Pancreatic Parenchymal Atrophy and Pancreatic Fat Accumulation Measured by Multidetector Computed Tomography as a Stable Marker of Chronic Progressive Type 2 Diabetes Mellitus—A Cross Sectional Observational Study

Abstract

Abstract Background The most crucial step in the management of type 2 diabetes is identifying its pathogenesis and progression. Fat accumulation in the pancreas and decreased parenchymal volume can influence pancreatic function due to insulin resistance or β-cell dysfunction. This study aims to find out the difference in pancreatic volume and fat content by using contrast-enhanced computed tomography (CECT) between normal subjects and patients with different durations of type 2 diabetes mellitus (T2DM). Methods This was a cross-sectional study. Patients who underwent CECT abdomen for the evaluation of conditions other than pancreatic origin were included. The study group was divided into three subgroups according to the duration of diabetes as <5 years, 5 to 10 years, and >10 years. In total, 40 nondiabetic controls were included. Pancreatic fat volume and parenchymal volume were measured in cm3 using CECT. Correlation between pancreatic parenchymal and fat volume with the duration of T2DM as well as with levels of hemoglobin A1c, random blood sugar, serum triglyceride, low-density lipoproteins, and high-density lipoproteins was done. Results T2DM patients had significantly (p < 0.001) lower pancreatic parenchymal volume (mean value of 57.08 ± 8.26 cm3 in diabetics and 72.23 ± 3.41 cm3 in controls) and higher pancreatic fat volume (mean value of 3.08 ± 1.90 cm3 in diabetics and 0.67 ± 0.27cm3 in controls) as compared to nondiabetic controls. In patients with T2DM, as the duration of T2DM increased, pancreatic parenchymal volume decreased and pancreatic fat volume increased. Conclusion Reduction in pancreatic volume and fat deposition may have a role in the onset and progression of diabetes. Determining the pancreatic volume and fat content would be useful for identifying high-risk patients and determining the pathogenesis of the development of diabetes.