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Selenium deficiency impairs corticosterone and leptin responses to adrenocorticotropin in the rat
Author(s) -
Chanoine JeanPierre,
Wong Alfred C.K.,
Lavoie JeanClaude
Publication year - 2004
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520200205
Subject(s) - medicine , endocrinology , leptin , corticosterone , selenium deficiency , oxidative stress , selenium , glutathione peroxidase , chemistry , adrenocorticotropic hormone , biology , hormone , superoxide dismutase , obesity , organic chemistry
Selenium deficiency causes oxidative stress and impairs steroidogenesis in vitro . Leptin is closely related to the hypothalamo‐pituitary‐adrenal (HPA) axis. Leptin inhibits the HPA axis at the central level while corticosteroids have been shown to stimulate leptin secretion in most studies. We hypothesized that oxidative stress impairs adrenal steroidogenesis and decreases leptin production in vivo. The goal of this study was to investigate in rats the effects of selenium deficiency and oxidative stress on adrenal function and on leptin concentrations. Weanling rats were fed a selenium‐deficient (Se‐) or selenium‐sufficient (Se+) diet for 4–10 weeks. Selenium deficiency caused a marked decrease in liver (≥ 99%) and adrenal (≥ 81%) glutathione peroxidase (GPx) activities. Selenium deficiency did not affect basal and short‐term adrenocorticotropin (ACTH) stimulated corticosterone or leptin concentrations. In contrast, after long‐term ACTH stimulation, selenium deficiency caused a doubling in adrenal isoprostane content and blunted the increase in corticosterone and leptin concentrations observed in Se+ animals. Plasma leptin concentrations were 50% lower in Se‐ compared to Se+ animals following long‐term ACTH. Our results suggest that oxidative stress causes a decrease in circulating corticosterone in response to ACTH, and, as a consequence, a decrease in plasma leptin concentrations.