| Project/Area Number |
26893080
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Pathological medical chemistry
|
|---|
| Research Institution | Niigata University |
|---|
Principal Investigator |
Shimizu Ippei 新潟大学, 医歯(薬)学総合研究科, 特任准教授 (60444056)
|
|---|
| Project Period (FY) |
2014-08-29 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| Keywords | 褐色脂肪 / 心不全 / 肥満 / NASH / 褐色アディポカイン / 褐色脂肪由来代謝産物 / 心筋代謝リモデリング / 褐色脂肪不全 |
|---|
| Outline of Final Research Achievements |
Accumulating evidence indicates that brown adipose tissue (BAT) is the critical regulator for systemic metabolic dysfunction. Our results suggested that BAT dysfunction develops upon left ventricular pressure overload in a murine heart failure model, and causal for the progression of heart failure. BAT transplantation ameliorated cardiac dysfunction. We are currently examining to find a novel metabolites involved in disturbing cardiac metabolism with metabolome analyses. We also found that in dietary obese model, obesity associated pro-fibrotic protein (OAFP) is produced and secreted predominantly from BAT and promotes fibrosis in the liver. OAFP level in the serum was also increased in non alcoholic steatohepatitis (NASH) patients, and OAFP gain of function model promoted fibrosis in the liver. Further studies would elucidate the pathological role of OAFP in NASH.
|
