Observational studyThe Journal of clinical endocrinology and metabolism2025
Abnormal Glucagon Secretion Contributes to a Longitudinal Decline in Glucose Tolerance.
Observational study in The Journal of clinical endocrinology and metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Hepatic steatosis in humans is associated with preserved glucagon action on amino acid metabolism.The Journal of clinical investigation · 2026Trial
- From beta-cell failure to islet dysfunction: the emerging role of the alpha cell.BMJ open diabetes research & care · 2026Article
- Nonlinear associations between the cholesterol, high-density lipoprotein, and glucose index and type 2 diabetes risk in Chinese prediabetic adults: a cohort study.Scientific reports · 2026Article
- Modeling the effect of glucagon on endogenous glucose production in healthy individuals under meal-like conditions.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Abnormal Glucagon Secretion Contributes to a Longitudinal Decline in Glucose Tolerance.The Journal of clinical endocrinology and metabolism · 2025Observational
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8 authors.
Funding
Abstract
contextDefects in insulin secretion and action contribute to the progression of prediabetes to diabetes. However, the contribution of α-cell dysfunction to this process has been unclear.
objectiveThis work aimed to understand the relative contributions of α-cell and β-cell dysfunction to declining glucose tolerance.
methodsA longitudinal, community-based observational study was conducted at a clinical research unit at an academic medical center. We studied 96 individuals without diabetes (age 55 ± 1 years; body mass index 27.7 ± 0.4) on 2 occasions, 3 years apart using an oral 75-g glucose challenge. Indices for insulin secretion and action were estimated using the oral minimal model. Glucagon secretion rate (GSR) was estimated by deconvolution from peripheral glucagon concentrations. Main outcome measures included glucose tolerance status (categorical variable) and then symmetrical percentage change in peak and 120-minute glucose (post oral glucose tolerance test) concentrations (continuous variables).
resultsA total of 32 individuals progressed from normal to impaired glucose tolerance (IGT) or from IGT to type 2 diabetes. The disposition index (DI) declined in the progressors (568 ± 98 vs 403 ± 65 10-4 dL/kg/min per μU/mL, baseline vs 3 years; P = .04). α-Cell suppression by glucose (δGSR/δglucose) did not change in the nonprogressors (1.5 ± 0.1 vs 1.3 ± 0.1 nmol/min/L; P = .37) but decreased (1.0 ± 0.2 vs 0.8 ± 0.2 nmol/min/L; P < .01) in those who progressed. Analysis of the entire cohort showed that DI and δGSR/δglucose were independently and inversely correlated with an increase in glycemic excursion.
conclusionThese data show that α-cell dysfunction accompanies a decline in β-cell function as IGT or overt type 2 diabetes develops.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.