2016 Fiscal Year Research-status Report
Novel murine model of congenital diabetes
| Project/Area Number |
16K07094
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| Research Institution | Kitasato University |
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Principal Investigator |
佐々木 宣哉 北里大学, 獣医学部, 教授 (20302614)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | Insulin / Diabetes / Pancreatic islet / Mutant |
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| Outline of Annual Research Achievements |
The ihs mice had significantly higher blood glucose concentrations than control mice throughout during the oral glucose tolerance test, whereas insulin tolerance test showed that ihs mice had normal insulin sensitivity. Thus, the glucose intolerance is thought to be caused by the impairment of insulin secretion, which was the main cause of diabetes in ihs mice. Histological examination of pancreatic islets showed normal islet number and B-cell mass in ihs mice compared with controls. Immunostaining and ultrastructural analysis showed the morphology of pancreas, stain intensities for insulin/glucagon, and the number or size of secretory vesicles was not significantly different between ihs and control mice.
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| Current Status of Research Progress |
Current Status of Research Progress
2: Research has progressed on the whole more than it was originally planned.
Reason
糖尿病原因遺伝子座の同定に成功し、この領域に約200の候補遺伝子が存在し、原因遺伝子の同定に着手する段階にある。
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| Strategy for Future Research Activity |
次世代シークエンサーによるエキソーム解析及びmRNA発現解析によって原因遺伝子を同定する。また原因遺伝子が同定された後は、KOマウスを作出することによって発症メカニズムの解析を行う。
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| Causes of Carryover |
原因遺伝子座の同定にかかる動物匹数を100匹から50匹に削減できたため、差額が生じた。
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| Expenditure Plan for Carryover Budget |
今年度生じた差額分は、次年度の次世代シークエンサーおよびKOマウスの作出に支出する。
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