Sweet Taste Receptor in Pancreatic Beta-cell : Investigation for Glucose Response

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591311
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Metabolomics
• Research Institution: Gunma University
• Principal Investigator: NAKAGAWA Yuko 群馬大学, 生体調節研究所, 助教 (90422500)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 膵β細胞 / 代謝 / ATP / 甘味受容体

Outline of Final Research Achievements

In the present study, we addressed whether or not the sweet taste receptor (STR) expressed in β-cells modulates metabolism of glucose. To this end, we monitored changes in intracellular ATP ([ATP]c) in MIN6 cells expressing luciferase. High concentrations of glucose induced biphasic increase in [ATP]c, which was inhibited by an addition of mannoheptulose or dinitrophenol. In the presence of 5.5 mM glucose, addition of sucralose, an activator of STR, induced an immediate and marked elevation of [ATP]c. Sucralose potentiated the effect of glucose and also augmented methylsuccinate-induced elevation of [ATP]c.
In the presence of 5.5 mM glucose, addition of 3-O-methylglucose (MeGlc), a non-metabolizable analogue of glucose, induced a transient increase in [ATP]c, which corresponded to the first peak of the glucose-induced elevation of [ATP]c. or dinitrophenol.These results indicate that activation of STR primes the metabolic pathway and enhances ATP production.

Free Research Field

内分泌学