title: The relationship between serum adiponectin and steatosis in patients with chronic hepatitis C genotype-4.
abstract: BACKGROUND
  The mechanisms underlying steatosis during hepatitis C virus (HCV) infection are complex and multifactorial. The aim of our study was to assess whether host metabolic factors influence the degree of hepatic steatosis and fibrosis in patients infected with hepatitis C virus genotype 4 by investigating the role of adiponectin, leptin and insulin resistance.
  
  
  METHODS
  Adiponectin and leptin levels, HCV genotypes, HCV-RNA, IR (HOMA-IR), body mass index and liver steatosis and fibrosis were assessed in 74 chronic patients with HCV genotype 4.
  
  
  RESULTS
  Chronic HCV patients with steatosis showed lower serum adiponectin levels and higher levels of leptin, HOMA, alanine aminotransferase, gamma-glutamiltransferase and fibrosis scores. Low adiponectin levels were independently associated with grades of steatosis and HOMA-IR. Adiponectin levels showed significant inverse correlation between adiponectin and steatosis grade, BMI, HOMA and fibrosis stage. The multivariate analysis of factors showed that steatosis was significantly associated with low adiponectin concentration while leptin, insulin, HOMA, ALT, gamma-GT and cholesterol were positively associated with steatosis.
  
  
  CONCLUSIONS
  This study stated that patients with HCV genotype-4 suffering from steatosis had a lower adiponectin level which is inversely correlated with insulin resistance. These data support a role for adiponectin in protecting against liver injury and also that hypoadiponectinaemia may contribute to the progression of hepatic steatosis. Further molecular and genetic studies with larger numbers of patients are required to confirm these results.
authors.affiliation: Biochemistry Department, National Research Center, Cairo, Egypt.
authors.forename: Esmat
authors.initials: E
authors.lastname: Ashour
authors.forename: Nervana
authors.initials: N
authors.lastname: Samy
authors.forename: Magda
authors.initials: M
authors.lastname: Sayed
authors.forename: Azza
authors.initials: A
authors.lastname: Imam
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D002784:Cholesterol / Q000097:blood; D005234:Fatty Liver / Q000097:blood* / Q000473:pathology; D005260:Female; D005355:Fibrosis / Q000097:blood; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics; D006526:Hepatitis C / Q000097:blood* / Q000235:genetics / Q000473:pathology; D018937:Hepatitis C Antibodies / Q000097:blood; D006801:Humans; D020738:Leptin / Q000097:blood; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D014280:Triglycerides / Q000097:blood; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D052242:Adiponectin; D018937:Hepatitis C Antibodies; D020738:Leptin; D012367:RNA, Viral; D014280:Triglycerides; D002784:Cholesterol; D005723:gamma-Glutamyltransferase; D000410:Alanine Transaminase