title: Hepatic lipase activity is increased in non-alcoholic fatty liver disease beyond insulin resistance.
abstract: OBJECTIVE
  Hepatic lipase is a lipolytic enzyme mostly synthesized and localized at the surface of liver sinusoidal capillaries, which hydrolyses triglycerides and phospholipids of intermediate density, large low density (LDL) and high density lipoproteins. Hepatic lipase activity is increased in insulin resistant states. Non-alcoholic fatty liver disease (NAFLD) is characterized by insulin resistance. However, at present, no data are available regarding the behaviour of hepatic lipase with regard to the degree of hepatic steatosis. Our aim was to evaluate hepatic lipase activity in NAFLD patients and its relationship to the severity of hepatic steatosis.
  
  
  METHODS
  We studied 48 patients with NAFLD (diagnosed by ultrasonography and confirmed by liver biopsy) and 30 controls. Steatosis was semi-quantitatively assessed and considered as mild or grade 1, moderate or grade 2 and severe or grade 3.
  
  
  METHODS
  hepatic lipase activity, lipid and lipoprotein profile (including intermediate density lipoproteins and dense LDL), adiponectin, insulin, glucose and high sensitivity C-reactive protein were measured. Homeostasis model assessment for insulin resistance (HOMA) index was calculated.
  
  
  RESULTS
  Patients with hepatic steatosis presented with higher hepatic lipase activity, HOMA and dense LDL and lower levels of adiponectin, high density lipoproteins, cholesterol and apoA-I. Hepatic lipase activity positively correlated significantly with the severity of hepatic steatosis. Hepatic lipase correlated with a more atherogenic profile and persisted higher in patients even after corrected for age, gender, body mass index, HOMA and adiponectin.
  
  
  CONCLUSIONS
  The higher hepatic lipase activity in NAFLD patients contributes to a more atherogenic profile linked to increased cardiovascular risk, beyond the insulin resistance and the reduction in adiponectin.
authors.affiliation: Laboratory of Lipids and Lipoproteins, Department of Clinical Biochemistry, INFIBIOC, University of Buenos Aires, Buenos Aires, Argentina.
authors.forename: V
authors.initials: V
authors.lastname: Miksztowicz
authors.forename: D
authors.initials: D
authors.lastname: Lucero
authors.forename: V
authors.initials: V
authors.lastname: Zago
authors.forename: L
authors.initials: L
authors.lastname: Cacciagiú
authors.forename: G
authors.initials: G
authors.lastname: Lopez
authors.forename: E
authors.initials: E
authors.lastname: Gonzalez Ballerga
authors.forename: J
authors.initials: J
authors.lastname: Sordá
authors.forename: E
authors.initials: E
authors.lastname: Fassio
authors.forename: L
authors.initials: L
authors.lastname: Schreier
authors.forename: G
authors.initials: G
authors.lastname: Berg
mesh_terms: D050197:Atherosclerosis / Q000209:etiology; D002318:Cardiovascular Diseases / Q000209:etiology; D005234:Fatty Liver / Q000201:enzymology* / Q000473:pathology; D006801:Humans; D007333:Insulin Resistance; D008049:Lipase / Q000378:metabolism*; D008099:Liver / Q000201:enzymology; D065626:Non-alcoholic Fatty Liver Disease; D012306:Risk
chemical_list: C504173:LIPC protein, human; D008049:Lipase