Resistin G–A haplotype at SNP‐420/‐358 is associated with the latent sarcopenic obesity index in the toon genome study

Author:

Ikeda Yosuke1ORCID,Kawamura Ryoichi1,Takata Yasunori1,Tabara Yasuharu23,Maruyama Koutatsu4,Takakado Misaki1,Hadate Toshimi1ORCID,Ohashi Jun5,Saito Isao6,Ogawa Yoshihiro7,Osawa Haruhiko1

Affiliation:

1. Department of Diabetes and Molecular Genetics Ehime University Graduate School of Medicine Ehime Japan

2. Graduate School of Public Health Shizuoka Graduate University of Public Health Shizuoka Japan

3. Center for Genomic Medicine Kyoto University Graduate School of Medicine Kyoto Japan

4. Department of Bioscience, Graduate School of Agriculture Ehime University Ehime Japan

5. Department of Biological Sciences, Graduate School of Science University of Tokyo Tokyo Japan

6. Department of Public Health and Epidemiology, Faculty of Medicine Oita University Oita Japan

7. Department of Medicine and Bioregulatory Science Graduate School of Medical Sciences, Kyushu University Fukuoka Japan

Abstract

ABSTRACTAim/IntroductionResistin, which induces insulin resistance, is mainly expressed in monocytes/macrophages in humans. We reported previously that serum resistin was highest in the G–A haplotype defined by resistin single nucleotide polymorphisms (SNPs) at −420 (rs1862513) and − 358 (rs3219175). As sarcopenic obesity is associated with insulin resistance, we aimed to examine whether serum resistin and its haplotypes were associated with sarcopenic obesity at a latent stage.Materials and MethodsWe cross‐sectionally analyzed 567 community‐dwelling Japanese participants attending annual medical check‐ups in which the sarcopenic obesity index was evaluated. The age‐ and gender‐matched normal glucose tolerance subjects with G–A homozygotes and those with C–G homozygotes were examined via RNA‐sequencing and pathway analysis (each n = 3), and RT‐PCR (each n = 8).ResultsIn multivariate logistic regression analyses, the fourth quartile (Q4) of serum resistin and G–A homozygotes were both associated with the latent sarcopenic obesity index defined by a visceral fat area of ≥ 100 cm2 and grip strength Q1 after adjustment for age and gender, with or without other confounding factors. RNA sequencing and pathway analysis showed that tumor necrosis factor (TNF) was involved in the top five pathways in the whole blood cells of G–A homozygotes compared with C–G homozygotes. RT‐PCR revealed that TNF mRNA was higher in G–A homozygotes than in C–G homozygotes.ConclusionsThe G–A haplotype was associated with the latent sarcopenic obesity index defined by grip strength in the Japanese cohort, could be mediated by TNF‐α.

Publisher

Wiley

Subject

General Medicine,Endocrinology, Diabetes and Metabolism,Internal Medicine

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