Cardiometabolic & kidneyMechanistic study
Site-Specific Apo AI Glycation Impairs HDL Function and Promotes Atherosclerosis in Diabetes
- Mechanistic study
- glycation proteomics
- training, testing and independent validation cohorts
- diabetic mouse models
Authors' conclusion
This study provides a comprehensive site-resolved map of apo AI glycation in patients with diabetes and identifies the Apo AI Glycation Index as a glycation signature associated with diabetic CAS and impaired HDL function.
Study context
- Population
- Patients with type 2 diabetes with or without coronary atherosclerosis; diabetic mouse models
- Participants
- 860 vs 294
- Comparison
- T2DM with coronary atherosclerosis (CAS) vs T2DM without CAS; glycation-resistant apo AICL vs glycated apo AI
- CASn = 860
- Controlsn = 294reference
Main finding
As reported in the abstract
Apo AI glycation sites and Apo AI Glycation Index in T2DM with vs without coronary atherosclerosis (CAS)
- Apo AI glycation patterns differed between T2DM with and without CAS; K96 and K106/107 prominent disease-associated glycation sites
- Apo AI Glycation Index independently associated with CAS and CAD in T2DM
- Apo AI Glycation Index inversely associated with HDL-mediated reverse cholesterol transport and lecithin-cholesterol acyltransferase activity
Original publication
Site-Specific Apo AI Glycation Impairs HDL Function and Promotes Atherosclerosis in Diabetes. Circulation. Published 25 August 2026. doi:10.1161/circulationaha.125.078171
Summarised from the published abstract; every number is checked against it