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At least 109 records · Page 6Linked to original sources

PubMed1996

Insulin-like growth factors enhance steroidogenic enzyme and corticotropin receptor messenger ribonucleic acid levels and corticotropin steroidogenic responsiveness in cultured human adrenocortical cells.

In several species, including the human fetus, insulin-like growth factors (IGF-I and IGF-II) have been reported to modulate adrenal steroidogenesis, thus contributing to adrenal cortical differentiation. In the present study, we examined the long term effects of IGF-I and -II on human adult adrenal fasciculata-reticularis cells cultured in a chemically defined medium and compared them to the effects of insulin, human GH, and ACTH. Treatment for 3 days with IGF-I or -II at nanomolar concentrations or with insulin at micromolar concentrations slightly increased the production of androstenedione, cortisol, and dehydroepiandrosterone about 1.5-fold over that by control cells. Moreover, the acute steroidogenic response to ACTH of cells pretreated with IGF-I, IGF-II, or insulin was 3- to 6-fold higher than that of control cells. For each hormone, these effects of IGF-I and -II were dose dependent between 0.1-26 nmol/L (1-200 ng/mL). The secretion of androstenedione was more potently stimulated than that of dehydroepiandrosterone and cortisol, and this effect was more clearly yielded by pretreatment with IGF-II than with IGF-I or insulin. Human GH had no effect on these cells. In cells treated with IGF-I or -II, the messenger ribonucleic acid (mRNA) levels of cytochrome P450 17 alpha-hydroxylase and of 3 beta-hydroxysteroid dehydrogenase were increased, and the abundance of ACTH receptor mRNA was also slightly enhanced, but the mRNA of cytochrome P450 cholesterol side-chain cleavage enzyme was unchanged. In conclusion, IGFs enhance the steroidogenesis and ACTH responsiveness of human adrenocortical cells in culture. We speculate, that by this mechanism, IGFs may contribute to clinical states with hyperandrogenemia.

3-Hydroxysteroid Dehydrogenases↗

PubMed1996

Plasma corticotropin and cortisol responses to ovine corticotropin-releasing hormone (CRH), arginine vasopressin (AVP), CRH plus AVP, and CRH plus metyrapone in patients with Cushing's disease.

The CRH test may sometimes be useful in the differential diagnosis of Cushing's syndrome, because most patients with pituitary ACTH-dependent Cushing's syndrome (Cushing's disease) respond to CRH, but those with other causes of Cushing's syndrome usually do not. However, about 10% of Cushing's disease patients fail to respond to CRH. We wondered if we could eliminate these false negative results either by exploiting the potential additive or synergistic effects of another ACTH secretagogue or by reducing glucocorticoid inhibition of CRH's ACTH-releasing effect. We compared the effect on plasma ACTH and cortisol in 51 patients with Cushing's disease of administering ovine CRH (1 microgram/kg BW, i.v.) alone, arginine vasopressin (AVP; 10 U, i.m.) alone, the combination of CRH and AVP, and CRH after pretreatment with metyrapone (1 g, orally, every 4 h for three doses; CRH + MET). The rates of nonresponse (ACTH increment, < 35%; cortisol increment, < 20%) to AVP and CRH alone were 26% and 8%, respectively; all patients responded to CRH + AVP. The lack of response was not due to improper administration or rapid metabolism of the agonist, because plasma CRH and AVP concentrations were similar in responders and nonresponders. A synergistic ACTH response to CRH + AVP occurred in 65% of the patients. MET pretreatment increased basal plasma ACTH levels in most patients and induced the greatest mean peak ACTH response to CRH, but 8% of the patients did not respond to CRH + MET with an ACTH increment of 35% or more. Because all of the Cushing's disease patients tested in this study responded to the combination of CRH + AVP, whereas 8% failed to respond to CRH alone, we conclude that CRH + AVP administration may provide a more reliable test for the differential diagnosis of ACTH-dependent Cushing's syndrome than administration of CRH alone. Whether this improved sensitivity is accompanied by unaltered specificity for Cushing's disease must be tested in patients with chronic ectopic ACTH syndrome.

Adolescent↗

PubMed1993

Corticotropin-releasing factor activates c-fos, NGFI-B, and corticotropin-releasing factor gene expression within the paraventricular nucleus of the rat hypothalamus.

Studies examining the regulation of hypothalamic CRF biosynthesis have provided substantial information regarding the relevance of this peptide in neuroendocrine homeostasis. However, the consequences of elevated CRF levels within the mammalian central nervous system on regulation of CRF production within the paraventricular nucleus (PVN) of the hypothalamus remain unclear. The expression of the immediate early gene c-fos has been used and validated as a marker for neural systems activated by a variety of extracellular stimuli and has been especially useful when examining activation of central neuroendocrine systems such as those involved in the response to stressful stimuli. The present study investigates the effects of injecting CRF into the lateral ventricle of conscious rats, firstly on the expression of two separate immediate early genes, c-fos and NGFI-B within the hypothalamic PVN, and secondly on the expression of CRF mRNA itself, as determined by quantitative in situ hybridization. Expression of Fos protein was also examined by immunohistochemical techniques. Intracerebroventricular (icv) injection of CRF increased the gene expression of both c-fos and NGFI-B in the parvocellular division of the PVN 30 min after injection. Fos immunoreactivity increased in this same region between 30-60 min, whereas expression of the CRF gene itself increased 2-fold 60 min after injection and remained elevated 2 h after treatment. A positive hybridization signal for CRF was observed over Fos-immunoreactive neurons within the parvocellular division of the PVN. Finally, we observed that all CRF-induced changes in gene expression were abolished by pretreatment with the competitive CRF antagonist alpha-helical CRF-(9-41). The time-related changes in expression of the genes measured imply that the expression of both c-fos and NGFI-B occurs before a significant increase in the expression of CRF. The results also suggest that CRF may act in a positive manner to regulate its own biosynthesis.

Animals↗

PubMed2002