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前列腺素E2对人体脂肪组织中腺苷酸环化酶活性及脂肪分解的影响。

Effects of prostaglandin E2 on adenylate cyclase activity and lipolysis in human adipose tissue.

作者信息

Kather H

出版信息

Int J Obes. 1981;5(6):659-63.

PMID:7319686
Abstract

To elucidate the mechanisms of prostaglandin action in human adipose tissue the effects of prostaglandin E2 on isoproterenol-stimulated lipolysis in intact human fat cells and on adenylate cyclase activity of fat-cell ghosts were compared. In intact fat cells prostaglandin E2 caused a dose-dependent inhibition of isoproterenol -stimulated lipolysis which has a maximum of about 40 per cent; half maximal effects were observed at approximately 30 nmol/l prostaglandin E2. In broken cell preparation prostaglandin E2 displayed biphasic effects on adenylate cyclase activity with inhibition occurring in the nanomolar concentration range and stimulation at prostaglandin E2-concentrations above 1 mumol/l. The inhibitory component of prostaglandin E2-action was critically dependent on relatively high concentrations of GTP (greater than 1 mumol/l) and was augmented by sodium ions. The inhibitory component of prostaglandin E2-action on adenylate cyclase reflected the antilipolytic effects of this C-20 fatty acid in intact fat cells with respect to the effective concentration range and degree of inhibition suggesting that the antilipolytic effects of prostaglandins are in fact mediated via inhibition of human fat-cell adenylate cyclase.

摘要

为阐明前列腺素在人体脂肪组织中的作用机制,比较了前列腺素E2对完整人体脂肪细胞中异丙肾上腺素刺激的脂肪分解作用以及对脂肪细胞空壳腺苷酸环化酶活性的影响。在完整脂肪细胞中,前列腺素E2对异丙肾上腺素刺激的脂肪分解产生剂量依赖性抑制,最大抑制率约为40%;在前列腺素E2浓度约为30 nmol/l时观察到半数最大效应。在破碎细胞制剂中,前列腺素E2对腺苷酸环化酶活性表现出双相作用,在纳摩尔浓度范围内出现抑制,在前列腺素E2浓度高于1 μmol/l时出现刺激。前列腺素E2作用的抑制成分严重依赖于相对高浓度的GTP(大于1 μmol/l),并被钠离子增强。前列腺素E2对腺苷酸环化酶作用的抑制成分反映了这种C-20脂肪酸在完整脂肪细胞中的抗脂解作用,就有效浓度范围和抑制程度而言,提示前列腺素的抗脂解作用实际上是通过抑制人体脂肪细胞腺苷酸环化酶介导的。

相似文献

1
Effects of prostaglandin E2 on adenylate cyclase activity and lipolysis in human adipose tissue.前列腺素E2对人体脂肪组织中腺苷酸环化酶活性及脂肪分解的影响。
Int J Obes. 1981;5(6):659-63.
2
Biphasic effects of prostaglandin E2 on the human fat cell adenylate cyclase.前列腺素E2对人脂肪细胞腺苷酸环化酶的双相效应。
J Clin Invest. 1979 Aug;64(2):609-12. doi: 10.1172/JCI109500.
3
Inhibition of hormone-stimulated human fat cell-lipolysis by prostaglandin E2 and its synthetic analogue sulprostrone.前列腺素E2及其合成类似物舒前列素对激素刺激的人脂肪细胞脂解的抑制作用。
Prostaglandins Leukot Med. 1982 May;8(5):525-9.
4
Sodium ions discriminate between stimulatory and inhibitory effects of prostaglandin E2 on human fat cell adenylate cyclase.钠离子可区分前列腺素E2对人脂肪细胞腺苷酸环化酶的刺激作用和抑制作用。
Prostaglandins Leukot Med. 1982 Nov;9(5):531-7. doi: 10.1016/0262-1746(82)90034-8.
5
Human fat cell lipolysis is primarily regulated by inhibitory modulators acting through distinct mechanisms.人类脂肪细胞的脂解作用主要受通过不同机制起作用的抑制性调节剂调控。
J Clin Invest. 1985 Oct;76(4):1559-65. doi: 10.1172/JCI112137.
6
Coupling of adenylate cyclase to lipolysis in permeabilized adipocytes: direct evidence that an antilipolytic effect of insulin is independent of adenylate cyclase.通透化脂肪细胞中腺苷酸环化酶与脂解作用的偶联:胰岛素抗脂解作用独立于腺苷酸环化酶的直接证据。
Endocrinology. 1986 Nov;119(5):2240-8. doi: 10.1210/endo-119-5-2240.
7
Antagonistic effects of prostaglandin E1 and nicotinic acid on the human fat cell adenylate cyclase.前列腺素E1与烟酸对人脂肪细胞腺苷酸环化酶的拮抗作用。
Res Commun Chem Pathol Pharmacol. 1979 Jan;23(1):81-8.
8
Inhibition of the stimulatory effect of adrenaline and prostaglandin E1 on the human fat cell adenylate cyclase by adenosine.腺苷对肾上腺素和前列腺素E1刺激人脂肪细胞腺苷酸环化酶作用的抑制
Horm Metab Res. 1980 Apr;12(4):169-72. doi: 10.1055/s-2007-996232.
9
Antilipolytic effect of prostaglandin E2 in perifused rat adipocytes.前列腺素E2对灌注大鼠脂肪细胞的抗脂解作用。
Endocrinology. 1987 Oct;121(4):1221-6. doi: 10.1210/endo-121-4-1221.
10
Mechanisms of prostaglandin action on human fat cell lipolysis.前列腺素对人脂肪细胞脂肪分解的作用机制。
Adv Prostaglandin Thromboxane Leukot Res. 1983;12:253-8.

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Clin Sci (Lond). 2020 Mar 13;134(5):473-512. doi: 10.1042/CS20190579.
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n3 and n6 polyunsaturated fatty acids differentially modulate prostaglandin E secretion but not markers of lipogenesis in adipocytes.n3 和 n6 多不饱和脂肪酸对脂肪细胞中前列腺素 E 分泌的调节作用不同,但对脂肪生成标志物无影响。
Nutr Metab (Lond). 2009 Jan 21;6:5. doi: 10.1186/1743-7075-6-5.