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Volume 41 Issue 9
Sep.  2025
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Article Navigation >  Journal of Clinical Hepatology  > 2025  >  41(9): 1802-1807

Association of growth hormone secretagogue receptor rs2922126 gene polymorphism with susceptibility to non-alcoholic fatty liver disease

DOI: 10.12449/JCH250915
  • 1.

    Department of Infectious Diseases, Qingdao Municipal Hospital，University of Health and Rehabilitation Sciences，Qingdao，Shandong 266011，China

  • 2.

    Purchasing Office, Qingdao Municipal Hospital，University of Health and Rehabilitation Sciences，Qingdao，Shandong 266011，China

  • 3.

    Clinical Research Center, Qingdao Municipal Hospital，University of Health and Rehabilitation Sciences，Qingdao，Shandong 266011，China

Research funding:

National Natural Science Foundation of China (32171277)

More Information
  • Corresponding author: XIN Yongning， xinyongning@163.com （0000-0002-3692-7655）; ZHAO Zhenzhen， qdzzz1987@163.com （0000-0002-5883-1056）
  • Received Date: 2025-02-21
  • Accepted Date: 2025-04-07
  • Published Date: 2025-09-25
    Abstract
  •   Objective  To investigate growth hormone secretagogue receptor （GHSR） rs2922126 gene polymorphisms and their association with genetic susceptibility to nonalcoholic fatty liver disease （NAFLD） in the Chinese Han population in Qingdao， China， and to provide a basis for diagnosis and treatment.  Methods  A total of 220 patients who were admitted to Qingdao Municipal Hospital from June 2022 to June 2023 and were diagnosed with NAFLD based on radiological examination were enrolled as NAFLD group， and 167 healthy individuals during the same period of time were enrolled as control group. Fasting blood samples were collected from all subjects， and related biochemical parameters were measured. Whole blood DNA was extracted， and polymerase chain reaction and MALDI-TOF mass spectrometer were used for genotyping. The chi-square test was used for comparison of categorical data between groups， and the independent-samples t test or the Mann-Whitney U test was used for comparison of continuous data between groups. The binary logistic regression analysis was used to investigate the risk of NAFLD.  Results  Compared with the control group， the NAFLD group had significantly higher age， body mass index （BMI）， fasting plasma glucose， triglyceride， gamma-glutamyl transpeptidase， alkaline phosphatase， alanine aminotransferase， and aspartate aminotransferase， as well as a significantly lower level of high-density lipoprotein （all P<0.05）. The distribution of GHSR rs2922126 genotypes was consistent with the Hardy-Weinberg equilibrium， suggesting population representativeness in the subjects enrolled （NAFLD group： P=0.106； control group： P=0.849）. There was no significant difference in the distribution of AA， TA， and TT genotypes at GHSR rs2922126 locus between the control group and the NAFLD group （P=0.099）， and there was also no significant difference in allele frequency between the two groups （P=0.063）. In the recessive model of A allele， there was a significant difference in the distribution of AA homozygote and TA+TT genotype between the NAFLD group and the control group （P=0.032）. The binary logistic regression analysis showed that in the recessive model of A allele， AA homozygote carriers had an increased risk of NAFLD compared with TA+TT genotype carriers （odds ratio ［OR］=1.712， 95% confidence interval ［CI］： 1.045 — 2.807， P=0.033）. There was still a significant difference after adjustment for sex， age， and BMI （OR=2.156， 95%CI： 1.221 — 3.808， P=0.008）. In the NAFLD group， AA genotype carriers had a significantly higher serum level of total cholesterol （TC） than TT+TA carriers （Z=-1.99，P=0.046）.  Conclusion  GHSR rs2922126 AA genotype may be associated with the increased risk of NAFLD in the Chinese Han population in Qingdao， and GHSR rs2922126 AA genotype is associated with the increase in TC in NAFLD patients.

     

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    • References(24)
  • [1]
    LU R, LIU Y, HONG TP. Epidemiological characteristics and management of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis in China: A narrative review[J]. Diabetes Obes Metab, 2023, 25( Suppl 1): 13- 26. DOI: 10.1111/dom.15014.
    [2]
    MA L, HU XX, ZHAO B, et al. Association of polymorphisms of the acetyl-coA acetyltransferase 1 gene and the melatonin receptor 1B gene with the susceptibility to nonalcoholic fatty liver disease[J]. J Clin Hepatol, 2024, 40( 4): 700- 705. DOI: 10.12449/JCH240410.

    马磊, 胡欣欣, 赵波, 等. ACAT1和MTNR1B基因多态性与非酒精性脂肪性肝病易感性的关系[J]. 临床肝胆病杂志, 2024, 40( 4): 700- 705. DOI: 10.12449/JCH240410.
    [3]
    DONGIOVANNI P, ROMEO S, VALENTI L. Genetic factors in the pathogenesis of nonalcoholic fatty liver and steatohepatitis[J]. Biomed Res Int, 2015, 2015: 460190. DOI: 10.1155/2015/460190.
    [4]
    LONGO M, MERONI M, PAOLINI E, et al. TM6SF2/PNPLA3/MBOAT7 loss-of-function genetic variants impact on NAFLD development and progression both in patients and in vitro models[J]. Cell Mol Gastroenterol Hepatol, 2022, 13( 3): 759- 788. DOI: 10.1016/j.jcmgh.2021.11.007.
    [5]
    AJMERA V, LOOMBA R. Advances in the genetics of nonalcoholic fatty liver disease[J]. Curr Opin Gastroenterol, 2023, 39( 3): 150- 155. DOI: 10.1097/MOG.0000000000000927.
    [6]
    BAESSLER A, HASINOFF MJ, FISCHER M, et al. Genetic linkage and association of the growth hormone secretagogue receptor(ghrelin receptor) gene in human obesity[J]. Diabetes, 2005, 54( 1): 259- 267. DOI: 10.2337/diabetes.54.1.259.
    [7]
    KISSEBAH AH, SONNENBERG GE, MYKLEBUST J, et al. Quantitative trait loci on chromosomes 3 and 17 influence phenotypes of the metabolic syndrome[J]. Proc Natl Acad Sci USA, 2000, 97( 26): 14478- 14483. DOI: 10.1073/pnas.97.26.14478.
    [8]
    GUEORGUIEV M, LECOEUR C, MEYRE D, et al. Association studies on ghrelin and ghrelin receptor gene polymorphisms with obesity[J]. Obesity(Silver Spring), 2009, 17( 4): 745- 754. DOI: 10.1038/oby.2008.589.
    [9]
    INOUE H, KANGAWA N, KINOUCHI A, et al. Identification and functional analysis of novel human growth hormone secretagogue receptor(GHSR) gene mutations in Japanese subjects with short stature[J]. J Clin Endocrinol Metab, 2011, 96( 2): E373- E378. DOI: 10.1210/jc.2010-1570.
    [10]
    TANG LY, HUANG H, ZHU LN, et al. Effects of GHSR rs572169 gene polymorphism on blood glucose and lipid levels in longevity population[J]. J Guangxi Med Univ, 2019, 36( 5): 837- 841. DOI: 10.16190/j.cnki.45-1211/r.2019.05.038.

    唐岚莹, 黄浩, 朱丽娜, 等. GHSR rs572169基因多态性对长寿人群血糖和血脂水平的影响[J]. 广西医科大学学报, 2019, 36( 5): 837- 841. DOI: 10.16190/j.cnki.45-1211/r.2019.05.038.
    [11]
    YANG YM, LI C. Association study of GHSR and hypercholesterolemia[J]. Med J West China, 2012, 24( 1): 155- 157. DOI: 10.3969/j.issn.1672-3511.2012.01.070.

    杨驭媒, 李岑. GHSR基因多态性与高胆固醇血症的关联研究[J]. 西部医学, 2012, 24( 1): 155- 157. DOI: 10.3969/j.issn.1672-3511.2012.01.070.
    [12]
    HUH Y, CHO YJ, GE NAM. Recent epidemiology and risk factors of nonalcoholic fatty liver disease[J]. J Obes Metab Syndr, 2022, 31( 1): 17- 27. DOI: 10.7570/jomes22021.
    [13]
    National Workshop on Fatty Liver and Alcoholic Liver Disease, Chinese Society of Hepatology, Chinese Medical Association: Fatty Liver Expert Committee, Chinese Medical Doctor Association. Guidelines of prevention and treatment for nonalcoholic fatty liver disease: a 2018 update[J]. J Clin Hepatol, 2018, 34( 5): 947- 957. DOI: 10.3969/j.issn.10015256.2018.05.007.

    中华医学会肝病学分会脂肪肝和酒精性肝病学组, 中国医师协会脂肪性肝病专家委员会. 非酒精性脂肪性肝病防治指南(2018年更新版)[J]. 临床肝胆病杂志, 2018, 34( 5): 947- 957. DOI: 10.3969/j.issn.10015256.2018.05.007.
    [14]
    BUZZETTI E, PINZANI M, TSOCHATZIS EA. The multiple-hit pathogenesis of non-alcoholic fatty liver disease(NAFLD)[J]. Metabolism, 2016, 65( 8): 1038- 1048. DOI: 10.1016/j.metabol.2015.12.012.
    [15]
    LV Y, LIANG TT, WANG GX, et al. Ghrelin, a gastrointestinal hormone, regulates energy balance and lipid metabolism[J]. Biosci Rep, 2018, 38( 5): BSR20181061. DOI: 10.1042/BSR20181061.
    [16]
    MÜLLER TD, NOGUEIRAS R, ANDERMANN ML, et al. Ghrelin[J]. Mol Metab, 2015, 4( 6): 437- 460. DOI: 10.1016/j.molmet.2015.03.005.
    [17]
    WANG Q, LIU C, UCHIDA A, et al. Arcuate AgRP neurons mediate orexigenic and glucoregulatory actions of ghrelin[J]. Mol Metab, 2013, 3( 1): 64- 72. DOI: 10.1016/j.molmet.2013.10.001.
    [18]
    REZAMAND G, MAHMOUDI T, TABAEIAN SP, et al. The“GG” genotype of rs26802 variant in the ghrelin gene is a potential protective factor against nonalcoholic fatty liver disease[J]. Physiol Int, 2021, 108( 3): 342- 352. DOI: 10.1556/2060.2021.00183.
    [19]
    TABAEIAN SP, MAHMOUDI T, SABZIKARIAN M, et al. The Leu72Met(rs696217 GT) polymorphism of the ghrelin gene might be a protective factor for nonalcoholic fatty liver disease[J]. J Gastrointestin Liver Dis, 2021, 30( 2): 233- 239. DOI: 10.15403/jgld-2703.
    [20]
    LI WJ, ZHEN YS, SUN K, et al. Ghrelin receptor gene polymorphisms are associated with female metabolic syndrome in Chinese population[J]. Chin Med J(Engl), 2008, 121( 17): 1666- 1669.
    [21]
    ARGUELLO G, BALBOA E, ARRESE M, et al. Recent insights on the role of cholesterol in non-alcoholic fatty liver disease[J]. Biochim Biophys Acta, 2015, 1852( 9): 1765- 1778. DOI: 10.1016/j.bbadis.2015.05.015.
    [22]
    PENG KP, MO ZN, TIAN GX. Serum lipid abnormalities and nonalcoholic fatty liver disease in adult males[J]. Am J Med Sci, 2017, 353( 3): 236- 241. DOI: 10.1016/j.amjms.2017.01.002.
    [23]
    ZHANG YX, WANG Y, YOU CL, et al. Analysis of related factors of abnormal liver function in patients with nonalcoholic fatty liver disease[J]. Clin J Med Offic, 2025, 53( 5): 522- 524, 528. DOI: 10.16680/j.1671-3826.2025.05.21.

    张月霞, 王宇, 尤丛蕾, 等. 非酒精性脂肪肝患者肝功能异常相关因素分析[J]. 临床军医杂志, 2025, 53( 5): 522- 524, 528. DOI: 10.16680/j.1671-3826.2025.05.21.
    [24]
    ZHANG YT, WANG AH, YANG JN, et al. Mechanisms of cholesterol metabolism imbalance in a PA-induced non-alcoholic fatty liver disease cell model[J]. J China Pharm Univ, 2023, 54( 4): 490- 500. DOI: 10.11665/j.issn.1000-5048.2023032401.

    章玉婷, 王安慧, 杨晋妮, 等. 非酒精性脂肪性肝病细胞模型中胆固醇代谢紊乱机制[J]. 中国药科大学学报, 2023, 54( 4): 490- 500. DOI: 10.11665/j.issn.1000-5048.2023032401.
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