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Article

The Association between SOCS1−1656G>A Polymorphism, Insulin Resistance and Obesity in Nonalcoholic Fatty Liver Disease (NAFLD) Patients

1
Department of Medical Biology, Pomeranian Medical University, 70-111 Szczecin, Poland
2
Translational Medicine Group, Pomeranian Medical University, 71-210 Szczecin, Poland
3
Liver and Internal Medicine Unit, Medical University of Warsaw, 02-097 Warsaw, Poland
4
Department of Human Nutrition and Metabolomics, Pomeranian Medical University, 71-460 Szczecin, Poland
*
Author to whom correspondence should be addressed.
J. Clin. Med. 2019, 8(11), 1912; https://doi.org/10.3390/jcm8111912
Received: 13 September 2019 / Revised: 31 October 2019 / Accepted: 6 November 2019 / Published: 8 November 2019
(This article belongs to the Special Issue Non-Alcoholic Steatohepatitis (NASH))
Suppressor of cytokine signaling (SOCS) proteins prevent uncontrolled cytokine signaling and appear to play a role in the pathological processes behind obesity and insulin resistance. The polymorphism of the SOCS1 gene (rs243330, −1656G>A) is associated with obesity and glucose sensitivity. To estimate the effect of this SOCS1 gene polymorphism on nonalcoholic fatty liver disease (NAFLD) susceptibility, we performed a study on 138 patients with ultrasound-confirmed NAFLD and 1000 healthy blood donors. The relationship between the SOCS1−1656G>A polymorphism and serum biochemical parameters in NAFLD was additionally investigated. The SOCS1 variant was genotyped using a dedicated TaqMan assay. The frequency of rs243330 polymorphism did not differ between patients and controls. However, in a cohort of obese individuals (BMI ≥ 30 kg/m2) the occurrence of the G allele of the SOCS1−1656G>A polymorphism was strongly associated with NAFLD (odds ratio (OR) 1.6; 95% CI,1.1–2.5; p = 0.009), and carriers of the AA genotype have lower risk of developing NAFLD (OR 0.4; 95% CI, 0.2–0.7; p = 0.004). Overweight NAFLD patients who were carriers of GG genotypes had significantly lower levels of homeostasis model assessment of insulin resistance (HOMA-IR) values (p = 0.03 vs. AA), and the obese GG homozygotes had lower serum concertation of triglyceride (GG vs. AA; p = 0.02). Serum liver enzyme activities were not modified by the presence of SOCS1 risk variants. In conclusion, the observed phenotype of overweight NAFLD patients with non-elevated levels of TG and HOMA-IR, which is associated with genetic variants of SOCS1, provides a rationale for further research on the pathophysiology of fatty liver disease. View Full-Text
Keywords: obesity; steatohepatitis; metabolic syndrome; cytokines obesity; steatohepatitis; metabolic syndrome; cytokines
MDPI and ACS Style

Kempinska-Podhorodecka, A.; Wunsch, E.; Milkiewicz, P.; Stachowska, E.; Milkiewicz, M. The Association between SOCS1−1656G>A Polymorphism, Insulin Resistance and Obesity in Nonalcoholic Fatty Liver Disease (NAFLD) Patients. J. Clin. Med. 2019, 8, 1912. https://doi.org/10.3390/jcm8111912

AMA Style

Kempinska-Podhorodecka A, Wunsch E, Milkiewicz P, Stachowska E, Milkiewicz M. The Association between SOCS1−1656G>A Polymorphism, Insulin Resistance and Obesity in Nonalcoholic Fatty Liver Disease (NAFLD) Patients. Journal of Clinical Medicine. 2019; 8(11):1912. https://doi.org/10.3390/jcm8111912

Chicago/Turabian Style

Kempinska-Podhorodecka, Agnieszka, Ewa Wunsch, Piotr Milkiewicz, Ewa Stachowska, and Malgorzata Milkiewicz. 2019. "The Association between SOCS1−1656G>A Polymorphism, Insulin Resistance and Obesity in Nonalcoholic Fatty Liver Disease (NAFLD) Patients" Journal of Clinical Medicine 8, no. 11: 1912. https://doi.org/10.3390/jcm8111912

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