Abstract
BackgroundHormone 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.MethodsA 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.ResultsIn 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.ConclusionAdipo-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.
Highlights
Hormone sensitive lipase (HSL) promoter (LIPE-60 C > G) polymorphism has been found to be involved in hepatic steatosis, obesity, diabetes and dyslipidemia
The hepatic TG content results from a complex interaction of lipid homeostasis, including (1) fatty acid influx derived by adipose lipolysis, (2) dietary fat intake from chylomicron (10- 15%), (3) de novo lipogenesis from plasma glucose (25- 30%), (4) fatty acid β-oxidation and (5) fatty acid export by esterification to secrete as a very low-density lipoprotein (VLDL) [7,8]
To standardize the de novo lipogenesis by fasting plasma glucose, our purely male population was divided into NTG (n = 729) and Glucose Intolerance (GI) (n = 299) groups
Summary
Hormone sensitive lipase (HSL) promoter (LIPE-60 C > G) polymorphism has been found to be involved in hepatic steatosis, obesity, diabetes and dyslipidemia. Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease in the world, and is growing especially quickly in Asia It is regarded as a hepatic manifestation of metabolic syndrome (MetS) because of its close concomitance with obesity, type 2 diabetes mellitus and dyslipidemia [1,2]. In the FA metabolism, adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL) are responsible for > 95% of TG hydrolysis. Both ATGL and HSL regulate the basal lipolysis, whereas only HSL determines the stimulated lipolysis. As there is a very low expression of ATGL in the liver, the activities of FAS and HSL seem to be essential for the regulation of fatty acid metabolism in the formation of NAFLD
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