A 3’-untranslated region variant (rs2289046) of insulin receptor substrate 2 gene is associated with susceptibility to nonalcoholic fatty liver disease
| Journal | Volume 83 - 2020 |
| Issue | Fasc.2 - Original articles |
| Author(s) | R. Dabiri 1, T. Mahmoudi 2, M. Sabzikarian 3, A. Asadi 4, H. Farahani 5, H. Nobakht 1, I. Maleki 6, F. Mansour-Ghanaei 7, F. Derakhshan 2, M.R. Zali 2 |
| Full article |
 PAGES 271-276 VIEW FREE PDF |
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Affiliations: (1) Internal Medicine Department, Semnan University of Medical Sciences, Semnan, Iran
(2) Gastroenterology and Liver Diseases Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran (3) Colorectal Research Center, Iran University of Medical Sciences, Tehran, Iran (4) Department of Biology, Faculty of Science, University of Mohaghegh Ardabili, Ardabil, Iran (5) Department of Physiology, School of Medicine, Qom University of Medical Sciences, Qom, Iran (6) Gut and Liver Research Center, Mazandaran University of Medical Sciences, Sari, Iran (7) Division of Gastroenterology and Hepatology, Gastrointestinal and Liver Diseases Research Center (GLDRC), Guilan University of Medical Sciences, Rasht, Iran |
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Purpose: Nonalcoholic fatty liver disease (NAFLD) is an increasing global health concern defined by excessive hepatic fat content in the absence of excessive alcohol consumption. Regarding the key role of insulin and insulin resistance in NAFLD, we investigated whether insulin receptor substrate 1 (IRS1) and insulin receptor substrate 2 (IRS2) gene variants were associated with NAFLD risk. Methods: In this case-control study, 305 subjects including 151 cases with biopsy-proven NAFLD and 154 controls were enrolled. All the subjects were genotyped for IRS1 (rs1801278) and IRS2 (rs2289046) gene variants using PCR-RFLP method. Results: Our findings showed that the IRS2 rs2289046 “GG+AG” genotype compared with “AA” genotype to be a marker of decreased NAFLD susceptibility and the difference remained significant even after adjustment for confounding factors including age, BMI, sex, smoking status, systolic blood pressure, and diastolic blood pressure (P=0.014; OR=0.50, 95%CI= 0.29-0.87). Furthermore, the IRS2 “G” allele was significantly underrepresented in the cases with NAFLD than controls (P=0.026 ; OR=0.62, 95%CI=0.41-0.94). However, no significant difference was found for IRS1 rs1801278 gene variant. Conclusions: This study suggests, for the first time, that the IRS2 gene rs2289046 variant may play a role in NAFLD susceptibility. Nevertheless, this observation warrants further investigations in other populations. Keywords: insulin, IRS1 gene, IRS2 gene, NAFLD, variant. |
| The authors declare that they have no conflict of interest. |
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© Acta Gastro-Enterologica Belgica. PMID 32603046 |
