Analysis of a novel metabolic syndrome model mouse and its molecular mechanism
| Project/Area Number |
21500386
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | University of Tsukuba |
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Principal Investigator |
ISHII Tetsuro 筑波大学, 医学医療系, 教授 (20111370)
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| Co-Investigator(Kenkyū-buntansha) |
WARABI Eiji 筑波大学, 医学医療系, 講師 (70396612)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 疾患モデル / sequestosome1 / レプチン / 肥満 / 視床下部 / 過食 / Seuestosome 1 / A170 / エストラジオール / 摂食 / 紫外線 / アポトーシス / sequestosome 1 |
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| Research Abstract |
A mutant mouse defective in sequestosome1 gene causes mature-onset obesity. A previous study suggested importance of sequestosome1 (SQSTM1/p62) in regulation of adipocyte differentiation as a cause of obesity formation. However, our studies show overeating is the cause of the obesity formation. We constructed brain-specific SQSTM1 knock-down mouse. We found the conditional knock-down mouse exhibited similar body weight increase as the whole body gene knock-out mouse. We showed SQSTM1 is highly expressed in neurons of hypothalamus, suggesting a possibility that SQSTM1 is involved in the intracellular signaling of anorexic hormone leptin. Interesting finding is a female hormone estradiol compensates the lack of SQSTM1 in body weight control. It inhibits obesity formation through suppression of overeating of the mutant mice.
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Report
(4 results)
Research Products
(32 results)
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[Journal Article] Enhanced neointimal hyperplasia and carotid artery remodeling in sequestosome 1 deficient mice2010
Author(s)
Sugimoto R, Warabi E, Katayanagi S, Sakai S, Uwayama J, Yanagawa T, WatanabeA, Harada H, Kitamura K, Noguchi N, YoshidaH, Siow RCM, Mann GE, Ishii T
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Journal Title
J Cell Mol Med
Volume: 14(6B)
Pages: 1546-1554
Related Report
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[Journal Article] Listeria monocytogenes ActA-mediated escape from autophagic recognition2009
Author(s)
Yoshikawa Y, Ogawa M, Hain T, YoshidaM, FukumatsuM, Kim M, Mimuro H, NakagawaI, Yanagawa T, Ishii T, Kakizuka A, SztulE, Chakraborty T, Sasakawa C
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Journal Title
Nature Cell Biol
Volume: 11
Pages: 1233-1240
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[Journal Article] A role of NBR1 in autophagosomal degradation of ubiquitinated substrates2009
Author(s)
Kirkin V., Lamark T., Sou Y-S, BjorkoyG., Nunn J. L., Bruun J-A., Shvets E., McEwan D. G., Clausen T. H., Wild P., Bilusic I., Theurillat J-P., Overvatn A., Ishii T., Elazar Z., Komatsu M., Dikic I., Johansen T
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Journal Title
Molecular Cell
Volume: 33
Pages: 1-12
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