title: Influence of visfatin on histopathological changes of non-alcoholic fatty liver disease.
abstract: BACKGROUND
  Non-alcoholic fatty liver disease (NAFLD) is a common liver disease. The aim of the present study was to explore the relation of visfatin with underlying histopathological changes of NAFLD patients.
  
  
  METHODS
  A population of 55 NAFLD patients was analyzed in a cross-sectional study. A liver biopsy was realized. Weight, basal glucose, insulin, insulin resistance (HOMA), total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, and visfatin levels were measured. A bioimpedance was performed.
  
  
  CONCLUSIONS
  The mean age was 42.8 +/- 11.2 years, the mean BMI was 33.1 +/- 10.2 with 37 males (67.3%) and 18 females (32.7%). Probabilities to have; portal inflammation increased 1.11 (CI95%:1.03-1.50) with each increment of 1 ng/ml of visfatin concentration, high grade of steatosis increased 1.25 (CI 95%:1.06-1.61) with each unit of insulin concentrations, fibrosis increased 1.12 (CI 95%:1.02-1.43) with each unit of fat mass and lobulillar inflammation increased 13.4 (CI 95%:1.3-147) with each unit of HOMA-IR. Portal inflammation frequencies were different between groups (low visfatin group 13.07 < ng/ml: 37.5% versus high visfatin group 13.07 > ng/ml: 62.5%; P < 0.05). In conclusion, several histopathological changes in liver biopsies could be explained by insulin concentrations, HOMA-IR, and fat mass amount. Moreover, visfatin plasma concentrations could predict the presence of portal inflammation in NAFLD patients.
authors.affiliation: Institute of Endocrinology and Nutrition, Medicine School and Unit of Investigation, Hospital Rio Hortega, University of Valladolid, C/Los perales 16, 47130, Simancas, Valladolid, Spain.
authors.forename: R
authors.initials: R
authors.lastname: Aller
authors.forename: D A
authors.initials: DA
authors.lastname: de Luis
authors.forename: O
authors.initials: O
authors.lastname: Izaola
authors.forename: M Gonzalez
authors.initials: MG
authors.lastname: Sagrado
authors.forename: R
authors.initials: R
authors.lastname: Conde
authors.forename: M C
authors.initials: MC
authors.lastname: Velasco
authors.forename: T
authors.initials: T
authors.lastname: Alvarez
authors.forename: D
authors.initials: D
authors.lastname: Pacheco
authors.forename: J M
authors.initials: JM
authors.lastname: González
mesh_terms: D000273:Adipose Tissue / Q000473:pathology; D000328:Adult; D001706:Biopsy; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003430:Cross-Sectional Studies; D017097:Electric Impedance; D005234:Fatty Liver / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology; D008099:Liver / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*; D011237:Predictive Value of Tests; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D007328:Insulin; D014280:Triglycerides; D002784:Cholesterol; D054409:Nicotinamide Phosphoribosyltransferase