肾上腺素能受体并非生长抑素对大鼠脂肪细胞脂解作用的介质。

Adrenergic receptors are not mediators in the lipolytic effect of somatostatin in rat adipocytes.

作者信息

Simón M A, Calle C

机构信息

Department of Biochemistry, School of Medicine, Complutense University, Madrid.

出版信息

Life Sci. 1987 Nov 23;41(21):2411-7. doi: 10.1016/0024-3205(87)90666-7.

DOI:10.1016/0024-3205(87)90666-7

PMID:2891012

Abstract

Beta-adrenergic receptors have been purported to act as possible mediators in the lipolytic effect of somatostatin in vivo. Investigations with isolated rat adipocytes studying the lipolytic activity of somatostatin (1.7 x 10(-7) M), glucagon (8.1 x 10(-8 M) and norepinephrine (10(-6) M), have shown that the lipolytic effect stimulated by somatostatin is not altered by 10(-5) M propranolol (beta-antagonist); is significantly enhanced by 10(-5) M isoproterenol (beta-agonist) and is not altered by the addition of 10(-6) M phenoxybenzamine (alpha-antagonist) or 10(-6) M phenylephrine (alpha-agonist). Similar results were found when lipolysis was stimulated by glucagon, whereas the lipolytic effect stimulated by norepinephrine was blocked by propranolol. These results indicate that the direct lipolytic effect of somatostatin on isolated rat adipocytes does not seem to be mediated through mechanisms involved with adrenergic receptors.

摘要

β-肾上腺素能受体被认为可能是生长抑素体内脂解作用的介质。对分离的大鼠脂肪细胞进行的研究，观察生长抑素（1.7×10⁻⁷M）、胰高血糖素（8.1×10⁻⁸M）和去甲肾上腺素（10⁻⁶M）的脂解活性，结果显示，10⁻⁵M普萘洛尔（β拮抗剂）不会改变生长抑素刺激的脂解作用；10⁻⁵M异丙肾上腺素（β激动剂）可显著增强该作用，而添加10⁻⁶M酚苄明（α拮抗剂）或10⁻⁶M去氧肾上腺素（α激动剂）不会改变该作用。当胰高血糖素刺激脂解时也发现了类似结果，而去甲肾上腺素刺激的脂解作用被普萘洛尔阻断。这些结果表明，生长抑素对分离的大鼠脂肪细胞的直接脂解作用似乎不是通过与肾上腺素能受体相关的机制介导的。