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Chronic Ethanol Feeding Suppresses ß-Adrenergic Receptor-Stimulated Lipolysis in Adipocytes Isolated from Epididymal Fat

Departments of Biochemistry (L.K.) and Nutrition (L.E.N.), Case Western Reserve University, Cleveland, Ohio 44106-4906

Address all correspondence and requests for reprints to: Laura E. Nagy, Department of Nutrition, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, Ohio 44106-4906. E-mail: len2{at}case.edu.

Chronic ethanol consumption disrupts G protein-dependent signaling pathways in rat adipocytes. Because lipolysis in adipocytes is regulated by G protein-mediated cAMP signal transduction, we hypothesized that cAMP-regulated lipolysis may be vulnerable to long-term ethanol exposure. Male Wistar rats were fed a liquid diet containing ethanol as 35% of total calories or pair-fed a control diet that isocalorically substituted maltose dextrins for ethanol for 4 wk. Lipolysis was measured by glycerol release over 1 h with or without agonists in adipocytes isolated from epididymal fat. Chronic ethanol feeding decreased ß-adrenergic receptor-stimulated lipolysis, but had no effect on basal lipolysis. In response to ß-adrenergic activation, the early peak of cAMP accumulation was suppressed after ethanol feeding, although the basal cAMP concentration in adipocytes did not differ between pair- and ethanol-fed rats. The suppression in cAMP accumulation caused by ethanol feeding was associated with increased activity of phosphodiesterase 4. Chronic ethanol feeding also decreased ß-adrenergic receptor-stimulated protein kinase A activation and phosphorylation of its downstream proteins, perilipin A and hormone-sensitive lipase, the primary lipase-mediating lipolysis. In conclusion, these data suggest that chronic ethanol feeding increased phosphodiesterase 4 activity in adipocytes, resulting in decreased accumulation of cAMP in response to ß-adrenergic activation and a suppression of ß-adrenergic stimulation of lipolysis.

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