Novel signaling function of adipocytes

Ghrelin可增加下丘脑弓状核神经肽Y神经元胞内游离钙离子浓度([Ca^&lt；2+&gt；]i)，而瘦素对此有拮抗作用，其中依赖磷酸二酯酶3(PDE3)的瘦素信号转导途径起着关键作用。腺病毒瞬时抵抗素基因表达的小鼠通过诱导SOCS-3表达和Akt磷酸化减少而在胰岛β细胞表现出胰岛素抵抗，并抑制葡萄糖诱导的胰岛素分泌。油酸(OA)通过PLC和L型钙离子通道与大鼠胰岛β细胞中的GPR40相互作用增加[Ca^&lt；2+&gt；]i。2+通道，促进胰岛素释放。阿托伐他汀抑制3T3-L1细胞中脂肪细胞的成熟、SLC2A4的表达和胰岛素的作用，并通过增加α细胞内[Ca^&lt；2+&gt；]i的释放来刺激高血糖素的释放。在NSY小鼠中，阿托伐他汀加速了由于胰岛素抵抗而导致的葡萄糖耐量增加，并减少了WAT中SLC2A4的表达。GK大鼠的青壮年吞噬功能亢进是由ARC NPY神经元过度活动、内脏脂肪堆积和瘦素抵抗引起的。

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.