2016 Fiscal Year Final Research Report
The molecular mechanism of GPR120 in chronic inflammation in diabetes and obesity-related metabolic disorders.
| Project/Area Number |
26860054
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Pharmacology in pharmacy
|
|---|
| Research Institution | Tokushima Bunri University (2016)
Kyoto University (2014-2015) |
|---|
Principal Investigator |
Hara Takafumi 徳島文理大学, 薬学部, 講師 (90546722)
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Keywords | 脂肪酸受容体 / 脂肪酸 / 炎症反応 / 糖尿病 / エネルギー代謝 |
|---|
| Outline of Final Research Achievements |
Free fatty acid receptors (FFARs) are G-protein coupled receptor activated by fatty acids. GPR120 is one of the FFARs specifically activated by medium- to long-chain fatty acids such as omega-3 fatty acids like DHA and EPA. It is reported that GPR120 plays important roles in the regulation of energy metabolism and inflammatory responses, however, the molecular mechanisms of GRP120 on the inflammatory responses remain to be elucidated in detail.
DNA expression database analysis suggested that GPR120 is expressed on macrophages and dendritic cells. The expression of GPR120 mRNA in mouse dendritic cells was enriched in a certain of DC subpopulation. The inflammatory responses in dendritic cells activated by the stimulation of lipopolysaccarides were suppressed by the stimulation of endogenous GPR120 ligands. The analysis of inflammatory disease model using GPR120KO mice suggested that GPR120 might play important role in the regulation of disease severity.
|
| Free Research Field |
分子薬理学
|
