At the 2026 European Congress on Obesity (ECO) in Istanbul, researchers presented a small observational study assessing fasting peptide YY (PYY), ghrelin and glucose-dependent insulinotropic polypeptide (GIP) levels in people living with type 1 diabetes (T1D), with or without obesity. While exploratory, the study adds to a growing body of evidence that obesity in T1D may not simply mirror obesity in type 2 diabetes (T2D) or the general population, and may require a more tailored clinical and commercial approach.
The study is timely as obesity pharmacotherapy continues to expand beyond traditional T2D and general obesity populations. People with T1D are increasingly affected by overweight and obesity, but remain underrepresented in obesity trials, creating uncertainty around how gut hormone biology, insulin use, glycemic variability and weight management interact in this group. For pharma companies developing or commercialising incretin-based and gut hormone-targeting therapies, this represents both a potential evidence gap and an opportunity for differentiation.
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The investigators recruited four groups: lean healthy controls, participants with obesity without T1D, lean participants with T1D, and participants with both obesity and T1D. Groups were evaluated using anthropometric measures, body composition and fasting circulating levels of PYY, ghrelin and GIP, allowing comparisons by both diabetes and obesity status.
The most relevant signal was observed with fasting PYY. The authors reported significantly lower PYY levels in participants with T1D, both with and without obesity, compared with their non-diabetes counterparts. This suggests that altered satiety signalling may be associated with T1D itself, rather than being driven solely by adiposity. If confirmed in larger studies, this could support the view that appetite regulation and weight management in T1D may require a distinct mechanistic framework from obesity without diabetes.
Fasting ghrelin findings also point toward a differentiated biology. While ghrelin was higher in lean controls than in participants with obesity, there were no significant differences between lean T1D and T1D with obesity groups. Lean T1D participants also had lower ghrelin levels than lean controls, suggesting that T1D may alter expected fasting ghrelin patterns. In contrast, fasting GIP levels were similar across all groups, indicating that GIP may be less informative as a fasting biomarker in this small dataset.
For industry stakeholders, the key implication is not immediate clinical practice change, but the need to avoid assuming that obesity in T1D behaves similarly to obesity in T2D. As GLP-1, dual agonist and multi-agonist therapies move into broader metabolic populations, T1D with obesity could become an increasingly important but evidence-light segment. Companies that proactively generate data in this population may be better positioned to shape future treatment algorithms, payer discussions and clinician confidence.
The findings also raise questions around endpoint strategy. Future studies in T1D with obesity may need to go beyond weight loss alone and include appetite regulation, insulin dose changes, glycemic variability, hypoglycemia risk, post-prandial hormone responses and patient-reported satiety outcomes. These measures could help determine whether altered PYY and ghrelin signalling translates into clinically meaningful differences in treatment response.
From a strategic perspective, this poster supports a broader “now what” for obesity drug developers: T1D with obesity should be considered a distinct research and evidence-generation opportunity. While the current study is small and cross-sectional, it highlights a biologically plausible rationale for dedicated trials or real-world evidence studies in this group. If validated, differentiated gut hormone profiles in T1D could influence product positioning, label expansion strategies, KOL messaging and future development of precision obesity approaches.
Looking ahead, larger studies incorporating post-prandial testing, glycemic control measures and longitudinal weight outcomes will be needed to confirm whether fasting PYY and ghrelin differences have therapeutic relevance. Until then, the study’s main value lies in drawing attention to an underserved population that may become increasingly relevant as obesity treatment expands across complex metabolic disease segments.
