What question did this study set out to answer?

This study examines how exocrine insufficiency impacts β-cell reserve and overall glycemic control in chronic pancreatitis.

June 10, 2026

1325-OR: Deficient β-Cell Reserve and Exocrine Insufficiency Synergistically Drive Glycemic Variability in Chronic Pancreatitis

Key Points

This study examines how exocrine insufficiency impacts β-cell reserve and overall glycemic control in chronic pancreatitis.
Analyzed 148 chronic pancreatitis patients using Mixed Meal Tolerance Tests and Continuous Glucose Monitoring.
Stratified patients by glucose tolerance levels and fecal elastase-1 to assess islet function and glycemic variability.
Used indices like HOMA, Insulinogenic Index, and measures like MAGE and Time in Range to evaluate correlations.
Patients with severe exocrine insufficiency had significantly higher fasting plasma glucose levels (P<0.05).
Fecal elastase-1 positively correlated with insulin secretion measures (P<0.001).
Negative correlation found between fecal elastase-1 and glycemic variability (MAGE) (P<0.05).

Abstract

Introduction and Objective: Post-pancreatitis diabetes mellitus (PPDM-C) is characterized by dual exocrine and endocrine failure. However, the impact of exocrine insufficiency (PEI) on β-cell reserve and glycemic variability remains underdefined. This study aims to elucidate the characteristics of islet function in CP and the influence of exocrine status on glucose homeostasis. Methods: We analyzed 148 CP patients using Mixed Meal Tolerance Tests (MMTT) and Continuous Glucose Monitoring (CGMS). Patients were stratified by glucose tolerance (NGT, IGT, DM) and fecal elastase-1 (FE-1) levels. We assessed islet function using HOMA indices, Insulinogenic Index (IGI), and Corrected Insulin Response (CIR), and glycemic variability via MAGE and Time in Range (TIR). Results: 1. Baseline 0.05), HOMA-β and early-phase secretion (IGI, 30min C-peptide) significantly declined from NGT to DM (P0.001). Notably, HOMA-IR showed no significant difference among groups (P0.05), indicating a defect in reserve rather than insulin resistance.2. Exocrine-Endocrine Correlation: In patients without decompensated diabetes, FE-1 levels showed a significant positive correlation with IGI, CIR, and HOMA-β (P0.001). Patients with severe PEI exhibited significantly higher FPG and glucose AUC compared to those with normal exocrine function (P0.05).3. Glycemic Variability: FE-1 levels were negatively correlated with MAGE (P0.05). Regression analysis confirmed that PEI is an independent risk factor for increased glycemic variability and reduced TIR, even after adjusting for insulin secretion. Conclusion: PPDM-C is primarily driven by insufficient β-cell reserve, specifically impaired early-phase secretion. This endocrine dysfunction parallels the severity of exocrine insufficiency. Thus, exocrine function is a key determinant of glycemic stability, highlighting that exocrine assessment and intervention are essential for optimal glycemic management in CP patients. Disclosure R. Wang: None.

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