Type 2 & other diabetes

Alpha cell dysfunction in type 2 diabetes: associations with insulin resistance and reduced insulin secretion

BMJ Open Diabetes Res CarePublished Retrospective cohort study

Authors' conclusion

In T2DM, impaired glucagon suppression during OGTT is associated with insulin resistance closely, highlighting insulin resistance as a key factor in alpha-cell dysfunction.

Study context

Population
Patients with T2D treated at Tianjin Medical University General Hospital, October 2022 to March 2025, who underwent a 75 g oral glucose tolerance tests (OGTT)
Participants
247 patients
Exposure
Glucagon levels across quartiles of insulin resistance and insulin secretion indices
Outcome
Associations of insulin resistance (HomaIR, CPRIR) and insulin secretion (AUCcp, HomaB, first PH, second PH) with glucagon levels during OGTT
Methodological detailssingle-centre, generalized linear models, mediation analysis
  • Single-centre
  • Generalized linear models
  • Mediation analysis

Main finding

As reported in the abstract

Glucagon levels during OGTT
  • Glucagon significantly elevated with severe insulin resistance (homeostasis model assessment of insulin resistance (HomaIR) Q3 and CPRIR Q1), even after adjusting for confounders
  • Poorest insulin secretion (AUCcp Q1, HomaB Q1, first PH Q1, second PH Q1) did not show elevated glucagon vs better secretion

Observational data: associations, not effects.

Further findings

Mediation analysis

Neither AUCcp nor HomaB mediated the relationship between insulin resistance and glucagon levels

Model fit and sensitivity analyses

Satisfactory model fit; sensitivity analyses (excluding influential points by Cook's distance; bootstrapped CIs) yielded consistent results

Original publication

Alpha cell dysfunction in type 2 diabetes: associations with insulin resistance and reduced insulin secretion. BMJ Open Diabetes Res Care. Published 30 June 2026. doi:10.1136/bmjdrc-2025-005653

Composed by AI from the published abstract and checked against it. How Briefs are made →

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