A new treatment for metabolic syndrome with references to fructose metabolism
Project/Area Number |
26500005
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Integrated Nutrition Science
|
Research Institution | Gifu University |
Principal Investigator |
Iizuka Katsumi 岐阜大学, 医学部附属病院, 講師 (40431712)
|
Co-Investigator(Kenkyū-buntansha) |
堀川 幸男 岐阜大学, 医学部附属病院, 准教授 (10323370)
武田 純 岐阜大学, 大学院医学系研究科, 教授 (40270855)
|
Research Collaborator |
KATO Takehiro
TAKAO Ken
NIWA Hiroyuki
WU Wudelehu
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | ChREBP / フルクトース / 小腸 / GLUT5 / ケトヘキソキナーゼ / 肝臓 / ブドウ糖 / 糖代謝 / Glut5 / フルクトキナーゼ / グルコース |
Outline of Final Research Achievements |
Excess intake of fructose is reported to cause dysmetabolic syndrome. We studied the role of glucose activated transcription factor, ChREBP, in fructose metabolism. We identified that ChREBP induces genes expression related to fructose metabolism and thereby promotes fructose uptake and its breakdown in intestine and conversion into other metabolites in liver. Fructose (Fruit sugar) has more potent cytotoxicity because of increased advanced glycation end product (AGE) production. This study showed that intestinal and hepatic ChREBP function has an important role in protecting from fructose toxicity.
|
Report
(4 results)
Research Products
(20 results)