Delayed improvement of insulin secretion after autologous islet transplantation in partially pancreatectomized patients

Hye Seung Jung, Seong Ho Choi, Sung Joo Kim, Dong Wook Choi, Jin Seok Heo, Kyu Taek Lee, Jong Kyun Lee, Kee Taek Jang, Byung Wan Lee, Jae Hwan Jee, Jung Hyun Noh, In Kyung Jeong, Tae Young Yang, Seung Hoon Oh, You Ran Ahn, Young Seok Kim, Heesung No, Moon Kyu Lee, Kwang Won Kim

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

The purpose of this study was to evaluate the effects of autologous islet transplantation (ITx) on glucose homeostasis and insulin secretory function after partial pancreatectomy (Px). Fourteen nondiabetic patients who underwent distal Px and autologous ITx for benign pancreatic tumors were enrolled in the study (Px + ITx group). Fourteen normal glucose-tolerant controls and 6 Px without ITx controls were recruited, and all groups were followed over a 24-month period. They performed the 75-g oral glucose tolerance test and the 1-mg glucagon stimulation test. Hemoglobin A1c was measured, and indices of insulin secretion were calculated. In the Px + ITx group, insulin secretion increased after a nadir at 6 months. Glucose tolerance, which had been abruptly impaired immediately after Px, recovered until 6 months and stabilized thereafter. As a result, differences in glucose intolerance emerged between the subjects in the Px group and those in the Px + ITx group at 24 months after Px. Characteristic variables in the better insulin secretory subjects in the Px + ITx group included younger age, less extensive pancreas resection, and a greater number of total islets. In summary, delayed amelioration of glucose intolerance was induced by autologous ITx after partial Px, even with a small number of islets.

Original languageEnglish
Pages (from-to)1629-1635
Number of pages7
JournalMetabolism: Clinical and Experimental
Volume58
Issue number11
DOIs
Publication statusPublished - 2009 Nov

Bibliographical note

Funding Information:
This study was supported by grants from the IN-SUNG Foundation for Medical Research (C-A7-801-1); from the Korea Health 21 R & D Project, Ministry of Health & Welfare, Republic of Korea (A060004); from the Samsung Biomedical Research Institute (C-A6-405-1); and from the Samsung Medical Center Research Development.

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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