Differential contribution of alpha and beta cell dysfunction to impaired fasting glucose and impaired glucose tolerance.

Alpha cell function Beta cell function Deconvolution Glucagon suppression Impaired fasting glucose Impaired insulin action Insulin secretion Prediabetes

Journal

Diabetologia
ISSN: 1432-0428
Titre abrégé: Diabetologia
Pays: Germany
ID NLM: 0006777

Informations de publication

Date de publication:
01 2023
Historique:
received: 18 05 2022
accepted: 02 08 2022
pmc-release: 01 01 2024
pubmed: 17 9 2022
medline: 15 12 2022
entrez: 16 9 2022
Statut: ppublish

Résumé

People with isolated impaired fasting glucose (IFG) have normal beta cell function. We hypothesised that an increased glucose threshold for beta cell secretion explains IFG. We used graded glucose infusion to examine the relationship of insulin secretion rate (ISR) and glucagon secretion rate (GSR) with rising glucose. We studied 39 non-diabetic individuals (53 ± 2 years, BMI 30 ± 1 kg/m The relationship of ISR with glucose was linear and the threshold for insulin secretion in isolated IFG did not differ from that in people with normal fasting glucose and normal glucose tolerance. GSR exhibited a single-exponential relationship with glucose that could be characterised by G These data show that, in non-diabetic humans, alpha cell dysfunction contributes to the pathogenesis of IFG independently of defects in insulin secretion. We also describe a new index that quantifies the suppression of glucagon secretion by glucose.

Identifiants

pubmed: 36112169
doi: 10.1007/s00125-022-05794-3
pii: 10.1007/s00125-022-05794-3
pmc: PMC9742343
mid: NIHMS1845110
doi:

Substances chimiques

Glucagon 9007-92-5
Glucose IY9XDZ35W2

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

201-212

Subventions

Organisme : NIDDK NIH HHS
ID : R01 DK078646
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK126206
Pays : United States

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

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Auteurs

Jacob D Kohlenberg (JD)

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

Marcello C Laurenti (MC)

Biomedical Engineering and Physiology Graduate Program, Mayo Clinic Graduate School of Biomedical Sciences, Rochester, MN, USA.

Aoife M Egan (AM)

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

Daniel Schembri Wismayer (DS)

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

Kent R Bailey (KR)

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

Claudio Cobelli (C)

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

Chiara Dalla Man (CD)

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

Adrian Vella (A)

Division of Endocrinology, Diabetes and Metabolism, Mayo Clinic College of Medicine, Rochester, MN, USA. vella.adrian@mayo.edu.

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Classifications MeSH