| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
EXPERIMENTAL STUDY |
1 Department of Anatomy-Histology-Embryology, University of Ioannina, School of Medicine, Ioannina 45110, Greece, 2 Developmental Endocrinology Branch, National Institute of Child Health and Human Development and 3 Neuroendocrinology Branch, National Institute of Mental Health, Bethesda, Maryland 20892, USA and 4 Department of Pediatrics, University of Athens, School of Medicine, Athens, Greece
(Correspondence should be addressed to E O Johnson, Department of Anatomy-Histology-Embryology, University of Ioannina, School of Medicine, Ioannina 45110, Greece; Email: ejohnson{at}cc.uoi.gr or soukakos{at}panafonet.gr)
Objective: Previous studies on the effects of altered thyroid function on the secretion and metabolism of adrenocortical hormones suggest a degree of adrenocortical hyperactivity in hyperthyroidism. We have previously shown that experimentally-induced hyperthyroidism is associated with significant alterations in pituitary–adrenal responsiveness to synthetic ovine corticotropin-releasing hormone (oCRH) that are contingent upon the duration of the altered thyroid function. The purpose of this study was to assess the time-dependent effects of hyperthyroidism on the functional integrity of the hypothalamic–pituitary–adrenal (HPA) axis by in vivo stimulation of the hypothalamic CRH neuron and adrenal cortex.
Methods: The functional integrity of the HPA axis was examined in vivo in sham-thyroidectomized male Sprague-Dawley rats given placebo or in thyroidectomized rats given 50 µg of thyroxine every day for 7 or 60 days. Responses to insulin-induced hypoglycemia and IL-1
stimulation were used to assess the hypothalamic CRH neuron. Adrenocortical reserve was assessed in response to low-dose adrenocorticotropic hormone (ACTH), following suppression of the HPA axis with dexamethasone. Adrenal and thymus tissue weight, in addition to basal plasma ACTH, corticosterone and thyroid indices were also determined.
Results: Basal plasma corticosterone and corticosterone binding globulin (CBG) concentrations were significantly increased in short- and long-term hyperthyroid rats, and by 60 days, cerebrospinal fluid (CSF) corticosterone levels were significantly increased. Basal plasma ACTH levels were similar to controls. Although plasma ACTH responses to hypoglycemic stress and IL-1 administration in both short- and long-term hyperthyroidism were normal, corticosterone responses to the ACTH release during the administration of these stimuli were significantly increased. The adrenal reserve was significantly elevated in short-term hyperthyroidsim. Long-term hyperthyroidism, however, was associated with a significant reduction in adrenocortical reserve. A significant increase in adrenal weights and a decrease in thymus weights were observed in both short- and long-term hyperthyroidism.
Conclusions: The available data confirms that hyperthyroidism is associated with hypercorticosteronemia, although the locus that is principally affected still remains unclear. Despite the sustained hyperactivity of the HPA axis, long-term experimentally-induced hyperthyroidism is associated with diminished adrenal functional reserve. The alterations in HPA function in states of disturbed thyroid function were found to be somewhat more pronounced as the duration of thyroid dysfunction increased.
This article has been cited by other articles:
|
|
 |
|
  N. Marissal-Arvy, A. Gaumont, A. Langlois, F. Dabertrand, M. Bouchecareilh, C. Tridon, and P. Mormede Strain differences in hypothalamic pituitary adrenocortical axis function and adipogenic effects of corticosterone in rats J. Endocrinol., December 1, 2007; 195(3): 473 - 484. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
