Affiliations: Endocrinology and Diabetes Unit, British Columbia's
Children's Hospital, University of British Columbia, Vancouver, BC,
Canada | Perinatal Research Center, Hôpital Sainte-
Justine, University of Montreal, Montreal, Quebec, Canada
Abstract: 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.
