Z Gastroenterol 2006; 44 - A2_24
DOI: 10.1055/s-2006-931691

Chronic and excessive alcohol consumption is causing elevated adiponectin serum levels

M Mühlbauer 1, A Schäffler 1, C Buechler 1, M Johann 2, N Wodarz 2, T Weiss 3, J Schölmerich 1, C Hellerbrand 1
  • 1Klinik und Poliklinik für Innere Medizin I der Universität Regensburg, Regensburg
  • 2Klinik und Poliklinik für Psychiatrie, Klinikum der Universität Regensburg, Regensburg
  • 3Klinik und Poliklinik für Chirurgie der Universität Regensburg, Regensburg

In animal models hepatic injury is causing elevated serum adiponectin levels, and adiponectin is revealing antifibrotic and hepatoprotective effects. Adiponectin is a plasma protein produced by the adipose tissue and decreased serum adiponectin levels are found in obese patients. The aim of this study was to analyze the effect of (chronic) excessive alcohol consumption on adiponectin expression and serum levels in vivo and in vitro.

Patients and Methods: Serum specimens were collected from a) 75 heavy drinkers (>=80g/day; >5 years) without clinical or sonomorphological indications for advanced liver damage recruited from an in-patient abstention program at the day of admission, and during the program; b) 118 patients with HCV infection, c) 36 patients with alcohol-associated cirrhosis, and d) 10 healthy probands that consumed excessive amounts of alcohol (140–500g/48h) after a period of alcohol abstinence of 4 weeks. In vitro primary human hepatocytes (PHH) and adipocytes were incubated with 100µM alcohol for 48h. Adiponectin mRNA and protein expression were analysed with real time PCR and ELISA.

Results: Patients with chronic excessive alcohol consumption had significantly higher serum adiponectin levels than HCV-patients. Adiponectin levels did not differ significantly between patients with or without liver cirrhosis but correlated significantly with the amount of alcohol consumption and transaminases. In contrast, in HCV patients serum adiponectin levels did not correlate with transaminases or grading. After chronic excessive alcohol consumption a significant reduction of adiponectin levels was found during the course of alcohol abstinence. After short term excessive alcohol consumption no elevated adiponectin levels were observed in healthy individuals. In vitro adiponectin expression was detected in adipocytes but not in PHH. Neither in adipocytes nor in PHH alcohol induced adiponectin expression.

Summary and Conclusions: Elevated adiponectin levels were found in patients with alcoholic but not in patients with viral liver damage, indicating a specific effect of alcohol on adiponectin expression. These effect seems to be dose and time dependent, and to correlate with the degree of hepatic damage. Hereby, alcohol does not seem to affect adiponectin expression directly in adipocytes but potentially via mediators released as a result of the alcoholic liver damage.