ArticleBMC medical genetics2013
Risk interaction of obesity, insulin resistance and hormone-sensitive lipase promoter polymorphisms (LIPE-60 C > G) in the development of fatty liver.
Article in BMC medical genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- First-in-Asian double-blind randomized trial to assess the efficacy and safety of insulin sensitizer in nonalcoholic steatohepatitis patients.Hepatology international · 2021Trial
- Hemoglobin A1c and abdominal obesity as predictors of diabetes and ASCVD in individuals with prediabetes in UK Biobank: a prospective observational study.Cardiovascular diabetology · 2024Observational
- Case report: First Chinese patient with family partial lipodystrophy type 6 due to novel compound heterozygous mutations in the LIPE gene.Frontiers in genetics · 2024Article
- Variation in theAnimals : an open access journal from MDPI · 2023Article
- Itemization difference of patient-reported outcome in patients with chronic liver disease.PloS one · 2022Article
- The protective roles of augmenter of liver regeneration in hepatocytes in the non-alcoholic fatty liver disease.Frontiers in pharmacology · 2022Review
- Co-inherited novel SNPs of the LIPE gene associated with increased carcass dressing and decreased fat-tail weight in Awassi breed.Tropical animal health and production · 2020Article
- Article
- Human Genetic Ancestral Composition Correlates with the Origin of Mycobacterium leprae Strains in a Leprosy Endemic Population.PLoS neglected tropical diseases · 2015Article
- Association between serum free fatty acid levels and nonalcoholic fatty liver disease: a cross-sectional study.Scientific reports · 2014Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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