title: Serum leptin levels correlate with hepatic steatosis in chronic hepatitis C.
abstract: OBJECTIVE
  Hepatic steatosis (HS) has been related to obesity and fibrosis in chronic hepatitis C (CHC). The aim of this study was to determine the role of leptin system in HS development.
  
  
  METHODS
  Patients (n = 131) with biopsy-proven CHC, positive HCV RNA, and raised ALT were enrolled. Body mass index, percentage of body fat by skin fold measurement, and bioelectrical impedance analysis was calculated and serum leptin concentration measured. Intrahepatic HCV RNA, HS, necroinflammatory activity, and fibrosis were determined in liver biopsy tissue.
  
  
  RESULTS
  HS was present in 63 patients (48.1%). Steatosis was evident in 32 of 91 patients (35.2%) infected with genotype 1 and in 22 of 27 patients (81.5%) with genotype 3a (p < 0.001). In patients infected by genotype 3a, HS correlated significantly with intrahepatic HCV RNA load (r = 0.78; p < 0.001). However, in genotype 1, HS was associated with host factors such as leptin, body mass index, percentage of body fat, and visceral obesity. Multivariate analysis showed genotype (OR = 11.54, 95% CI = 1.13-117.14, p = 0.038), leptin levels (OR = 1.09, 95% CI = 1.03-1.17, p = 0.008) and fibrosis (OR = 9.86, 95% CI = 2.11-5.86, p = 0.03) as independent variables of HS development.
  
  
  CONCLUSIONS
  Hepatic steatosis was related to genotype, fibrosis degree, and serum leptin levels. Genotype 3 seems to have a viral specific steatogenic effect. Leptin seems to be a link between obesity and steatosis development in CHC genotype 1-infected patients.
authors.affiliation: Units of Hepatology, Hospital Universitario de Valme, Sevilla, Spain.
authors.forename: Manuel
authors.initials: M
authors.lastname: Romero-Gómez
authors.forename: Victor M
authors.initials: VM
authors.lastname: Castellano-Megias
authors.forename: Lourdes
authors.initials: L
authors.lastname: Grande
authors.forename: José A
authors.initials: JA
authors.lastname: Irles
authors.forename: Marina
authors.initials: M
authors.lastname: Cruz
authors.forename: Marí Carmen
authors.initials: MC
authors.lastname: Nogales
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Alcón
authors.forename: Antonio
authors.initials: A
authors.lastname: Robles
mesh_terms: D000328:Adult; D000428:Alcohol Drinking; D015992:Body Mass Index; D002986:Clinical Trials as Topic; D005234:Fatty Liver / Q000097:blood* / Q000503:physiopathology; D005260:Female; D005355:Fibrosis / Q000209:etiology / Q000473:pathology; D005838:Genotype; D016174:Hepacivirus / Q000302:isolation & purification*; D019698:Hepatitis C, Chronic / Q000097:blood* / Q000503:physiopathology; D006801:Humans; D020738:Leptin / Q000097:blood*; D008103:Liver Cirrhosis / Q000097:blood / Q000503:physiopathology; D008111:Liver Function Tests; D008297:Male; D015999:Multivariate Analysis; D016133:Polymerase Chain Reaction; D012367:RNA, Viral / Q000032:analysis; D012044:Regression Analysis; D019562:Viral Load
chemical_list: D020738:Leptin; D012367:RNA, Viral