Haplotype testing of MTTP alleles on insulin resistance in patients with chronic hepatitis C

IF 1 Q4 GENETICS & HEREDITY

Gene Reports Pub Date : 2024-06-10 DOI:10.1016/j.genrep.2024.101951

Thamiris Vaz Gago Prata , Bianca Peixoto Dantas , Caroline Manchiero , Arielle Karen da Silva Nunes , Victória Gonçalves de Paula , Fátima Mitiko Tengan , Mariana Cavalheiro Magri

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引用次数: 0

Abstract

Background

Insulin resistance is a common manifestation among patients with chronic hepatitis C. The aim of this study was to investigate the effect of haplotypes in the microsomal triglyceride transfer protein (MTTP) gene on insulin resistance in Brazilian patients with chronic hepatitis C.

Methods

Genetic variants in the MTTP gene were genotyped by PCR-RFLP.

Results: Of the 232 patients with chronic hepatitis C, 34.5 % had insulin resistance (HOMA-IR ≥3) and the majority were ≥50 years old. The minor allele frequencies for the -400A/T (rs1800803), -164T/C (rs1800804), H297Q (rs2306985), I128T (rs3816873), Q95H (rs61733139), Q244E (rs17599091) and -493G/T (rs1800591) variants in the MTTP gene were 0.41, 0.30, 0.49, 0.30, 0.08, 0.06 and 0.32. In multivariate analysis, elevated levels of gamma-glutamyl transpeptidase (GGT) was associated with insulin resistance (p = 0.006). Haplotype-based association testing presented that the haplotype ATCTGGG of the -400A/T, -164T/C, H297Q, I128T, Q95H, Q244E and -493G/T variants was associated with the presence of insulin resistance (p = 0.028) and the haplotype TTGTGCG may be a protective factor (p = 0.012).

Conclusion

The combination of alleles in the -400A/T, -164T/C, H297Q, I128T, Q95H, Q244E and -493G/T genetic variants in the MTTP gene may play a relevant role in insulin resistance among patients with chronic hepatitis C.

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慢性丙型肝炎患者胰岛素抵抗的 MTTP 等位基因单倍型检测

本研究的目的是调查微粒体甘油三酯转移蛋白（MTTP）基因单倍型对巴西慢性丙型肝炎患者胰岛素抵抗的影响：结果：在 232 名慢性丙型肝炎患者中，34.5% 有胰岛素抵抗（HOMA-IR ≥3），大多数患者年龄≥50 岁。MTTP 基因中 -400A/T (rs1800803), -164T/C (rs1800804), H297Q (rs2306985), I128T (rs3816873), Q95H (rs61733139), Q244E (rs17599091) 和 -493G/T (rs1800591) 变体的小等位基因频率分别为 0.41、0.30、0.49、0.30、0.08、0.06 和 0.32。在多变量分析中，γ-谷氨酰转肽酶（GGT）水平升高与胰岛素抵抗有关（p = 0.006）。基于单倍型的关联测试表明，-400A/T、-164T/C、H297Q、I128T、Q95H、Q244E 和 -493G/T 变体的单倍型 ATCTGG 与胰岛素抵抗有关（p = 0.028），而单倍型 TTGTGCG 可能是一个保护因素（p = 0.012）。结论 MTTP基因中的-400A/T、-164T/C、H297Q、I128T、Q95H、Q244E和-493G/T等位基因组合可能在慢性丙型肝炎患者的胰岛素抵抗中发挥相关作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Gene Reports Biochemistry, Genetics and Molecular Biology-Genetics

CiteScore

3.30

自引率

7.70%

发文量

246

审稿时长

49 days

期刊介绍： Gene Reports publishes papers that focus on the regulation, expression, function and evolution of genes in all biological contexts, including all prokaryotic and eukaryotic organisms, as well as viruses. Gene Reports strives to be a very diverse journal and topics in all fields will be considered for publication. Although not limited to the following, some general topics include: DNA Organization, Replication & Evolution -Focus on genomic DNA (chromosomal organization, comparative genomics, DNA replication, DNA repair, mobile DNA, mitochondrial DNA, chloroplast DNA). Expression & Function - Focus on functional RNAs (microRNAs, tRNAs, rRNAs, mRNA splicing, alternative polyadenylation) Regulation - Focus on processes that mediate gene-read out (epigenetics, chromatin, histone code, transcription, translation, protein degradation). Cell Signaling - Focus on mechanisms that control information flow into the nucleus to control gene expression (kinase and phosphatase pathways controlled by extra-cellular ligands, Wnt, Notch, TGFbeta/BMPs, FGFs, IGFs etc.) Profiling of gene expression and genetic variation - Focus on high throughput approaches (e.g., DeepSeq, ChIP-Seq, Affymetrix microarrays, proteomics) that define gene regulatory circuitry, molecular pathways and protein/protein networks. Genetics - Focus on development in model organisms (e.g., mouse, frog, fruit fly, worm), human genetic variation, population genetics, as well as agricultural and veterinary genetics. Molecular Pathology & Regenerative Medicine - Focus on the deregulation of molecular processes in human diseases and mechanisms supporting regeneration of tissues through pluripotent or multipotent stem cells.