ArticleHuman genetics2013
Identification of genetic variation that determines human trehalase activity and its association with type 2 diabetes.
Article in Human genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Trehalose's untapped mechanisms in alzheimer's: gut-brain-autophagy signalling beyond the usual targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- Integrated bulk and single-cell transcriptomics reveals TREH as a novel protective biomarker and prognostic predictor in clear cell renal cell carcinoma.Frontiers in oncology · 2026Article
- Assessing the efficacy of the natural disaccharide trehalose in ameliorating diet-induced obesity and metabolic dysfunction.Frontiers in nutrition · 2025Article
- Genetic Variants Associated with Body Mass Index Changes in Korean Adults: The Anseong and Ansan Cohorts of the Korean Genome and Epidemiology Study.Current issues in molecular biology · 2024Article
- Prevalence of genetically determined trehalase deficiency in populations of Siberia and Russian Far East.International journal of circumpolar health · 2023Article
- Individual and joint effects of trehalose and glutamate on diabetic retinopathy: a propensity score-matched case-control study.Endocrine connections · 2022Article
- Identification and analysis of circulating long non-coding RNAs with high significance in diabetic cardiomyopathy.Scientific reports · 2021Article
- Using trehalose to prevent and treat metabolic function: effectiveness and mechanisms.Current opinion in clinical nutrition and metabolic care · 2019Review
- Genetic correlations among psychiatric and immune-related phenotypes based on genome-wide association data.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2018Article
- Analysis of type 2 diabetes and obesity genetic variants in Mexican Pima Indians: Marked allelic differentiation among Amerindians at HLA.Annals of human genetics · 2018Article
- Mechanism of neuroprotection by trehalose: controversy surrounding autophagy induction.Cell death & disease · 2018Review
- Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis.Nature communications · 2017Article
- Flies without trehalose.The Journal of biological chemistry · 2015Article
- Article
- Study design of the Maycoba Project: obesity and diabetes in Mexican Pimas.American journal of health behavior · 2014Article
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Authors and funding
15 authors.
Funding
Abstract
A prior linkage scan in Pima Indians identified a putative locus for type two diabetes (T2D) and body mass index (BMI) on chromosome 11q23-25. Association mapping across this region identified single nucleotide polymorphisms (SNPs) in the trehalase gene (TREH) that were associated with T2D. To assess the putative connection between trehalase activity and T2D, we performed a linkage study for trehalase activity in 570 Pima Indians who had measures of trehalase activity. Strong evidence of linkage of plasma trehalase activity (LOD = 7.0) was observed in the TREH locus. Four tag SNPs in TREH were genotyped in these subjects and plasma trehalase activity was highly associated with three SNPs: rs2276064, rs117619140 and rs558907 (p = 2.2 × 10(-11)-1.4 × 10(-23)), and the fourth SNP, rs10790256, was associated conditionally on these three (p = 2.9 × 10(-7)). Together, the four tag SNPs explained 51 % of the variance in plasma trehalase activity and 79 % of the variance attributed to the linked locus. These four tag SNPs were further genotyped in 828 subjects used for association mapping of T2D, and rs558907 was associated with T2D (odds ratio (OR) 1.94, p = 0.002). To assess replication of the T2D association, all four tag SNPs were additionally genotyped in two non-overlapping samples of Native Americans. Rs558907 was reproducibly associated with T2D in 2,942 full-heritage Pima Indians (OR 1.27 p = 0.03) and 3,897 "mixed" heritage Native Americans (OR 1.21, p = 0.03), and the strongest evidence for association came from combining all samples (OR 1.27 p = 1.6 × 10(-4), n = 7,667). However, among 320 longitudinally studied subjects, measures of trehalase activity from a non-diabetic exam did not predict those who would eventually develop diabetes versus those who would remain non-diabetic (hazard ratio 0.94 per SD of trehalase activity, p = 0.29). We conclude that variants in TREH control trehalase activity, and although one of these variants is also reproducibly associated with T2D, it is likely that the effect of the SNP on risk of T2D occurs by a mechanism different than affecting trehalase activity. Alternatively, TREH variants may be tagging a nearby T2D locus.
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