Analyzing the mechanism of obesity in novel genetic obese C57Black mouse
| Project/Area Number |
23650237
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Laboratory animal science
|
|---|
| Research Institution | University of Miyazaki |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | 疾患モデル / 肥満 / レプチン / 内臓脂肪 / 褐色脂肪 / 肥満モデルマウス / 肥満マウス / Darumaマウス / インスリン / レプチン抵抗性 / インスリン抵抗性 |
|---|
| Research Abstract |
We established a C57Black mouse demonstrating spontaneous obesity, and named it “C57Black-Daruma”. In the C57 Black -Daruma mouse, the leptin receptor gene sequence carried two base mutations, which are good candidates for the variation(s) responsible for the obese phenotype. As well as ICR-Daruma, C57 Black -Daruma mice developed characteristic visceral fat accumulation at 4 weeks of age, and the white adipose and liver tissues exhibited increases in cell size and lipid droplets, respectively. Moreover, the onset of impaired leptin signaling was early and manifested as hyperleptinemia and hyperinsulinemia. Pair-feeding completely inhibited obesity, although these mice rapidly developed hyperphagia and obesity followed by hyperleptinemia when pair-feeding ceased and free-access feeding was permitted.
|
Report
(3 results)
Research Products
(15 results)
