title: Risk interaction of obesity, insulin resistance and hormone-sensitive lipase promoter polymorphisms (LIPE-60 C > G) in the development of fatty liver.
abstract: BACKGROUND
  Hormone sensitive lipase (HSL) promoter (LIPE-60 C > G) polymorphism has been found to be involved in hepatic steatosis, obesity, diabetes and dyslipidemia. The precise interactions between these risk factors and genetic susceptibility that may affect non-alcoholic fatty liver disease (NAFLD) are still not fully determined.
  
  
  METHODS
  A cross-sectional study was conducted in 1056 men. To avoid the confounding effect of plasma glucose, the study population was classified into normal glucose tolerance (NGT, n = 729) and glucose intolerance (GI, n = 299) groups. NAFLD was diagnosed by abdominal ultrasound after ruling out any history of alcohol abuse. A multivariate regression model was used to estimate the impact of these factors on NAFLD.
  
  
  RESULTS
  In the NGT group, subjects with NAFLD often have complicated metabolic abnormalities. The coexistence of NAFLD and GI has been demonstrated to have a synergistic effect raising BMI, serum insulin and HOMA-insulin resistance (HOMA-IR). BMI and adipose-insulin resistance (Adipo-IR), but not HOMA-IR, significantly contributed to a greater risk of developing NAFLD. Serum triglyceride was significantly up-regulated in men with the (CG + GG) genotype of HSL promoter polymorphism, NAFLD and Adiopo-IR in sequence.
  
  
  CONCLUSIONS
  Adipo-IR, rather than HOMA-IR, appears to be a consistent insulin resistance index in the study of NAFLD. G allele of the HSL promoter polymorphism may contribute the greatest impact raising serum triglyceride in a state of glucose intolerance.
authors.affiliation: Department of Internal Medicine, Division of Endocrinology and Metabolism, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
authors.forename: Pi-Jung
authors.initials: PJ
authors.lastname: Hsiao
authors.forename: Zhih-Cherg
authors.initials: ZC
authors.lastname: Chen
authors.forename: Wei-Wen
authors.initials: WW
authors.lastname: Hung
authors.forename: Yi-Hsin Connie
authors.initials: YH
authors.lastname: Yang
authors.forename: Mei-Yueh
authors.initials: MY
authors.lastname: Lee
authors.forename: Jee-Fu
authors.initials: JF
authors.lastname: Huang
authors.forename: Kung-Kai
authors.initials: KK
authors.lastname: Kuo
mesh_terms: D000328:Adult; D003430:Cross-Sectional Studies; D000431:Ethanol / Q000378:metabolism; D005234:Fatty Liver / Q000201:enzymology / Q000235:genetics* / Q000378:metabolism*; D020022:Genetic Predisposition to Disease; D018149:Glucose Intolerance / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood / Q000235:genetics / Q000378:metabolism; D007333:Insulin Resistance / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D065626:Non-alcoholic Fatty Liver Disease; D009765:Obesity / Q000235:genetics* / Q000378:metabolism*; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics*; D012307:Risk Factors; D002787:Sterol Esterase / Q000235:genetics* / Q000378:metabolism; D014280:Triglycerides / Q000097:blood / Q000235:genetics / Q000378:metabolism
chemical_list: D007328:Insulin; D014280:Triglycerides; D000431:Ethanol; D002787:Sterol Esterase