Impact of Antidiabetic Medications on IgG and Plasma Protein N-Glycosylation in Type 2 Diabetes Patients
Abstract
ABSTRACT:
Introduction: Diabetes is a growing global health challenge, necessitating effective management strategies. Glycosylation, a highly regulated post-translational protein modification, has emerged as a pivotal factor in diabetes pathophysiology. However, the modulation of protein glycosylation by antidiabetic treatment is still largely unknown. This study explored the longitudinal effects of four distinct antidiabetic therapies – metformin, insulin, sodium-glucose cotransporter-2 (SGLT2) inhibitors, and glucagon-like peptide-1 receptor agonists (GLP-1RA) – on plasma protein and immunoglobulin G (IgG) glycosylation in patients with type 2 diabetes (T2D).
Research Design and Methods: Plasma protein and IgG N-glycans were enzymatically released, purified and chromatographically profiled in a cohort of 124 patients, examined at four time points, to assess therapy-induced glycan alterations. Linear mixed models adjusting for covariates and multiple testing (FDR<0.05) were used to investigate the associations between plasma protein and IgG N-glycosylation and antidiabetic therapy.
Results: Our findings reveal that metformin, SGLT2 inhibitors, and GLP-1RA induce significant alterations in IgG glycosylation, including the increased core fucosylation and galactosylation, features associated with a reduced inflammatory IgG potential. Notably, IgG monogalactosylation, previously linked to cardioprotective effects in women, was elevated in response to GLP-1RA and SGLT2 inhibitor…
How strong is the evidence?
Evidence Hub reads this as a cohort study, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence. Reported size: 124 participants or records.
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