[Case of disseminated hemangioendotheliosarcoma].
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Biomedical subjects
Publications and source records attributed to A Markowska.
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Leptin is a peptide secreted by adipose tissue, which regulates satiety, metabolic rate, and thermogenesis. Since corticosteroids regulate the mass of adipose tissue, and leptin synthesis and secretion by adipocytes, we have examined whether leptin in turn is able to directly affect adrenal steroid secretion. Recombinant murine leptin was found to increase basal aldosterone and corticosterone production by dispersed rat zona glomerulosa and zona fasciculata-reticularis cells, respectively. In contrast, leptin did not affect maximally ACTH (10(-9) M)-stimulated steroid secretion. These findings, coupled with the recent observation that leptin is able to stimulate hypothalamo-pituitary CRH-ACTH system, may indicate a role for leptin as a regulator of adrenocortical function in the rat.
The effects of neurotensin (NT) and ACTH on the dexamethasone (Dx)-induced atrophy of the rat adrenal cortex (120 micrograms Dx/rat/day for 4 days) were investigated. NT at a dose of 8 micrograms/rat/day for 2 days prevented Dx-induced adrenal atrophy, and a similar effect was exerted by 10 micrograms/rat/day of ACTH for 2 days. Lower doses of NT were ineffective. ACTH markedly enhanced 3H-thymidine incorporation by adrenal slices, while NT did not. Neither ACTH nor NT had any effect on the number of metaphases per section of the adrenal gland. These findings indicate that NT, like ACTH, prevents Dx-induced adrenocortical atrophy, and that this effect does not depend, as does that of ACTH, upon the stimulation of proliferation of adrenocortical cells.