Insulin secretory defect plays a major role in the development of diabetes in patients with distal pancreatectomy

Byung Wan Lee, Hahn Wook Kang, Jin Seok Heo, Seong Ho Choi, Sang Yong Kim, Yong Ki Min, Jae Hoon Chung, Moon Kyu Lee, Myung Shik Lee, Kwang Won Kim

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20 Citations (Scopus)


To investigate the pathogenesis of distal pancreatectomy (d-Px)-induced diabetes in Korean patients, we investigated insulin secretory and sensitivity indexes obtained by oral glucose tolerance testing in 20 patients that had received d-Px (10 with d-Px-induced diabetes and 10 with normal glucose tolerance with d-Px [NGT d-Px]) and in 164 control subjects (77 with type 2 diabetes mellitus and 87 with NGT) that did not receive d-Px. The pancreatectomized subjects had lower fasting serum insulin, homeostasis model assessment of pancreatic beta-cell function (HOMA-β) levels, and insulinogenic indices than the NGT controls. The HOMA-β values of nonobese NGT d-Px- and d-Px-induced diabetic subjects were 73.7% and 38.7% of those for nonobese NGT controls, respectively, and HOMA-β was significantly lower only for d-Px-induced diabetic subjects (P < .01). In obese subjects, the HOMA-β values of obese d-Px-induced diabetic subjects were significantly lower than those of obese NGT controls (P < .05). The insulin sensitivity was significantly lower in nonobese type 2 diabetes mellitus controls than in nonobese NGT d-Px or in nonobese d-Px-induced diabetic subjects (P < .001 and .05, respectively). These results show that a reduced insulin secretory function is a typical feature of glucose homeostasis in distal pancreatectomized patients and that insulin secretory defect plays a major role in the development of diabetes in these patients. In addition, the study suggests that pancreatic resections of 60% or less and body mass index are not the main causes of diabetes onset after d-Px in this study.

Original languageEnglish
Pages (from-to)135-141
Number of pages7
JournalMetabolism: Clinical and Experimental
Issue number1
Publication statusPublished - 2006 Jan

Bibliographical note

Funding Information:
This work was supported by grants from the Samsung Biomedical Research Institute (C-98-008 and C-A3-116).

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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