Identification of the role of type 2 diabetes susceptible gene SLC30A8

2014 Fiscal Year Final Research Report

• Project/Area Number: 24790933
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Metabolomics
• Research Institution: The University of Tokushima (2014); Juntendo University (2012-2013)
• Principal Investigator: TAMAKI MOTOYUKI 徳島大学, 糖尿病臨床・研究開発センター, 助教 (60624400)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 膵β細胞 / インスリン / 糖尿病

Outline of Final Research Achievements

We revealed the physiological expression site of SLC30A8, and expression levels of SLC30A8/ZnT8 was markedly decreased in diabetic model mice (Tamaki M. et al. Islets. 1(2); 124-128, 2009). We next generate pancreatic beta cell specific SLC30A8 knock out mice. These mice showed that loss of SLC30A8 was associated with not only beta cell dysfunction, but also worsening hepatic insulin clearance. We reported these findings in Journal of Clinical Investigation (Tamaki M. et al. J Clin Invest. 123(10); 4513-4524, 2013).

Free Research Field

代謝学