糖皮质激素和胰岛素对体内脂肪组织中磷酸烯醇式丙酮酸羧激酶（GTP）的调节作用。

Regulation of phosphoenolpyruvate carboxykinase (GTP) in adipose tissue in vivo by glucocorticoids and insulin.

作者信息

Meyuhas O, Reshef L, Gunn J M, Hanson R W, Ballard F J

出版信息

Biochem J. 1976 Jul 15;158(1):1-7. doi: 10.1042/bj1580001.

DOI:10.1042/bj1580001

PMID:962885

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1163929/

Abstract

The regulation of the synthesis of phosphoenolpyruvate carboxykinase (GTP) (EC 4.1.1.32) in epididymal adipose tissue, liver and kidney in vivo was studied immunochemically. 2. Phosphoenolpyruvate carboxykinase (GTP) synthesis in adipose tissue is increased by starvation, diabetes and noradrenaline, and decreased by re-feeding and insulin. These changes were also seen in adrenalectomized rats and are qualitatively similar to those observed for the liver enzyme. This indicates the involvement of cyclic AMP as an inducer and insulin as a de-inducer in the regulation of phosphoenolpyruvate carboxykinase (GTP) in both tissues. (Induction and de-induction are defined as selective increase and decrease respectively in the rate of enzyme synthesis, regardless of the mechanism involved.)3. Adrenalectomy had little effect on phosphoenolpyruvate carboxykinase (GTP) synthesis in liver and kidney, but increased the synthesis rate of the adipose-tissue enzyme. Starvation and adrenalectomy had additive effects in increasing the synthesis rate of adipose-tissue phosphoenolpyruvate carboxykinase (GTP). In adrenalectomized diabetic rats glucocorticoids increased phosphoenolpyruvate carboxykinase (GTP) synthesis in liver and kidney while decreasing enzyme synthesis in adipose tissue. De-induction of adipose tissue phosphoenolpyruvate carboxykinase (GTP) is therefore regulated independently by glucocorticoids and insulin. 4. Although liver, kidney and adipose-tissue phosphoenolpyruvate carboxykinases (GTP) are seemingly identical, there is an apparent tissue-specific differentiation in regulatory systems for the enzyme.

摘要

采用免疫化学方法研究了体内附睾脂肪组织、肝脏和肾脏中磷酸烯醇丙酮酸羧激酶（GTP）（EC 4.1.1.32）的合成调控。2. 脂肪组织中磷酸烯醇丙酮酸羧激酶（GTP）的合成在饥饿、糖尿病和去甲肾上腺素作用下增加，在重新喂食和胰岛素作用下减少。这些变化在肾上腺切除的大鼠中也可见，并且在性质上与肝脏酶所观察到的变化相似。这表明环磷酸腺苷作为诱导剂以及胰岛素作为去诱导剂参与了两种组织中磷酸烯醇丙酮酸羧激酶（GTP）的调控。（诱导和去诱导分别定义为酶合成速率的选择性增加和减少，而不考虑所涉及的机制。）3. 肾上腺切除对肝脏和肾脏中磷酸烯醇丙酮酸羧激酶（GTP）的合成影响不大，但增加了脂肪组织中该酶的合成速率。饥饿和肾上腺切除在增加脂肪组织磷酸烯醇丙酮酸羧激酶（GTP）合成速率方面具有累加效应。在肾上腺切除的糖尿病大鼠中，糖皮质激素增加了肝脏和肾脏中磷酸烯醇丙酮酸羧激酶（GTP）的合成，同时降低了脂肪组织中的酶合成。因此，脂肪组织磷酸烯醇丙酮酸羧激酶（GTP）的去诱导由糖皮质激素和胰岛素独立调控。4. 尽管肝脏、肾脏和脂肪组织中的磷酸烯醇丙酮酸羧激酶（GTP）看似相同，但该酶的调控系统存在明显的组织特异性分化。