Effects of systemic tumour necrosis factor (TNF) inhibition on postprandial glucose-regulatory hormones in inflammatory arthritis
Authors' conclusion
In patients initiating TNFi therapy, serum levels of GIP, amylin and PP increase regardless of systemic inflammation.
Study context
- Population
- Non-diabetic patients with RA, PsA or axial spondylarthritis (axSpA) undergoing TNFi therapynon-diabetic
- Participants
- 64 patients
- Exposure
- Baseline vs 12, 24 and 52 weeks of TNFi therapy
- RAn = 22
- PsAn = 13
- axSpAn = 29
- Outcome
- Serum GIP, amylin and PP
- Follow-up
- 12, 24 and 52 weeks
Methodological detailsmultivariable linear mixed-effects models
- Multivariable linear mixed-effects models
Main finding
As reported in the abstract
Serum basal GIP, amylin and PP
- Serum basal gastric inhibitory polypeptide (GIP), amylin and pancreatic polypeptide (PP) significantly increased in the univariable model, consistent after adjusting for CRP
- Effects consistent across TNFi types and diagnoses, except PP, with a significant interaction with type of arthritis
Observational data: associations, not effects.
Further findings
Basal insulin resistance indices
- No significant change throughout the study in RA, PsA or axSpA
Original publication
Effects of systemic TNF inhibition on postprandial glucose-regulatory hormones in inflammatory arthritis. Rheumatology (Oxford). Published 17 November 2025. doi:10.
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