Physiological and pathophysilogical roles of acinar-like cell cluster touching Langerhans islet with thin interstitial surrounding (ATLANTIS) on regeneration and maintenance of beta cell.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09406
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Metabolomics
• Research Institution: Okinaka Memorial Institute for Medical Research
• Principal Investigator: Kobayashi Tetsuro (財)冲中記念成人病研究所, その他部局等, 研究員 (30113442)
• Co-Investigator(Kenkyū-buntansha): 永淵 正法 佐賀大学, 医学部, 客員研究員 (00150441) ; 雨宮 三千代 (財)冲中記念成人病研究所, その他部局等, 研究員 (00288101) ; 會田 薫 山梨大学, 大学院総合研究部, 医学研究員 (50184015)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 糖尿病 / ウイルス / 再生医学

Outline of Final Research Achievements

We examined 1) the presence or absence of acinar-like cell clusters touching Langerhans islets with thin interstitial surrounding (ATLANTIS) in homozygous Reg I deficient (Reg I-/-) and wild-type mice, and 2) the possible role of ATLANTIS in the regeneration of beta cell clusters after encephalomyocarditis (EMC) virus (D-variant) infection in Reg I-/- and wild-type mice. ATLANTIS was found in both wild-type and Reg I-/- mice. At 12 days after EMC virus infection, lower BrdU labeling indices were observed in islet beta cells of Reg I-/- mice compared to wild-type mice. Beta cell volume 12 days after EMC virus infection in Reg I-/- mice did not differ from that of wild-type mice.
These results suggest that Reg I, which is released from ATLANTIS to islet beta cell clusters, has a crucial role in beta cell regeneration in EMC virus-induced diabetes. The presence of mechanism(s) other than that mediated by Reg I in beta cell restoration after destruction by EMC virus was also suggested.

Free Research Field

糖尿病学