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Circulating corticosterone in the infant rat: the mechanism of age and thyroxine effects
Insights
Thyroid hormones influence infant rat corticosterone levels by affecting its metabolic clearance, not direct production. This impacts how the body regulates stress hormones during development.
Area of Science:
- Endocrinology
- Developmental Biology
- Physiology
Background:
- Serum corticosterone, a key stress hormone, significantly increases in infant rats between postnatal days 12-24.
- This rise is thought to be influenced by L-thyroxine, suggesting a role for thyroid status in corticosterone regulation during development.
Purpose of the Study:
- To investigate the physiological mechanisms underlying the age- and thyroid-dependent regulation of serum corticosterone in infant rats.
- To differentiate between central (pituitary-adrenal axis) and peripheral (hormone clearance) contributions to these changes.
Main Methods:
- In vivo studies assessed the adrenal response to adrenocorticotropic hormone and cyclic AMP in rats of different ages and thyroid statuses (hyperthyroid, hypothyroid).
- In vitro adrenal incubations examined basal and stimulated corticosterone production.
- Chronic administration of exogenous corticosterone was used to assess metabolic clearance differences.
Main Results:
- The in vivo adrenal response to stimulation increased with age and was modulated by thyroid status (advanced in hyperthyroidism, delayed in hypothyroidism).
- In vitro studies showed no age-related differences in adrenal corticosterone production.
- Hyperthyroid rats exhibited higher serum corticosterone levels after exogenous administration compared to hypothyroid rats, linked to increased corticosteroid-binding globulin.
Conclusions:
- Age- and thyroid-dependent changes in serum corticosterone in infant rats are primarily mediated by alterations in the hormone's metabolic clearance rate.
- Increased corticosteroid-binding globulin in hyperthyroidism contributes to elevated circulating corticosterone levels.
Abstract:
Infant rats exhibit a marked rise in serum concentrations of corticosterone between postnatal days 12 and 24. As this rise appears to be cued by L-thyroxine, the aim of the current study was to determine the physiological bases of the effects of both age and thyroid status on serum corticosterone. The in vivo response to either adrenocorticotropic hormone (60 mU/g body weight) or dibutyryl 3',5'-cyclic adenylate (0.3 mg/g body weight) increased between 10 and 16 days and was advanced and delayed by hyper- and hypothyroidism, respectively. In contrast, in vitro studies with adrenals from rats aged 10 and 16 days showed no effect of age on either basal or adrenocorticotropic hormone-stimulated production of corticosterone. Chronic administration of exogenous corticosterone to hyperthyroid animals resulted in significantly higher concentrations of serum corticosterone than did an identical administration to hypothyroid animals. As hyperthyroidism was associated with marked elevations in the concentration of corticosteroid-binding globulin and in the extent of binding of corticosterone, these results suggest that the effects of both age and thyroid status on serum concentrations of corticosterone may reflect changes in the metabolic clearance of the hormone.