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2017 Fiscal Year Final Research Report

Significance of simultaneous secretion of insulin and incretin regulated by SKIP molecule

Research Project

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Project/Area Number 15K09384
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Metabolomics
Research InstitutionKyoto University

Principal Investigator

Harashima Shinichi  京都大学, 医学研究科, 客員研究員 (80444793)

Co-Investigator(Renkei-kenkyūsha) HOSODA Kiminori  京都大学, 大学院医学研究科, 教授 (40271598)
TOMITA Tsutomu  京都大学, 大学院医学研究科, 助教 (50402897)
MASHIMO Tomoji  京都大学, 大学院医学研究科, 准教授 (80397554)
Project Period (FY) 2015-04-01 – 2018-03-31
Keywordsインスリン分泌 / インクレチン分泌 / 糖尿病
Outline of Final Research Achievements

We find here that sphingosine kinase 1-interacting protein (SKIP, also called Sphkap) is highly expressed in pancreatic b-cells but not in a-cells. Intraperitoneal glucose tolerance test showed that plasma glucose levels were decreased and insulin levels were increased in SKIP-/- mice compared to SKIP+/+ mice, but exendin-4-enhanced insulin secretion was masked. GSIS was amplified more in SKIP-/- but exendin-4-enhanced insulin secretion was masked compared to that in SKIP+/+ islets. The ATP and cAMP content were similarly increased in SKIP+/+ and SKIP-/- islets; depolarization-evoked, PKA and cAMP-mediated insulin secretion were not affected. Inhibition of PDE activity equally augmented GSIS in SKIP+/+ and SKIP-/- islets. These results indicate that SKIP modulates GSIS by a pathway distinct from that of cAMP-, PDE- and sphingosine kinase-dependent pathways.

Free Research Field

代謝・内分泌

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Published: 2019-03-29  

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