Diabetes-associated Genetic Variation in

MTNR1B TCF7L2 alpha-cell function beta-cell function glucagon suppression insulin secretion

Journal

Journal of the Endocrine Society
ISSN: 2472-1972
Titre abrégé: J Endocr Soc
Pays: United States
ID NLM: 101697997

Informations de publication

Date de publication:
01 Jul 2024
Historique:
received: 16 05 2024
medline: 16 7 2024
pubmed: 16 7 2024
entrez: 16 7 2024
Statut: epublish

Résumé

Multiple common genetic variants have been associated with type 2 diabetes, but the mechanism by which they predispose to diabetes is incompletely understood. One such example is variation in To characterize the effect of diabetes-associated genetic variation at rs10830963 in the The association of genetic variation at rs10830963 with glucose, insulin, C-peptide, glucagon, and indices of insulin secretion and action were tested in a cohort of 294 individuals who had previously undergone an oral glucose tolerance test (OGTT). Insulin sensitivity, β-cell responsivity to glucose, and Disposition Indices were measured using the oral minimal model. The Clinical Research and Translation Unit at Mayo Clinic, Rochester, MN. Two cohorts were utilized for this analysis: 1 cohort was recruited on the basis of prior participation in a population-based study in Olmsted County. The other cohort was recruited on the basis of Two-hour, 7-sample OGTT. Fasting, nadir, and integrated glucagon concentrations. One or 2 copies of the G-allele at rs10830963 were associated with increased postchallenge glucose and glucagon concentrations compared to subjects with the CC genotype. The effects of rs10830963 on glucose homeostasis and predisposition to type 2 diabetes are likely to be partially mediated through changes in α-cell function.

Identifiants

pubmed: 39011323
doi: 10.1210/jendso/bvae130
pii: bvae130
pmc: PMC11249077
doi:

Types de publication

Journal Article

Langues

eng

Pagination

bvae130

Informations de copyright

© The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society.

Auteurs

Max Vella (M)

Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.

Sneha Mohan (S)

Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.

Hannah Christie (H)

Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.

Kent R Bailey (KR)

Division of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, MN 55905, USA.

Claudio Cobelli (C)

Department of Women and Children's Health, University of Padova, 35128 Padova, Italy.

Chiara Dalla Man (C)

Department of Information Engineering, University of Padova, 35128 Padova, Italy.

Aleksey Matveyenko (A)

Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN 55905, USA.

Aoife M Egan (AM)

Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.

Adrian Vella (A)

Division of Endocrinology, Diabetes & Metabolism, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.

Classifications MeSH