期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1980
卷号：77
期号：12
页码：7189-7193
DOI：10.1073/pnas.77.12.7189
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Intraperitoneal injection of maximally effective doses of corticotropin(1-24) [ACTH(1-24)] provoked maximal increases in rat adrenal phospholipids as follows: phosphatidic acid within 1.5-2 min, phosphatidylinositol and phosphatidylglycerol within 4-6 min, and polyphosphoinositides and corticosterone within 5-15 min. Continued maximal adrenal stimulation by ACTH(1-18) treatment caused sustained increases in adrenal phosphatidic acid, phosphatidylinositol, phosphatidylglycerol, polyphosphoinositides, and corticosterone. Treatment with cycloheximide during this steady-state caused rapid decreases in all of these substances to basal levels. The observed half-lives of adrenal phosphatide acid, phosphatidylinositol, polyphosphoinositides, phosphatidylglycerol, and corticosterone during cycloheximide inhibition were 0.15, 1.0, 1.7, 3.3, and 3.5 min, respectively. Calculated production rates during maximal ACTH stimulation were 1060, 991, 90, 34, and 41 nmol/g of tissue per min, respectively. These findings suggest that (i) an initial effect of ACTH on de novo synthesis of phosphatidic acid can account for all subsequently observed increases in other phospholipid derivatives of CDP-diacylglycerol, (ii) a labile protein is required for the ACTH-induced increase in phosphatidic acid, (iii) the phosphatidate leads to polyphosphoinositide-polyglycerophospholipid pathway is rapidly and dramatically responsive to hormonal stimulation, (iv) changes in steroidogenesis correlate well with changes in this phospholipid pathway, and (v) stimulation of this pathway is rapidly reversible.
