Persistent hyperglycemia induces beta-to-pancreatic polypeptide cell transdifferentiation

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08306
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pathological medical chemistry
• Research Institution: The University of Tokushima
• Principal Investigator: TAMAKI Motoyuki 徳島大学, 先端酵素学研究所(糖尿病), 徳島大学専門研究員 (60624400)
• Co-Investigator(Kenkyū-buntansha): 藤谷 与士夫 群馬大学, 生体調節研究所, 教授 (30433783)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 膵β細胞 / 糖尿病 / ランゲルハンス島

Outline of Final Research Achievements

Persistent hyperglycemia decreases pancreatic β- cell function and survival. As a possible explanation for the reduced β-cell mass, previous reports suggested that non-β cells are increased in obese diabetic mice, although the origin of these cells remains to be elucidated. In this study, we investigated whether persistent hyperglycemia contributes to the increase in non-β cells, and whether this is due to the fate conversion of β cells. We employed genetically non-diabetic and lineage traceable mice, and fed them a high fat diet and treated them with a low dose of streptozotocin. The mice became hyperglycemic and obese, and their non-β cells were significantly increased similarly to that of the genetically obese diabetic mice. Interestingly, the increased pancreatic polypeptide (PP)-positive producing cells were found to originate from the pre-existing β cells.

Free Research Field

代謝内分泌学