The mechanism of high fat diet induced neural inflammation and obese
Project/Area Number |
16K09761
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Metabolomics
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Research Institution | University of Miyazaki |
Principal Investigator |
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Project Period (FY) |
2016-04-01 – 2019-03-31
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Project Status |
Completed (Fiscal Year 2018)
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Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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Keywords | グレリン / 肥満 / 摂食中枢 / 自律神経 / 炎症 / 糖尿病 / 糖脂質代謝 / ペプチド / エネルギー・糖質代謝異常 |
Outline of Final Research Achievements |
In mice, ghrelin’s orexigenic activity was abolished after 2-4 weeks HFD, consistent with the timing of accumulation and activation of macrophages and microglia in the nodose ganglion and hypothalamus. Calorie-restricted weight loss restored ghrelin responsiveness and alleviated the upregulation of macrophage/microglia activation markers and inflammatory cytokines. Aged mice easily gained weight during short-term HFD feeding, and required many days to adapt their energy intake. One-day HFD in aged mice induced inflammation in the distal colon, but not in the nodose ganglion or hypothalamus. The anorexic effect of GLP-1 was attenuated in aged mice. mRNA expression of the gene encoding the GLP-1 receptor in the nodose ganglion was significantly lower in aged mice than in young mice. These findings suggest that adaptation of energy intake regulation was attenuated in aged mice, causing them to become obese in response to short-term HFD feeding.
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Academic Significance and Societal Importance of the Research Achievements |
過栄養や糖代謝異常による慢性炎症が、迷走神経節や視床下部にも及び、ペプチド受容体の発現低下から摂食行動の異常に至る分子機序を明らかにした。加齢によって自律神経を介する摂食調節機構が減弱し高脂肪食による肥満を生じやすくなる可能性が示唆された。
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Report
(4 results)
Research Products
(14 results)
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[Journal Article] Prolyl Isomerase Pin1 Suppresses Thermogenic Programs in Adipocytes by Promoting Degradation of Transcriptional Co-activator PRDM16.2019
Author(s)
Nakatsu Y, Matsunaga Y, Yamamotoya T, Ueda K, Inoue MK, Mizuno Y, Nakanishi M, Sano T, Yamawaki Y, Kushiyama A, Sakoda H, Fujishiro M, Ryo A, Ono H, Minamino T, Takahashi SI, Ohno H, Yoneda M, Takahashi K, Ishihara H, Katagiri H, Nishimura F, Kanematsu T, Yamada T, Asano T.
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Journal Title
Cell Rep.
Volume: 26
Issue: 12
Pages: 3221-3230
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Trk-fused gene (TFG) regulates pancreatic β cell mass and insulin secretory activity.2017
Author(s)
Yamamotoya T, Nakatsu Y, Kushiyama A, Matsunaga Y, Ueda K, Inoue Y, Inoue MK, Sakoda H, Fujishiro M, Ono H, Kiyonari H, Ishihara H, Asano T.
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Journal Title
Sci Rep.
Volume: 7
Issue: 1
Pages: 1-13
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Reduced SHARPIN and LUBAC formation may contribute to CCl4- or acetaminophen-induced liver cirrhosis in mice.2017
Author(s)
Yamamotoya T, Nakatsu Y, Matsunaga Y, Fukushima T, Yamazaki H, Kaneko S, Fujishiro M, Kikuchi T, Kushiyama A, Tokunaga F, Asano T, and Sakoda H.
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Journal Title
Int. J. Mol. Sci.
Volume: 18
Issue: 2
Pages: 326-326
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] Canagliflozin, a sodium glucose cotransporter 2 inhibitor, attenuates obesity-induced inflammation in the nodose ganglion, hypothalamus, and skeletal muscle of mice2016
Author(s)
Naznin F, Sakoda H, Okada T, Tsubouchi H, Waise TM, Arakawa K, Nakazato M
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Journal Title
Eur J Pharmacol
Volume: 794
Pages: 37-44
DOI
Related Report
Peer Reviewed / Open Access
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