Anti-leptin receptor antibody mimics the stimulation of lipolysis induced by leptin in isolated mouse fat pads.

Anti-leptin receptor antibody mimics the stimulation of lipolysis induced by leptin in isolated mouse fat pads.
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抗瘦素受体抗体模拟瘦素在离体小鼠脂肪垫中诱导的脂肪分解刺激。

DOI:
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发表时间:
2001
影响因子:
6.5
通讯作者:
H. Ueki
H. Ueki
中科院分区:
生物学2区
文献类型:
--
作者:
N. Kawaji;A. Yoshida;T. Motoyashiki;T. Morita;H. Ueki

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抗瘦素受体多克隆抗体(受体抗体),以及瘦素,以一种时间依赖性的方式刺激游离脂肪酸从分离的小鼠脂肪垫释放。孵育90 min后,在6 μ g/ml受体抗体和0.1 nM瘦素浓度下,脂肪溶解最大。受体抗体未显示出对瘦素诱导的脂肪分解刺激的任何附加效应,表明它们通过涉及瘦素受体的类似机制发挥作用。N-[2-(对溴肉桂胺)乙基]-5-异喹啉磺酰胺(H-89)、quin - 2- am、N-(6-氨基己基)-5-氯-1-萘磺酰胺(W-7)和硫酸新霉素(新霉素)均能有效抑制受体抗体和瘦素对脂肪分解的刺激。用受体抗体或瘦素对脂肪垫进行短期孵育,发现cAMP和肌醇1,4,5-三磷酸(IP3)的细胞含量短暂增加,其浓度与游离脂肪酸释放的浓度相似。Quin 2- am和W-7也抑制了cAMP含量的增加,提示Ca(2)+/钙调素依赖性过程可能参与了受体抗体和瘦素发挥作用的部分机制。通过对新霉素敏感的磷酸肌苷特异性磷脂酶C (PLC)增加细胞IP3含量似乎是启动细胞内事件的首要步骤。受体抗体和瘦素都可能通过细胞IP3含量的短暂增加以及cAMP的产生来刺激脂肪分解,从而导致cAMP依赖性蛋白激酶的激活。
An anti-leptin receptor polyclonal antibody (receptor antibody), as well as leptin, stimulated the release of free fatty acids from isolated mouse fat pads in a time-dependent manner. Following a 90-min incubation, maximal lipolysis was observed at 6 microg/ml receptor antibody and 0.1 nM leptin. The receptor antibody did not show any additive effect to the stimulation of lipolysis induced by leptin, suggesting that they exert their actions through a similar mechanism involving the leptin receptor. N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89), quin 2-AM, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7), and neomycin sulfate (neomycin) all potently inhibited the stimulation of lipolysis by the receptor antibody and leptin. Short-term incubation of the fat pads with the receptor antibody or leptin showed a transient increase in the cellular content of cAMP and myo-inositol 1,4,5-trisphosphate (IP3) in similar concentrations to the free fatty acid release. Quin 2-AM and W-7 also inhibited the increase in cAMP content, suggesting that a Ca(2)+/calmodulin-dependent process may be involved in a part of the mechanism in which the receptor antibody and leptin exert their effects. The increase in cellular IP3 content via phosphoinositide-specific phospholipase C (PLC) sensitive to neomycin appears to be a primary step to initiate intracellular events. Both the receptor antibody and leptin may stimulate the lipolysis through mechanisms involving a transient increase in the cellular IP3 content followed by cAMP production, which leads to the activation of cAMP-dependent protein kinase.
DOI: --
发表时间: 1986
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发表时间: 1989
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