epidemiological evidence and scientific literature that considers how alcohol consumption interacts with components of the metabolic syndrome to exert synergistic or supra-additive effects on the development and progression of liver disease, before discussing how these interactions may be addressed in clinical practice.

show abstract

“…The present results show that liver steatosis in the obese rats was less when diet E was given than when diet C was given. In a subsequent study (Karsenty et al 1985), an investigation of liver biochemical indices (glycogenesis, enzyme activities) led to the determination of one of the causes of this decrease: lowered hepatic lipogenesis activity in f a / f a rats eating diet E. The decrease in liver and adipose tissue lipogenesis and lipid synthesis is insufficient to affect the development of obesity and hyperlipidaemia, so these syndromes remain comparable for both diets.…”

Section: Hyperlipidaemia In the Fa/ Fa Zucker Rat After Alcohol Intoxmentioning

confidence: 99%

Influence of chronic ethanol intake on obesity, liver steatosis and hyperlipidaemia in the Zucker fa/fa rat

et al. 1985

Self Cite

View full text Add to dashboard Cite

1. The effect of chronic alcohol intoxication on metabolic disturbances and fatty infiltration and degeneration was studied in genetically obese, hyperlipoproteinaemic, fa/fa Zucker rats.2. Sixteen obese Zucker (fa/fa) rats, sixteen lean Zucker rats (Fa/-) and sixteen Wistar rats, all male rats aged 7-8 weeks, weregiveneitheracontrol (C)diet (13% ofenergyfromprotein, 37% fromfat, 50% fromcarbohydrate) or an ethanol (E) diet (13% of energy from protein, 37% from fat, 14% from carbohydrate, 36% from ethanol) for 4 weeks.3. Thefalfa rats given diet E consumed more energy than those given diet C, but after 4 weeks the weight gains and degrees of obesity were similar for both groups. With both diets, the developed hyperlipidaemia could be explained by the hyperinsulinaemia. Both hypertriglyceridaemia and hypercholesterolaemia were lower in fa/fa rats eating diet E than in those given diet C . Fatty infiltration of the liver, as assessed by hepatic triacylglycerol and cholesterol contents, was observed with both diets, but for fa/fa rats it was less extreme in those given diet E.Chronic alcohol intoxication in rats leads to liver steatosis (fatty infiltration and degeneration of the liver) (Lieber et al. 1965; De Carli & Lieber, 1967; Baraona & Lieber, 1979;Reitz, 1979) with (Redgrave & Martin, 1977;Lederer et al. 1978) or without hyperlipoproteinaemia (Hirayama et al. 1979). As the genetically obesefalfa Zucker rat has both these metabolic disorders, we have studied this species to determine if these conditions are exacerbated by chronic alcohol intoxication. MATERIALS A N D METHODS AnimalsForty-eight male rats were used : sixteen Wistar rats (CESAL, Vigneul-sous-Montmedy), sixteen obese (fa/'a) and sixteen lean (Fa/-) Zucker rats (CNRS, Orleans-la-Source). They were housed individually in randomly assigned cages and allowed to adapt over a 2-week period, during which they were allowed free access to a standard diet (UAR no. A 04, Villemoisson-sur-Orge) containing (g/kg) : protein 170, carbohydrate 587, lipid 30. At 7-8 weeks of age, equal numbers of each strain were randomly assigned to a control (C) or an ethanol-containing (E) diet, and they were allowed free access to food and tap water for a 4-week experimental period. The rats were weighed on arrival and at weekly intervals thereafter. DietsThe compositions of diets C and E are given in Table 1. The diets were given in a semi-liquid form to simplify ethanol incorporation and preserve a homogenous appearance. The proportion of ethanol in diet E was progressively increased at the expense of maize starch over the first 5 d. Amounts of ethanol given (g/kg dry diet) were 180 for the first 2 d, 240

show abstract

Paradoxical effect of ethanol on liver lipogenesis in the genetically-obese Zucker rat

Cited by 6 publications

References 19 publications

Premorbid obesity, but not nutrition, prevents critical illness‐induced muscle wasting and weakness

Premorbid obesity, but not nutrition, prevents critical illness‐induced muscle wasting and weakness

The bidirectional impacts of alcohol consumption and the metabolic syndrome: Cofactors for progressive fatty liver disease

Influence of chronic ethanol intake on obesity, liver steatosis and hyperlipidaemia in the Zucker fa/fa rat

Contact Info

Product

Resources

About