Novel signaling function of adipocytes

脂肪细胞的新信号传导功能

• 批准号: 15081211
• 负责人: YADA Toshihiko
• 金额: $ 24.58万
• 依托单位: Jichi Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research on Priority Areas
• 财政年份: 2003
• 资助国家: 日本
• 起止时间: 2003 至 2007
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15081211/
• 关键词: 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

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.

Ghrelin increases cytosolic Ca^<2+> concentration ([Ca^<2+>]i) in NPY neurons in the hypothalamic arcuate nuclearus, 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细胞通过诱导SOCS-3表达和Akt磷酸化的降低并损害葡萄糖诱导的胰岛素分泌。奥利酸（OA）在大鼠胰岛β细胞中与GPR40相互作用，以增加[Ca^<2+>] _ I通过PLC-and PLC-and L-type CA^<2+2 <2+<2+> Channel，潜在地释放。 OA还通过在α-cells.atorvastatin中释放[Ca^<2+>] _ I来刺激胰高血糖素的释放。在NSY小鼠中，atorvastatin由于胰岛素抵抗和GK大鼠的WAT.Young-Adult Alyphagia在GK大鼠中的SLC2A4表达改善而加速葡萄糖耐，这是由ARC NPY神经元，内脏脂肪积累和耐瘦素的耐药性过度活跃引起的。

项目成果

内分泌・糖尿病科:グレリンによるインスリン分泌・血糖値調節機構

内分泌/糖尿病：生长素释放肽的胰岛素分泌和血糖水平调节机制

• 发表时间: 2007
• 作者: K Ono;et al;出崎克也
• 通讯作者: 出崎克也

脂肪細胞と摂食調節機構

脂肪细胞与摄食调节机制

• 发表时间: 2004
• 期刊: ホルモンと臨床 52・12
• 作者: 益崎 裕章;泰江 慎太郎;中尾 一和;N. GUETG;Kato M.;Kihara S;河野 大輔
• 通讯作者: 河野 大輔

Cytosolic CA^<2+> responses to sub-picomolar and nanomolar PAUAP in pancreatic β-cells are mediated by VPAC2 and PAC1 receptors.

胰腺β细胞中对亚皮摩尔和纳摩尔PAUAP的胞质CA 2+ 反应由VPAC2和PAC1受体介导。

• 发表时间: 2004
• 期刊: Regulatory Peptides 123
• 作者: 益崎 裕章;田中 智洋;中尾 一和;Yamada H
• 通讯作者: Yamada H

Leptin potentiates ADP-induced Ca^<2+> increase via JAK2 and tyrosine kinases in a megakaryoblast cell line.

在巨核细胞系中，瘦素通过JAK2和酪氨酸激酶增强ADP诱导的Ca 2+ 增加。

• 发表时间: 2005
• 期刊: Diabetes Res Clin Pract 70
• 作者: Hashimoto;M.;Maekawa F;Kuramochi M;Nakata M;Kuramochi M;Kuramochi M;Fujiwara K;Oneka T;Muroya S;Fujiwara K;Nakata M;Ikeda Y;Kuramochi M;Onaka T;Fujiwara K;Nakata M
• 通讯作者: Nakata M

Galanin-like peptide increases cytosolic Ca^<2+> in neurons containing growth hormone-releasing hormone in the arcuate nucleus.

甘丙肽样肽增加弓状核中含有生长激素释放激素的神经元中的胞质Ca 2+ 。

• 发表时间: 2005
• 期刊: Regulatory Peptides 126
• 作者: Hashimoto;M.;Maekawa F;Kuramochi M;Nakata M;Kuramochi M;Kuramochi M;Fujiwara K;Oneka T;Muroya S;Fujiwara K;Nakata M;Ikeda Y;Kuramochi M
• 通讯作者: Kuramochi M