The effect of acute, chronic, and prenatal ethanol exposure on insulin sensitivity

Ting, Justin W.; Lautt, W. Wayne

doi:10.1016/j.pharmthera.2005.10.004

Cited by 61 publications

(56 citation statements)

References 135 publications

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“…AAA leads to impaired CNS activity due to alcohol's effect on synthesis [22] , release [23] and signaling [23,24] of neurotransmitters, including serotonin [25,26] , glutamate [27] , GABA [28] , endocannabinoids [29,30] and their receptors. AAA causes damage and functional impairment of the gastrointestinal (GI) tract, including luminal GI [31][32][33][34][35][36][37][38] , liver [39][40][41][42][43][44][45][46][47][48][49][50][51][52][53][54][55] , and pancreas [56][57][58][59][60][61][62] ; it also affects the protein, carbohydrate, and fat metabolism [58,[63][64][65][66] . AAA leads to insufficient immune system responses to infections; such deficiency was observed both in organ-specific [67][68][69] and systemic infections [70][71][72] .…”

Section: Aaa: Biomedical Impactmentioning

confidence: 99%

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In vitroandin vivomodels of acute alcohol exposure

Dolganiuc

Szabó

2009

WJG

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Alcohol abuse is a global problem due to the financial burden on society and the healthcare system. While the harmful health effects of chronic alcohol abuse are well established, more recent data suggest that acute alcohol consumption also affects human wellbeing. Thus, there is a need for research models in order to fully understand the effect of acute alcohol abuse on different body systems and organs. The present manuscript summarizes the interdisciplinary advantages and disadvantages of currently available human and non-human models of acute alcohol abuse, and identifies their suitability for biomedical research.

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Section: Aaa: Biomedical Impactmentioning

confidence: 99%

“…The vertebrate AAA models are widely used in research of biomedical effects of AAA, including brain [23][24][25][26][27][28][29][30]116] , gastrointestinal [38][39][40][41][42][43][44][46][47][48][64][65][66]154] , vascular [73,153] , muscle [97] and immune [68][69][70][71][72]74] systems.…”

Section: S I M I L a R T O H U M A N A A A M O D E L S T H E N O Nh mentioning

confidence: 99%

In vitroandin vivomodels of acute alcohol exposure

Dolganiuc

Szabó

2009

WJG

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“…The impairments in CNS activities are due to alcohol's effect on synthesis, release, and signaling of neuron transmitters, including glutamate, GABA, and other neuron transmitters (1)(2)(3). Alcohol use also affects insulin sensitivity that regulates protein, carbohydrate, and fat metabolism (4). Chronic abuse of alcohol can result in tolerance and physical dependence.…”

Section: Introductionmentioning

confidence: 99%

Increased brain uptake and oxidation of acetate in heavy drinkers

Jiang

Gulanski²,

Feyter³

et al. 2013

J. Clin. Invest.

118

114

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When a person consumes ethanol, the body quickly begins to convert it to acetic acid, which circulates in the blood and can serve as a source of energy for the brain and other organs. This study used 13 C magnetic resonance spectroscopy to test whether chronic heavy drinking is associated with greater brain uptake and oxidation of acetic acid, providing a potential metabolic reward or adenosinergic effect as a consequence of drinking. Seven heavy drinkers, who regularly consumed at least 8 drinks per week and at least 4 drinks per day at least once per week, and 7 light drinkers, who consumed fewer than 2 drinks per week were recruited. The subjects were administered [2-13 C]acetate for 2 hours and scanned throughout that time with magnetic resonance spectroscopy of the brain to observe natural 13 C abundance of N-acetylaspartate (NAA) and the appearance of 13 C-labeled glutamate, glutamine, and acetate. Heavy drinkers had approximately 2-fold more brain acetate relative to blood and twice as much labeled glutamate and glutamine. The results show that acetate transport and oxidation are faster in heavy drinkers compared with that in light drinkers. Our finding suggests that a new therapeutic approach to supply acetate during alcohol detoxification may be beneficial.

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“…However, although alcohol abuse is undoubtedly detrimental to human health, there is evidence that light-to-moderate alcohol consumption may have some beneficial effects, in particular regarding cardiovascular events, insulin resistance, and type 2 diabetes (Howard et al, 2004;Ting and Lautt, 2006;Kloner and Rezkalla, 2007). In addition, a recent study suggests that modest wine drinking could significantly reduce the prevalence of nonalcoholic fatty liver disease, which is closely related to obesity and metabolic syndrome (Dunn et al, 2008).…”

mentioning

confidence: 99%

“…It is interesting that moderate alcohol intake could lower the risk of type 2 diabetes through an improvement of insulin sensitivity (Howard et al, 2004;Sierksma et al, 2004;Ting and Lautt, 2006). The mechanisms whereby moderate alcohol consumption ameliorates insulin sensitivity are currently poorly understood, but some studies pointed to a reduction of body weight (in particular in women) and increased adiponectin levels (Sierksma et al, 2004;Ting and Lautt, 2006;Imhof et al, 2009).…”

mentioning

confidence: 99%

Chronic Ethanol Consumption Lessens the Gain of Body Weight, Liver Triglycerides, and Diabetes in Obese ob/ob Mice

Fromenty

Vadrot²,

Massart³

et al. 2009

J Pharmacol Exp Ther

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Clinical studies suggest that moderate alcohol consumption can have beneficial effects, in particular regarding cardiovascular events, insulin resistance, and type 2 diabetes. In this study, lean and obese diabetic ob/ob mice were submitted or not to chronic ethanol intake via the drinking water for 6 months, which was associated with moderate levels of plasma ethanol. Plasma levels of alanine aminotransferase and aspartate aminotransferase were not increased by alcohol intake. Ethanol consumption progressively reduced the gain of body weight in ob/ob mice, but not in lean mice, and this was observed despite higher calorie intake. Increased plasma free fatty acids and glycerol in ethanol-treated ob/ob mice suggested peripheral lipolysis. Glycemia and insulinemia were significantly reduced, whereas adiponectinemia was increased in ethanol-treated ob/ob mice. Liver weight and triglycerides were significantly decreased in ethanol-treated ob/ob mice, and this was associated with less microvesicular steatosis. Hepatic levels of AMP-activated protein kinase and the phosphorylated form of acetyl-CoA carboxylase were higher in ethanol-treated ob/ob mice, suggesting better fatty acid oxidation. However, hepatic mRNA expression of several lipogenic genes was not reduced by ethanol consumption. Finally, mild oxidative stress was noticed in the liver of ethanol-treated mice, regardless of their genotype. Hence, our data are in keeping with clinical studies suggesting that moderate ethanol intake can have beneficial effects on type 2 diabetes and insulin sensitivity, at least in part through increased levels of plasma adiponectin. However, further studies are needed to determine whether longterm drinking of light-to-moderate amounts of ethanol is safe for the liver.

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The effect of acute, chronic, and prenatal ethanol exposure on insulin sensitivity

Cited by 61 publications

References 135 publications

In vitroandin vivomodels of acute alcohol exposure

In vitroandin vivomodels of acute alcohol exposure

Increased brain uptake and oxidation of acetate in heavy drinkers

Chronic Ethanol Consumption Lessens the Gain of Body Weight, Liver Triglycerides, and Diabetes in Obese ob/ob Mice

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