Chronic ethanol feeding decreases expression of adiponectin by adipocytes and circulating adiponectin. Adiponectin treatment during chronic ethanol feeding prevents liver injury in mice. Chronic ethanol feeding also increases oxidative and endoplasmic reticulum (ER) stress in adipose tissue. Here we tested the hypothesis that supplemental taurine, an amino acid that functions as a chemical chaperone/osmolyte and enhances cellular antioxidant activity, would prevent ethanol-induced decreases in adiponectin expression and attenuate liver injury. Serum adiponectin concentrations decreased as early as 4 to 7 days after feeding rats a 36% ethanol diet. This rapid decrease was associated with increased oxidative, but not ER, stress in subcutaneous adipose tissue. Taurine prevented ethanol-induced oxidative stress and increased inflammatory cytokine expression in adipose tissue. Ethanol feeding also rapidly decreased expression of transcription factors regulating adiponectin expression (CCAAT/enhancer binding protein ␣; peroxisome proliferator-activated receptor ␣/␥) in subcutaneous adipose tissue. Taurine prevented the ethanol-induced decrease in CCAAT/enhancer binding protein ␣ and peroxisome proliferator-activated receptor ␣, normalizing adiponectin messenger (m)RNA and serum adiponectin concentrations. In the liver, taurine prevented ethanol-induced oxidative stress and attenuated tumor necrosis factor ␣ expression and steatosis, at least in part, by increasing expression of genes involved in fatty acid oxidation. Conclusion: In subcutaneous adipose tissue, taurine decreased ethanol-induced oxidative stress and cytokine expression, as well as normalized expression of adiponectin mRNA. Taurine prevented ethanol-induced decreases in serum adiponectin; normalized adiponectin was associated with a reduction in hepatic oxidative stress, tumor necrosis factor ␣ expression, and steatosis. Taken together, these data demonstrate that taurine has important protective effects against ethanol-induced tissue injury in both adipose and liver tissue.

Background: Chronic alcohol consumption leads to inflammation in adipose tissue, disrupting normal metabolic activity of adipocytes. Results: Expression of an alcohol metabolizing enzyme, cytochrome P4502E1, initiates inflammation in adipose. Bid-dependent apoptosis and activation of complement then exacerbate this initial response. Conclusion: Adipose inflammation during alcohol feeding develops in response to cytochrome P450 expression. Significance: Preventing adipose inflammation may prevent the pathphysiological effects of ethanol.

These data demonstrate that chronic ethanol feeding results in the development of insulin resistance, associated with impaired insulin-mediated suppression of hepatic glucose production and decreased insulin-stimulated glucose uptake into adipose tissue. Chronic ethanol-induced insulin resistance was associated with increased macrophage infiltration into adipose tissue, as well as changes in the expression of adipocytokines by adipose tissue.

Chronic ethanol consumption disrupts whole-body lipid metabolism. Here we tested the hypothesis that regulation of triglyceride homeostasis in adipose tissue is vulnerable to longterm ethanol exposure. After chronic ethanol feeding, total body fat content as well as the quantity of epididymal adipose tissue of male Wistar rats was decreased compared with pair-fed controls. Integrated rates of in vivo triglyceride turnover in epididymal adipose tissue were measured using 2 H 2 O as a tracer. Triglyceride turnover in adipose tissue was increased due to a 2.3-fold increase in triglyceride degradation in ethanol-fed rats compared with pair-fed controls with no effect of ethanol on triglyceride synthesis. Because increased lipolysis accompanied by the release of free fatty acids into the circulation is associated with insulin resistance and liver injury, we focused on determining the mechanisms for increased lipolysis in adipose tissue after chronic ethanol feeding. Chronic ethanol feeding suppressed ␤-adrenergic receptor-stimulated lipolysis in both in vivo and ex vivo assays; thus, enhanced triglyceride degradation during ethanol feeding was not due to increased ␤-adrenergic-mediated lipolysis. Instead, chronic ethanol feeding markedly impaired insulin-mediated suppression of lipolysis in conscious rats during a hyperinsulinemic-euglycemic clamp as well as in adipocytes isolated from epididymal and subcutaneous adipose tissue. These data demonstrate for the first time that chronic ethanol feeding increased the rate of triglyceride degradation in adipose tissue. Furthermore, this enhanced rate of lipolysis was due to a suppression of the anti-lipolytic effects of insulin in adipocytes after chronic ethanol feeding.Alcohol consumption is causally related to more than 60 different medical conditions, including hepatic diseases and cardiovascular disorders as well as diabetes mellitus (1). In humans chronic ethanol exposure causes excessive lipid accumulation in liver with the eventual development of hepatic steatosis (2).These pathophysiological effects of ethanol can be modeled in rodents fed diets containing ethanol; chronic ethanol feeding to rats induces hepatic steatosis coupled with the development of hyperlipidemia, characterized by elevated plasma cholesterol and triglyceride concentrations (2). These data suggest that the disruption of lipid homeostasis by ethanol is likely a mediator of alcohol-related disease progression. However, the effects of chronic ethanol feeding on lipid metabolism in adipose tissue, the biggest storage pool of lipids, are unknown.Adipose tissue is a specialized connective tissue that functions as the major storage site for fat in the form of triglycerides. Serving as an energy reserve, adipose tissue synthesizes triglycerides when energy intake exceeds energy output. During fasting or in response to infection and inflammation, adipose tissue mobilizes free fatty acids and glycerol, providing other tissues with metabolites and energy substrates (3). Mobilization of fatty acids and gl...