Project/Area Number |
15K21474
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Eating habits
Applied health science
|
Research Institution | Health Science University |
Principal Investigator |
Shimo Satoshi 健康科学大学, 健康科学部, 准教授 (80734607)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
Keywords | 高脂肪食 / 小腸吸収上皮細胞 / SGLT / 腸管免疫 / IgA / アウエルバッハ神経叢 / SBF-SEM / 腸管上皮 / 蠕動運動 |
Outline of Final Research Achievements |
In this study, we established a mouse hyperglycemia model using prolonged high-fat diet (HFD) ingestion, and analyzed the changes in the distribution of immunoglobulins in the lamina propria and the effect of an SGLT inhibitor (phlorizin) on neurons in the myenteric plexus. In HFD mice, a significant increase in the blood glucose level was observed at the age of 20 weeks as compared with the normal diet mice. Furthermore, the number of IgA plasma cells decreased in the lamina propria. Compared to STD mice, those on a prolonged HFD had decreased varicosity number and smaller varicosity minor axis in the neurons of the myenteric plexus. In HFD mice, phlorizin treatment resulted in ameliorated hyperglycemia and increased synaptic vesicle of varicosities in the myenteric plexus. These results support the notion that nerve damage underlies diabetic symptoms of mucosal immune functions and dysmotility, and reveals adaptive enteric nerve system responses to the prolonged ingestion of a HFD.
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