Type 1 diabetes involves dysfunctional GIP, GLP-1, and glucagon signaling that contributes to cardiovascular risk, and emerging incretin-based therapies may directly target these metabolic deficits.
Underserved populationT1D patients have significantly increased cardiovascular risk but no approved incretin-based therapies despite clear metabolic rationale
What the researchers found
T1D involves dysfunctional GIP, GLP-1, and glucagon signaling that contributes to dysglycemia and cardiovascular risk, with semaglutide and tirzepatide emerging as potential therapeutic options targeting these specific metabolic deficits.
Why it matters
T1D patients have no approved incretin-based therapies despite clear metabolic rationale. Demonstrating cardiovascular benefits could expand GLP-1 drug indications to T1D.
How the study worked
Narrative review of incretin hormone physiology in T1D, focusing on GIP, GLP-1, and glucagon dysfunction and emerging therapeutic opportunities with incretin-based drugs.
What this study cannot tell us
Mostly conceptual/review without new data. Clinical trials of GLP-1 drugs in T1D for cardiovascular outcomes are limited. Dosing and safety in T1D need separate validation.
How to read the evidence
Narrative review presenting mechanistic rationale. Limited clinical data for GLP-1 drugs in T1D cardiovascular outcomes.
When this study was published
Published in 2025.
The bigger picture
Extending incretin-based therapies from T2D to T1D could address cardiovascular risk in a population that has been largely excluded from the GLP-1 revolution.
Questions still open
- Would cardiovascular outcome trials of semaglutide in T1D be feasible and ethical?
- How does incretin dysfunction in T1D differ from T2D?
- Could tirzepatide's dual mechanism offer advantages over GLP-1 monotherapy in T1D?
Common questions
Can people with type 1 diabetes take GLP-1 drugs?
Why do T1D patients have high heart risk?
Read the original research
Targeting cardiometabolic risk in type 1 diabetes through incretin physiology.
Trends in endocrinology and metabolism: TEM, 37(2), 135-150
Citation
Frampton, Ruth; Hocking, Samantha; Snaith, Jennifer R; Greenfield, Jerry R. (2026). Targeting cardiometabolic risk in type 1 diabetes through incretin physiology.. Trends in endocrinology and metabolism: TEM, 37(2), 135-150. https://doi.org/10.1016/j.tem.2025.06.004