What question did this study set out to answer?

This research aims to assess if pancreas size and fecal elastase levels predict T1D risk and progression.

June 13, 2026

2116-P: The Exocrine Pancreas in the Pathway to Type 1 Diabetes: Size, Function, and Progression

Key Points

This research aims to assess if pancreas size and fecal elastase levels predict T1D risk and progression.
Participants included T1D islet autoantibody negative relatives and those with single/multiple autoantibodies (n=135).
Evaluated pancreas volume via MRI and fecal elastase at baseline and one year.
Nonparametric tests analyzed associations between fecal elastase and pancreas volume, comparing euglycemic and dysglycemic participants.
Baseline relative pancreas volume (RPV) was smaller in groups with more autoantibodies (p=0.009).
No change in RPV slope over one year across different groups (p=0.88).
Significant differences in fecal elastase levels were found between euglycemic and dysglycemic participants (median 2311 vs 1350 mcg/g, p=0.009).

Abstract

Introduction and Objective: Exocrine pancreas dysfunction and atrophy are characteristic of presymptomatic T1D. We sought to determine whether pancreas size by MRI or fecal elastase (FE-1) predicts T1D risk and whether a decline over time is predictive of progression. Methods: T1D islet autoantibody negative relatives (Aab-; n=60), single (sAab+; n=29) and multiple autoantibody positives (mAab+; n=46) aged 8-45 participating in TrialNet Pathway to Prevention were recruited across seven centers in the US and Australia. Relative pancreas volume by MRI (RPV; calculated as volume/BMI; n=135) and FE-1 (n=85) were measured at baseline and one year. A linear model with age and sex as covariates estimated an intercept and slopes across the groups. Nonparametric tests were used to correlate FE-1 with RPV, estimate differences in baseline FE-1, and document trajectories among euglycemic vs dysglycemic participants. Results: Aab-, sAab+, and mAab+ groups had sequentially smaller RPV measured at baseline (p=0.009). However, there was no observable decrease or differences in RPV slope after one year among the groups (p=0.88). FE-1 was not correlated with RPV (rs=0.14, p=0.22). Differences were observed in FE-1 at baseline in euglycemic vs dysglycemic participants (median 2311 vs 1350 mcg/g, p=0.009). Progressors from euglycemia to dysglycemia at one year (n=10) had a downward FE-1 trajectory vs non-progressors (n=20) (median one year value 65% vs 111% of baseline, p=0.02), largely due to a higher baseline FE-1 in progressors vs nonprogressors (FE-1 median 2230 vs 1623 mcg/g, p=0.01). Conclusion: RPV is sequentially smaller in Aab-, sAab+, and mAab+ groups, however, in our study no differences were observed in trajectory over time. Additional analyses incorporating glycemic status are expected. Baseline differences and differences in FE-1 trajectory were apparent in euglycemic vs dysglycemic participants and in euglycemic participants progressing to dysglycemia. Further study is warranted to determine the utility of these exocrine biomarkers as predictors of T1D progression. Disclosure B.S. Bruggeman: Research Support; Current; GentiBio. K. Morneault-Gill: None. J.R. Grajo: None. M. Guyot: None. S. Peeling: None. M.J. Haller: Advisory Panel; Current; MannKind Corporation, Sanofi, SAB Biotherapeutics, Inc. M.L. Campbell-Thompson: None. Funding National Institutes of Health (R01DK123329, K23DK131363)

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