BMC Medical Genetics | |
Risk interaction of obesity, insulin resistance and hormone-sensitive lipase promoter polymorphisms (LIPE-60 C > G) in the development of fatty liver | |
Kung-Kai Kuo2  Jee-Fu Huang3  Mei-Yueh Lee4  Yi-Hsin Connie Yang3  Wei-Wen Hung4  Zhih-Cherg Chen1  Pi-Jung Hsiao3  | |
[1] Department of Medical Research, Section of Internal Medicine, Chi-Mei Medical Center, Tainan, Taiwan;Department of Surgery, Division of Hepato-Bilio-Pancreatic Surgery, Kaohsiung Medical University, Hospital 100 Tzyou 1st Rd, Kaohsiung 807, Taiwan;School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan;Department of Internal Medicine, Division of Endocrinology and Metabolism, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan | |
关键词: Metabolic syndrome; Insulin resistance; Hormone-sensitive lipase (HSL); Non-alcoholic fatty liver disease (NAFLD); | |
Others : 1177698 DOI : 10.1186/1471-2350-14-54 |
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received in 2012-09-09, accepted in 2013-05-09, 发布年份 2013 | |
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【 摘 要 】
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.
Conclusion
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.
【 授权许可】
2013 Hsiao et al.; licensee BioMed Central Ltd.
【 预 览 】
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20150504021724206.pdf | 216KB | ![]() |
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