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GCKR基因多态性增加了患有代谢相关脂肪性肝病和高尿酸血症的年轻非肥胖患者低骨密度的风险。

GCKR Polymorphisms Increase the Risks of Low Bone Mineral Density in Young and Non-Obese Patients With MASLD and Hyperuricemia.

作者信息

Li Tzu-Hao, Huang Yu-Shin, Ma Chia-Chen, Tsai Shin-Yu, Tsai Hung-Cheng, Yeh Hsiao-Yun, Shen Hsiao-Chin, Hong Shiao-Ya, Su Chien-Wei, Yang Hwai-I, Yang Ying-Ying, Hou Ming-Chih

机构信息

Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.

Institute of Clinical Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.

出版信息

Kaohsiung J Med Sci. 2025 Jun;41(6):e70017. doi: 10.1002/kjm2.70017. Epub 2025 Apr 9.

DOI:10.1002/kjm2.70017
PMID:40202351
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12199583/
Abstract

Metabolic-associated steatotic liver disease (MASLD) encompasses common comorbidities including low bone mineral density (BMD) and hyperuricemia (HU), yet relevant genetic analyses are limited. This study aimed to investigate the genetic effects of risk single nucleotide polymorphisms (SNPs) on the occurrence of low BMD in patients with MASLD and HU, particularly focusing on relatively young or non-obese populations. We conducted a cross-sectional study utilizing data from the Taiwan Biobank, screening a total of 150,709 participants who were prospectively enrolled over a period of 13 years. The risk SNPs for MASLD were identified. Genotype analyses of HU and its effects on the occurrence of low BMD in the general population were evaluated, with further analyses of common SNPs focusing on patients with MASLD, including subgroup analyses on relatively young and non-obese populations. A total of 20,496 participants were eligible for analysis, including 7526 patients with MASLD. Several risk SNPs for MASLD were identified. Furthermore, MASLD patients carrying the PNPLA3-rs738409 C_C, PNPLA3-rs2896019 T_T, GCKR-rs780094 T_T, and GCKR-rs1260326 T_T genotypes exhibited an increased risk of comorbidity with HU. Trend analysis revealed that the T alleles in GCKR-rs780094 and GCKR-rs1260326 were associated with the occurrence of low BMD in MASLD individuals comorbid with HU, particularly among relatively young or non-obese populations. In relatively young, non-obese patients with MASLD and HU, genetic effects significantly increase the risk of occurrence of low BMD. Given the presence of genetic effects in these ostensibly low-risk groups, heightened awareness and close follow-up are recommended.

摘要

代谢相关脂肪性肝病（MASLD）包含常见的合并症，如低骨密度（BMD）和高尿酸血症（HU），但相关的基因分析有限。本研究旨在探讨风险单核苷酸多态性（SNP）对MASLD和HU患者低BMD发生的遗传影响，特别关注相对年轻或非肥胖人群。我们利用台湾生物银行的数据进行了一项横断面研究，筛选了在13年期间前瞻性招募的总共150,709名参与者。确定了MASLD的风险SNP。评估了HU的基因型分析及其对一般人群中低BMD发生的影响，并对MASLD患者的常见SNP进行了进一步分析，包括对相对年轻和非肥胖人群的亚组分析。共有20,496名参与者符合分析条件，其中包括7526名MASLD患者。确定了几个MASLD的风险SNP。此外，携带PNPLA3-rs738409 C_C、PNPLA3-rs2896019 T_T、GCKR-rs780094 T_T和GCKR-rs1260326 T_T基因型的MASLD患者合并HU的风险增加。趋势分析显示，GCKR-rs780094和GCKR-rs1260326中的T等位基因与合并HU的MASLD个体中低BMD的发生有关，特别是在相对年轻或非肥胖人群中。在相对年轻、非肥胖的MASLD和HU患者中，遗传效应显著增加了低BMD发生的风险。鉴于这些表面上低风险群体中存在遗传效应，建议提高认识并密切随访。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2a/12199583/34df3d998ee6/KJM2-41-e70017-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2a/12199583/1be61e4579a2/KJM2-41-e70017-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2a/12199583/e84e50911839/KJM2-41-e70017-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2a/12199583/0c9d704f5e16/KJM2-41-e70017-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2a/12199583/34df3d998ee6/KJM2-41-e70017-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2a/12199583/1be61e4579a2/KJM2-41-e70017-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2a/12199583/e84e50911839/KJM2-41-e70017-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2a/12199583/0c9d704f5e16/KJM2-41-e70017-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ee2a/12199583/34df3d998ee6/KJM2-41-e70017-g003.jpg

相似文献

[1]
GCKR Polymorphisms Increase the Risks of Low Bone Mineral Density in Young and Non-Obese Patients With MASLD and Hyperuricemia.

Kaohsiung J Med Sci. 2025-6

[2]
Clinical Utility of Genetic Variants in PNPLA3 and TM6SF2 to Predict Liver-Related Events in Metabolic Dysfunction-Associated Steatotic Liver Disease.

Liver Int. 2025-4

[3]
Genetic Variations in GCKR and PNPLA3 Regulate Metabolic Balance Across the Liver.

Diabetes. 2025-7-1

[4]
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[5]
PNPLA3 and SAMM50 variants are associated with lean nonalcoholic fatty liver disease in Asian population.

Ann Hepatol. 2025

[6]
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Arthritis Res Ther. 2017-7-5

[7]
AZD2693, a PNPLA3 antisense oligonucleotide, for the treatment of MASH in 148M homozygous participants: Two randomized phase I trials.

J Hepatol. 2025-1-9

[8]
Silymarin for adults with metabolic dysfunction-associated steatotic liver disease.

Cochrane Database Syst Rev. 2025-6-24

[9]
Dietary manganese intake is positively associated with metabolic dysfunction-associated steatotic liver disease: a multicohort study.

Eur J Nutr. 2025-5-26

[10]
Effectiveness and safety of vitamin D in relation to bone health.

Evid Rep Technol Assess (Full Rep). 2007-8

本文引用的文献

[1]
Metabolic dysfunction-associated fatty liver disease and osteoporosis: the mechanisms and roles of adiposity.

Osteoporos Int. 2024-12

[2]
Polygenic risk score of metabolic dysfunction-associated steatotic liver disease amplifies the health impact on severe liver disease and metabolism-related outcomes.

J Transl Med. 2024-7-12

[3]
Metabolic Dysfunction-Associated Steatotic Liver Disease: From Pathogenesis to Current Therapeutic Options.

Int J Mol Sci. 2024-5-22

[4]
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Osteoporos Int. 2024-9

[5]
New point-of-care calcaneal ultrasound densitometer (Osteosys BeeTLE) compared to standard dual-energy X-ray absorptiometry (DXA).

Sci Rep. 2024-3-22

[6]
Metabolic dysfunction-associated steatotic liver disease: Update and impact of new nomenclature on the American Association for the Study of Liver Diseases practice guidance on nonalcoholic fatty liver disease.

Hepatology. 2024-5-1

[7]
MSCs-derived extracellular vesicles alleviate sepsis-associated liver dysfunction by inhibiting macrophage glycolysis-mediated inflammatory response.

Int Immunopharmacol. 2024-2-15

[8]
Glucokinase regulatory protein: a balancing act between glucose and lipid metabolism in NAFLD.

Front Endocrinol (Lausanne). 2023

[9]
Linking metabolic syndrome with low bone mass through insights from BMI and health behaviors.

Sci Rep. 2023-9-1

[10]
Aging Affects Insulin Resistance, Insulin Secretion, and Glucose Effectiveness in Subjects with Normal Blood Glucose and Body Weight.

Diagnostics (Basel). 2023-6-24

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