| Project/Area Number |
15081211
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| Research Category |
Grant-in-Aid for Scientific Research on Priority Areas
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| Allocation Type | Single-year Grants |
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| Review Section |
Biological Sciences
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| Research Institution | Jichi Medical University |
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Principal Investigator |
YADA Toshihiko Jichi Medical University, School of Medicine, Professor (60166527)
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| Co-Investigator(Kenkyū-buntansha) |
NAKATA Masanori Jichi Medical University, School of Medicine, Associate Professor (10305120)
DEZAKI Katsuya Jichi Medical University, School of Medicine, Associate Professur (90337329)
MAEJIMA Yuko Jichi Medical University, School of Medicine, Assistant Professor (40438669)
TORIYA Masako Jichi Medical University, School of Medicine, 21st Century COE Program, post-doctral fellow (90420819)
尾仲 達史 自治医科大学, 医学部, 助教授 (90177254)
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| Project Period (FY) |
2003 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥38,400,000 (Direct Cost: ¥38,400,000)
Fiscal Year 2007: ¥7,200,000 (Direct Cost: ¥7,200,000)
Fiscal Year 2006: ¥7,200,000 (Direct Cost: ¥7,200,000)
Fiscal Year 2005: ¥8,000,000 (Direct Cost: ¥8,000,000)
Fiscal Year 2004: ¥8,000,000 (Direct Cost: ¥8,000,000)
Fiscal Year 2003: ¥8,000,000 (Direct Cost: ¥8,000,000)
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| Keywords | visceral fat / leptin / resistin / fatty acid / HMG CoA reductase inhibitor / insulin / GK rat / hyperphagia / 摂食 / グレリン / NPYニューロン / Nesfatin-1 / カンナビノイド / 内臓脂肪蓄積 / 脂肪細胞分化 / 膵島 / インスリン抵抗性 / GPR40 / インスリン分泌 / カルシウム / 脂肪細胞 / 血小板凝集 / 摂食中枢 / オレキシン / PACAP / 肥満 / オレイン酸 / 膵β細胞 / ホスホリパーゼC |
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| Research Abstract |
Ghrelin increases cytosolic Ca^<2+> concentration ([Ca^<2+>]i) in NPY neurons in the hypothalamic arcuate nucleus, and leptin counteracted it, in which phosphodiesterase 3 (PDE3)-dependent leptin signaling plays a crucial role.
Transiently resistin-expressing mice using adenovirus show insulin resistance in islet β-cells via induction of SOCS-3 expression and reduction of Akt phosphorylation and impairs glucose-induced insulin secretion.
Oleic acid (OA), interacts with GPR40 in rat islet β-cells to increase [Ca^<2+>]_i via PLC-and L-type Ca^<2+> channel, potentiating insulin release. OA also stimulates glucagon release by increasing [Ca^<2+>]_i via ER Ca^<2+> release in α-cells.
Atorvastatin inhibits adipocyte maturation, SLC2A4 expression and insulin action in 3T3-L1 cells. In NSY mice, atorvastatin accelerates glucose intolerance due to insulin resistance and decreased SLC2A4 expression in WAT.
Young-adult hyperphagia in GK rats is caused by hyperactivity of ARC NPY neurons, visceral fat accumulation and leptin resistance.
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