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Assessment of insulin sensitivity and secretion in patients with fibrocalculous pancreatic diabetes

Authors Aiswarya Y, Shivaprasad C, Anish K, Sridevi A, Anupam B, Amit G

Received 7 February 2019

Accepted for publication 17 April 2019

Published 22 May 2019 Volume 2019:12 Pages 779—788

DOI https://doi.org/10.2147/DMSO.S204254

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 4

Editor who approved publication: Dr Juei-Tang Cheng


Yalamanchi Aiswarya, Channabasappa Shivaprasad, Kolly Anish, Atluri Sridevi, Biswas Anupam, Goel Amit

Department of Endocrinology, Vydehi Institute of Medical Sciences and Research Centre, Bangalore, India

Background: Fibrocalculous pancreatic diabetes (FCPD) is a secondary form of diabetes seen in patients with tropical chronic pancreatitis. Insulin deficiency plays a major role in the etiopathogenesis of FCPD. Limited data suggest a possible role of insulin resistance (IR) in the pathogenesis of FCPD. Sparse data exist on measures of insulin sensitivity (IS) and secretion in patients with FCPD and its comparison to type 2 diabetes mellitus (T2D) patients.
Method: Eighty patients with FCPD, 36 patients with T2D and 36 healthy subjects were included. A 75 g oral glucose tolerance test (OGTT) was performed in the morning after an overnight fast. We evaluated IS and secretion using indices derived from fasting (homeostasis model assessment of insulin resistance [HOMA-IR], quantitativeinsulin sensitivity check index [QUICKI] and homeostasis model assessment of beta-cell function [HOMA-ß]) and OGTT (Matsuda, insulin sensitivity index by Kanauchi [ISI-K], oral glucose insulin sensitivity index [OGIS], Stumvoll, insulinogenic index and oral disposition index [ODI]) measurements of glucose and insulin.
Results: HOMA-IR was significantly higher and QUICKI significantly lower in patients with FCPD and T2D than in healthy controls (P<0.001). Matsuda, ISI-K, OGIS and Stumvoll were significantly lower in patients with FCPD and T2D than in healthy controls (P<0.001), indicating reduced IS in both FCPD and T2D patients. HOMA-ß, insulinogenic index and ODI were significantly lower in patients with FCPD and T2D compared to healthy controls (P<0.001).
Conclusion: FCPD is associated with reduced IS as assessed by fasting and OGTT-based indices. FCPD is also associated with a greater degree of impairment in insulin secretion than in T2D. IR may play a role in the pathogenesis of FCPD.

Keywords: fibrocalculous pancreatic diabetes, tropical chronic pancreatitis, insulin resistance, beta-cell function, HOMA-IR, QUICKI


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