期刊
PANCREAS
卷 40, 期 6, 页码 855-860出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MPA.0b013e318214832d
关键词
islet; islet transplantation; pancreatectomy; GLP-1; DPP-4 inhibitor
资金
- Merck
- Ministry of Health & Welfare, Republic of Korea [A080009]
- Samsung Biomedical Research Institute [C-A6-405]
- Korean Ministry of Education, Science and Technology
- IN-SUNG Foundation for Medical Research
- Korea Health Promotion Institute [A080009] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Objective: Glucagon-like peptide-1 (GLP-1) is known to promote beta cell proliferation, and dipeptidyl peptidase-4 (DPP-4) inhibitor increases GLP-1 levels by preventing its degradation. This study was designed to evaluate the effects of sitagliptin (sita), a DPP-4 inhibitor, on the outcome of islet transplantation (ITx) in diabetic mice after partial pancreatectomy (Px). Methods: A diabetic mouse model was prepared by performing 70% Px in C57BL/6 mice. The diabetic mice were treated with sita, subjected to ITx, or both treated with sita and subjected to ITx. After 12 days of sita treatment, the pancreatic remnants and transplanted islets were histologically examined. Results: Dipeptidyl peptidase-4 inhibitor increased the concentration of plasma active GLP-1 regardless of ITx and improved glycemic control in the ITx group. The beta cell mass of the pancreatic remnants increased in the ITx group, and mice that received combined treatment with ITx and sita showed a greater increase in the beta cell mass. Dipeptidyl peptidase-4 inhibitor seems to induce proliferation and inhibit apoptosis of beta cells in pancreatic remnants. Conclusions: The DPP-4 inhibitor favorably affects ITx in partially pancreatectomized diabetic mice by increasing the beta cell mass through cell proliferation and inhibition of beta cell apoptosis.
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