In type 2 diabetes, the pancreas is 30% smaller with irregular borders. The lack of rapid postprandial rise in insulin may explain the loss of exocrine tissues mass was postulated to be reversible on remission of diabetes. 90 people (38/52 F/M, 52.8±7.9 years, initial weight 100.2±16.3kg, and BMI 34.7±4.3 kg/m2) were randomized (Diabetes Remission Clinical Trial) to low calorie diet or to continue with routine diabetes management. A group of nondiabetic controls (n=25) matched to the post-diet weight was studied in one occasion. MR techniques were used for anatomical and fat fraction images of the pancreas (3T Philips, Netherlands). Specifically developed methods were used to quantify intrapancreatic fat, change in pancreas volume and irregularity of the border. At baseline, pancreas volume was lower in diabetes (63.8±1.8 vs. 79.8±2.9cm3, p<0.0001). It was unchanged after 5 months, increased at 12 months, and at 24 months had increased further by 12.6±1.5cm3 in responders compared with 4.5±1.3cm3 in non-responders (p<0.0001). Over 24 months, pancreas fat content decreased only in responders (p<0.0001) and responders lost 1.56±0.3% vs. 0.51±0.4% (p<0.05). At 12 months, there were negative correlations between decrease in pancreas fat and increase of insulin secretion (r=-0.55, p<0.0001), and increase in pancreas volume and the decrease of pancreas fat within the whole study (r=-0.35, p=0.02). Reflecting irregularity, Fractal Dimension (FD) of the pancreas borders was higher in the diabetic group (1.116±0.013 vs. 1.097±0.005, p<0.0001) and decreased to 24 months only in those who achieved remission (1.097±0.008, p=0.0003). The low pancreas volume of type 2 diabetes is likely to be related to deficiency of acute insulin secretion over many years of disease progression. Fat removal from the pancreas can restore β cells function and may lead to restoration of exocrine tissues mass via trophic effects of insulin. Pancreas morphology appears to reflect the pathophysiology of type 2 diabetes.

Disclosure

R. Taylor: Speaker’s Bureau; Self; Novo Nordisk Foundation. S.V. Zhyzhneuskaya: None. C. Peters: Speaker’s Bureau; Self; Sanofi-Aventis. A.C. Barnes: None. K.G. Hollingsworth: None. N. Sattar: Advisory Panel; Self; Amgen, AstraZeneca, Boehringer Ingelheim International GmbH, Eli Lilly and Company, Novo Nordisk A/S, Pfizer Inc., Sanofi. Research Support; Self; Boehringer Ingelheim Pharmaceuticals, Inc. M.E. Lean: None. A. Al-Mrabeh: None.

Funding

Diabetes UK

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