title: Elevated adiponectin serum levels in patients with chronic alcohol abuse rapidly decline during alcohol withdrawal.
abstract: BACKGROUND
  Adiponectin is a circulating protein with hepatoprotective effects.
  
  
  OBJECTIVE
  To study the relationship of excessive alcohol consumption and serum adiponectin levels (SAL).
  
  
  METHODS
  The SAL were determined in (i) heavy drinkers without advanced liver damage during the course of alcohol withdrawal, (ii) patients with chronic hepatitis C virus (HCV) infection, (iii) patients with alcohol-associated cirrhosis, and (iv) healthy volunteers that consumed excessive amounts of alcohol for only a short period of time. Further, primary human hepatocytes (PHH) and adipocytes were incubated in vitro with alcohol or serum of patients.
  
  
  RESULTS
  Patients with chronic alcohol consumption had significantly higher SAL than HCV-patients with comparable degrees of liver damage. In alcoholics, but not in HCV patients, SAL positively correlated with serum levels of aminotransferases. Further, SAL correlated with the amount of alcohol consumption but declined during the course of alcohol abstinence. After short-term excessive alcohol consumption SAL were not elevated in healthy individuals. Adiponectin mRNA was detectable in adipocytes but not in hepatocytes, and alcohol failed to induce adiponectin in both cell types. In contrast, serum of active drinkers induced adiponectin expression in adipocytes while serum from the same individuals collected after alcohol withdrawal had no effect.
  
  
  CONCLUSIONS
  Alcohol exhibits a specific effect on SAL that is dose and time dependent, and correlates with the degree of hepatic damage. Alcohol does not seem to affect adiponectin expression directly in adipocytes but potentially via mediators systemically released as a result of the chronic alcohol intake.
authors.affiliation: Department of Internal Medicine I, University of Regensburg, Regensburg D-93042, Germany.
authors.forename: Christa
authors.initials: C
authors.lastname: Buechler
authors.forename: Andreas
authors.initials: A
authors.lastname: Schäffler
authors.forename: Monika
authors.initials: M
authors.lastname: Johann
authors.forename: Markus
authors.initials: M
authors.lastname: Neumeier
authors.forename: Philip
authors.initials: P
authors.lastname: Köhl
authors.forename: Thomas
authors.initials: T
authors.lastname: Weiss
authors.forename: Norbert
authors.initials: N
authors.lastname: Wodarz
authors.forename: Paul
authors.initials: P
authors.lastname: Kiefer
authors.forename: Claus
authors.initials: C
authors.lastname: Hellerbrand
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects / Q000378:metabolism; D052242:Adiponectin / Q000097:blood / Q000235:genetics; D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D000428:Alcohol Drinking / Q000097:blood* / Q000473:pathology; D000437:Alcoholism / Q000097:blood* / Q000150:complications / Q000473:pathology / Q000628:therapy; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000097:blood; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000633:toxicity; D005260:Female; D019698:Hepatitis C, Chronic / Q000097:blood* / Q000150:complications / Q000473:pathology; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D008099:Liver / Q000201:enzymology / Q000473:pathology* / Q000821:virology; D008103:Liver Cirrhosis / Q000097:blood* / Q000473:pathology / Q000821:virology; D008104:Liver Cirrhosis, Alcoholic / Q000097:blood / Q000209:etiology* / Q000473:pathology; D008297:Male; D051379:Mice; D008875:Middle Aged; D012333:RNA, Messenger / Q000378:metabolism; D013375:Substance Withdrawal Syndrome / Q000097:blood* / Q000473:pathology / Q000628:therapy; D013997:Time Factors; D015854:Up-Regulation
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D015415:Biomarkers; D012333:RNA, Messenger; D000431:Ethanol; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase