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PubMed1986

CT diagnosis of adrenal abnormalities in patients with primary non-adrenal malignancies.

Fifty-seven patients with primary non-adrenal malignancy were found to have unsuspected adrenal abnormality on CT. In 33, comparison of histopathologic findings and/or the patients' hospital course or follow-up lead to the diagnosis of adrenal metastases (23), benign non-functioning adenomas (7), metastasis with hyperplasia (1), benign hyperplasia (1), and fatty infiltration (1). The analysis of CT findings indicated that: I) A heterogeneous adrenal mass showing contrast enhancement was always metastatic, II) Nonfunctioning adenomas were always 3 cm or smaller in diameter, III) Bilateral adrenal masses and growth of adrenal mass on follow-up CT or regression on treatment indicated metastases, and IV) metastatic disease could not be excluded purely on the basis of the size of the adrenal mass.

Adrenal Gland Neoplasms↗
PubMed1981

Immunologic cross-reactivity of the low density lipoprotein receptor from bovine adrenal cortex, human fibroblasts, canine liver and adrenal gland, and rat liver.

An antibody to the low density lipoprotein (LDL) receptor was prepared by immunization of rabbits with a partially purified receptor preparation from bovine adrenal cortex. Immunoglobulin G (IgG) isolated from the serum of immunized rabbits blocked the binding of 125I-LDL to intact bovine adrenal membranes as well as to the partially purified bovine adrenal LDL receptor. The anti-receptor IgG also blocked the binding, uptake, and degradation of 125I-LDL by monolayers of human fibroblasts and thus prevented the LDL-mediated suppression of 3-hydroxy-3-methylglutaryl coenzyme A reductase. A monovalent Fab fragment of th anti-receptor IgG retained the ability to inhibit LDL receptors of partially purified bovine adrenal cortex and monolayers of human fibroblasts. By immunofluorescence staining, the anti-receptor IgG was shown to bind to normal fibroblasts in discrete foci that were linearly arranged on the cell surface. No such foci were seen on fibroblasts from a patient with the receptor-negative form of homozygous familial hypercholesterolemia. The rabbit anti-receptor IgG also blocked the binding of 125I-LDL to membranes from dog and rat liver, but it did not prevent LDL binding to rabbit adrenal membranes or rabbit fibroblasts. The immunologic cross-reactivity of LDL receptors from bovine adrenal cortex, human fibroblasts, canine liver and adrenal gland, and rat liver indicates that the structure of this receptor has been widely conserved among animal species and tissues.

Adrenal Cortex↗
PubMed1998

bcl-2 expression in normal adrenal glands and in adrenal neoplasms.

Archival paraffin-embedded tissue from 5 normal adrenal glands (including 1 from a fetus of 28 weeks' gestation), 6 cases of adrenal cortical hyperplasia, 9 cortical adenomas, 14 cortical carcinomas, and 11 pheochromocytomas were immunostained with monoclonal antibody against bcl-2. Ultrastructural localization of bcl-2 protein was also performed on selected cases. Positive immunostaining for bcl-2 was seen in all of the layers of the normal adrenal cortex, with different staining characteristics. bcl-2 expression was never observed in the normal adrenal medulla. Electron microscopic studies revealed bcl-2 to be localized predominantly to mitochondria, with a small number of labels along the nuclear envelope. Analysis of adrenal neoplasms showed expression of bcl-2 in cortical tumors, but only one positive case in pheochromocytomas. Restriction of bcl-2 expression to adrenal cortex-derived tissue versus adrenal medulla-derived tissue might prove to be helpful for the differential diagnosis between cortical and medullary tumors.

Adolescent↗
PubMed1996

Expression of the steroidogenic acute regulatory protein mRNA in adrenal tumors and cultured adrenal cells.

The steroidogenic acute regulatory protein (StAR) has recently been shown to be a factor necessary for cholesterol transport into adrenal and gonadal mitochondria, which is the regulated, rate-limiting step in steroidogenesis. We show here that StAR mRNA is highly expressed in normal adult adrenals (n = 9), adrenocortical adenomas (n = 16), adrenal hyperplasias (n = 6), adrenocortical carcinomas (n = 6) and adrenals adjacent to tumor tissues (n = 9). There was a good correlation between the expression of StAR and the cholesterol side-chain cleavage enzyme/20,22-desmolase (P450 scc) mRNAs both in normal (r = 0.93; P < 0.01) and in tumor (r = 0.97; P < 0.001) tissues. No StAR mRNA was detected in Northern blots of liver, kidney, breast, parathyroid or phaeochromocytoma RNAs. In cultured adrenocortical cells, adrenocorticortropin (ACTH), (Bu)2cAMP, and cholera toxin increased StAR and P450 scc mRNA accumulation 6- to 18-fold, dose- and time-dependently. StAR (and P450 scc) mRNA increased relatively slowly in response to ACTH treatment, with the maximal increment at 24 h, while the mRNA of the early response gene c-fos peaked within 2 h. The protein kinase inhibitor H-7 inhibited basal and ACTH-induced StAR mRNA expression. Our results show that StAR mRNA is expressed at high levels in normal human adrenals and adrenocortical neoplasms. It is up-regulated in parallel with P450 scc by ACTH in adult adrenocortical cells, which suggests that ACTH is at least one of the key regulators of adrenal StAR expression.

Adenoma↗
PubMed1982

Neural regulation of adrenal chromaffin cell function in the mouse--stress effect on the distribution of [3H]dopamine in denervated adrenal medulla.

Effects of adrenal denervation and stress on the distribution of radioactivity in the adrenal medulla after [3H]dopamine injection was studied by light microscopic autoradiography. Denervation of the adrenal gland abolished the stress (restraint plus water immersion) induced degranulation of adrenal chromaffin cells and decreased uptake of [3H]dopamine. Denervated chromaffin cell of stress mice incorporated as high radioactivity as those of no stress mice. Adrenal denervation increased the uptake in adrenaline-storing (A) cells but not in noradrenaline-storing (NA) cells. The characteristic distribution of radioactivity (high radioactivity along the cortico-medullary junction) was reinforced by adrenal denervation. Under stress conditions, increase in pituitary adrenocortical system did not enhance the uptake of [3H]dopamine in chromaffin cell while increase in nerve activity suppressed the uptake. Spontaneous activity of the splanchnic nerve to adrenal chromaffin cells suppresses the uptake of [3H]dopamine. The neural influence is stronger on A cells than on NA cells. Chromaffin cells in the subcortical zone are more intensely controlled by the neural influence than those in the central zone.

Adrenal Medulla↗
PubMed1993

Effect of adrenal demedullation on neuropeptide Y content of the capsule/glomerulosa zone of the rat adrenal gland.

The capsule/glomerulosa zone of the adrenal gland is richly innervated by neuropeptide Y (NPY)-containing nerve fibers. The content and concentration of NPY in the capsule/glomerulosa zone of the female rat adrenal were determined by radioimmunoassay both in unoperated females (controls) and in operated ones, a week after in situ unilateral demedullation which excludes both the medulla and the fasciculata/reticularis zones. Demedullation induced a significant weight increase of the capsule/glomerulosa zone of the operated gland (compared to contralateral intact one) as well as of the medulla/fasciculata-reticularis zone of the contralateral intact one (compared to the corresponding part of the gland of controls). Both NPY content and concentration in the capsule/glomerulosa zone of the demedullated adrenal were significantly reduced in comparison with those in the corresponding part of the contralateral intact gland. NPY immunoreactive fibers, revealed by immunofluorescence, were present in the capsule/glomerular zone of both intact and contralateral demedullated adrenal gland. In the former, NPY fibers were regularly distributed in this part of the gland, while in the latter, some areas were devoid of immunoreactive fibers. NPY content, but not concentration, was increased in the medulla/fasciculata-reticularis zone of the contralateral intact gland. Present data support a dual origin for the NPY nerves present in the capsule/glomerulosa zone of the adrenal cortex: one part could arise from extra-adrenal site possibly the suprarenal ganglia while the other part could arise from intra adrenal ganglia cells which also contain NPY.

Adrenal Medulla↗
PubMed2003

Adrenal-preserving laparoscopic surgery in selected patients with bilateral adrenal tumors.

BACKGROUND: There have been few reports of laparoscopic adrenal-sparing surgery for bilateral adrenal tumors. We review our experience with this type of surgery with the aim of evaluating its feasibility and safety. METHODS: Over a 4-year period, we treated 9 patients with bilateral benign adrenal tumors. Seven patients had bilateral pheochromocytomas (MEN 2: 5, VHL: 1, sporadic: 1), and 2 patients had Cushing's syndrome caused by bilateral adrenocortical adenomas. Laparoscopic procedures were performed by a flank approach. The mean diameter of the tumors was 3.7 cm (range, 2.0-8.5 cm). RESULTS: All the tumors were removed laparoscopically. Four patients with hereditary pheochromocytomas underwent bilateral total adrenalectomy because of the large tumor size and multiplicity. The other 5 patients were treated successfully with preservation of adrenocortical function. In 4 of these 5 patients, the adrenal tumors were 3 cm or less in diameter. None of the patients experienced surgical complications. At a mean follow-up of 16 months (range, 4-40 months), none of the 5 patients who were treated by adrenal-sparing surgery required corticosteroid replacement. CONCLUSION: Laparoscopic surgery is feasible for the treatment of bilateral adrenal tumors. Adrenal-preserving laparoscopic surgery may be practicable for the removal of these tumors, if the tumor on either side is 3 cm or less in diameter; however, our follow up is short (mean, 16 months).

Adrenal Gland Neoplasms↗
PubMed2003

Adenomatoid tumor of the adrenal gland with micronodular adrenal cortical hyperplasia.

We report a case of an adenomatoid tumor (AT) of an adrenal gland with micronodular adrenal cortical hyperplasia (ACH). A 51-year-old man was found to have newly developed hypertension with clinical evidence of primary aldosteronism. A computerized tomogram of the abdomen revealed a solitary mass in the right adrenal gland. He underwent a right adrenalectomy for a presumptive clinical diagnosis of a solitary aldosterone-producing adrenal cortical adenoma. On histopathologic examination, the adrenal gland demonstrated an AT, diagnosed by the characteristic histological features, immunohistochemical stain results, and electron microscopic findings. The surrounding adrenal cortex showed multiple small hyperplastic cortical nodules. After the adrenalectomy, the patient's blood pressure normalized. Primary AT of the adrenal gland coexisting with micronodular ACH associated with hypertension has not been previously reported.

Adrenal Cortex Neoplasms↗
PubMed2004

Bilateral adrenal haemorrhage and acute adrenal insufficiency in a blunt abdominal trauma: a case-report and literature review.

Blunt abdominal trauma is frequently associated with adrenal haemorrhage, and is preferentially diagnosed by computed tomography scan. Lesions are mostly unilateral and asymptomatic and are therefore frequently overlooked. Bilateral haemorrhage, however, has a high mortality rate as a result of acute adrenal insufficiency. We report on a 30-year-old polytraumatic patient who developed cardiocirculatory arrest when all lesions were surgically controlled and stable and without evidence of a primary cardiac problem. Autopsy revealed bilateral adrenal haemorrhage, leading to the diagnosis of acute adrenal insufficiency as the cause of death. We conclude that adrenal haemorrhage should be looked for in every polytrauma patient, and that although it is a rare occurrence, acute adrenal insufficiency caused by bilateral adrenal haemorrhage should be considered in every patient with unexplained cardiocirculatory failure. Such patients may benefit from the prompt administration of corticosteroid replacement, which can be life saving.

Abdominal Injuries↗
PubMed1969

Adrenal secretion rates and adrenal tissue concentrations of pregnenolone, progesterone, 11 beta OH-androstenedione and some other steroids in young pigs and dogs.

1. The rates were measured at which a number of different steroids were secreted by the adrenal gland of the eviscerated and nephrectomized young pig and dog.2. In addition to cortisol and corticosterone the following steroids were consistently found to be present in the adrenal venous blood: pregnenolone, progesterone, 11betaOH-progesterone, androstenedione, 11betaOH-androstenedione and adrenosterone.3. The sum of the latter steroids could amount to as much as 30% of the total steroid secretion.4. A severe deficit in the blood volume increased the secretion of pregnenolone and the 17-oxo steroids in the pig.5. alpha-ethyltryptamine failed to inhibit ACTH release if the animals were eviscerated and nephrectomized, or if they were anaesthetized with chloralose instead of pentobarbitone sodium.6. The same steroids as in the adrenal venous blood were found in extracts from the adrenal glands of a number of species.7. The amount of individual steroids present in the adrenal gland of the stressed pig and dog was compared with the rate at which each had been secreted immediately before the excision of the gland.8. There was a positive correlation between the adrenal concentrations and the secretion rates of cortisol, the major glucocorticoid secreted by the pig and the dog.9. In contrast, the rate at which pregnenolone was secreted did not show a consistent relationship to its concentration in the gland.10. A storage mechanism for pregnenolone in the adrenal cortex is proposed.

Adrenal Glands↗
PubMed2000

Adrenocorticotropin-independent macronodular adrenal hyperplasia: an uncommon cause of primary adrenal hypercortisolism.

PURPOSE: To describe the imaging findings in the adrenal glands of 12 patients with adrenocorticotropin (ACTH)-independent macronodular adrenocortical hyperplasia (AIMAH). MATERIALS AND METHODS: Computed tomographic (CT) and magnetic resonance (MR) imaging findings in the adrenal glands were reviewed retrospectively in 12 patients (three men, nine women) with ACTH-independent Cushing syndrome and with bilateral nonpigmented multinodular adrenal hyperplasia. The results of pituitary MR imaging, adrenal scintigraphy, and petrosal sampling were available in nine, five, and six patients, respectively. Eleven patients underwent bilateral and one patient underwent unilateral adrenalectomy. RESULTS: Eleven patients had enlarged multinodular adrenal glands: Nodules were 0.1-5.5 cm. The combined weight of both adrenal specimens for the 11 bilateral adrenalectomy specimens was 28-297 g, with a mean weight of 122 g. Glands were hypointense compared with the liver on T1-weighted images and were hyperintense on T2-weighted images. Pituitary MR imaging findings were negative in nine of nine patients. Iodomethylnorcholesterol scintigraphy showed bilateral uptake in four of five patients. Petrosal sinus sampling revealed no petrosal-to-peripheral ACTH gradients before corticotropin-releasing hormone (CRH) stimulation in six of six patients, but three patients had gradients after CRH stimulation. After undergoing bilateral or unilateral adrenalectomy, all patients were cured. CONCLUSION: AIMAH is a rare cause of ACTH-independent Cushing syndrome, with characteristic CT findings of massively enlarged multinodular adrenal glands. Bilateral adrenalectomy is indicated on the basis of clinical and CT findings.

Adrenal Glands↗
PubMed1981

The developmental changes in plasma adrenal androgens during infancy and adrenarche are associated with changing activities of adrenal microsomal 17-hydroxylase and 17,20-desmolase.

The plasma concentrations of dehydroepiandrosterone, androstenedione, and dehydroepiandrosterone sulfate decrease during the first year of life, remain low during childhood, and then increase during adrenarche. To determine whether alterations in adrenal enzyme activity might explain the changing secretory pattern of the adrenal androgens, we measured human adrenal microsomal 3 beta-hydroxysteroid dehydrogenase-isomerase, 17,20-desmolase, 17-hydroxylase, and 21-hydroxylase activities. 12 adrenals from individuals aged 3 mo to 60 yr were studied. The patients were divided into three groups based upon the age of the patient when the adrenal glands were obtained: group 1, infants aged 3--8 mo (n = 3); group 2, preadrenarchal or early adrenarchal children aged 2--9 yr (n = 4); and group 3, adults aged 20--60 yr (n = 5). The mean activity of the 17,20-desmolase, 17-hydroxylase, and 21-hydroxylase fell by 50% and that of 3 beta-hydroxysteroid dehydrogenase-isomerase activity rose 80% from group 1 to 2. A fourfold increase in 17,20-desmolase (P less than 0.002) and 17-hydroxylase (P less than 0.001) activity and a doubling in 21-hydroxylase activity (P less than 0.005) occurred between groups 2 and 3. We conclude that the decline in plasma adrenal androgens after birth appears to be associated with a rise in 3 beta-hydroxysteroid dehydrogenase-isomerase and a fall in 17,20-desmolase and 17-hydroxylase activity. The subsequent increase in plasma adrenal androgen concentration during adrenarche is coincident with a rise in 17,20-desmolase and 17-hydroxylase activity.

3-Hydroxysteroid Dehydrogenases↗
PubMed1978

Rat adrenal androgen receptor: a possible mediator of androgen-induced decreased in rat adrenal weight.

Many previous studies have demonstrated effects of gonadal steroids on adrenal weight in the rat. Most of these effects are indirect, depending upon alterations in the pituitary-adrenal axis for their expression. In this study we have attempted to examine the direct effects of gonadal steroids on adrenal weight in the rat. This was done using hypophysectomized, castrated male rats receiving ACTH replacement, a model which excludes pituitary-adrenal feedback effects. Estradiol-treated rats did not differ from controls, whereas testosterone-treated rats exhibited a small but statistically significant decrease in adrenal weight. As a first step in exploring the mechanism of this androgen effect, we have identified a specific dihydrotestosterone-binding protein in the rat adrenal gland. A single class of high affinity (Kd = 0.6-2.0 x 10(-8) M), saturable (28 fmol/mg cytosol protein), cytoplasmic binding sites was found using both protamine sulfate precipitation and dextran-coated charcoal assays. The specificity, sedimentation coefficient on sucrose gradient, and sensitivity to sulfhydryl reagents and heat of this dihydrotestosterone-binding protein are typical of the cytoplasmic androgen receptor from other androgen target tissues such as prostrate. We conclude that testosterone can decrease rat adrenal weight directly, and that the mechanism may involve a high affinity binding protein, as has been shown in other androgen-responsive systems.

Adrenal Glands↗
PubMed1982

Rapid regression of fetal adrenal zone and absence of adrenal reticular zone in the marmoset.

Developmental changes in plasma dehydropiandrosterone (DHA) and in adrenal histology were studied in several marmoset species (Callithrix jacchus and Saguinus labiatus, nigricollis, and fuscicollis) to evaluate these primates as experimental models for the study of fetal adrenal zone regression. Newborn marmosets had a prominent fetal adrenal zone, plasma DHA levels above 1000 ng/dl, and plasma DHA sulfate (DHAS) levels of 140 micrograms/dl. The fetal zone regressed dramatically during the first week of life, paralleled by a marked decline in plasma DHA, the plasma DHA to cortisol ratio, and plasma DHAS. The adult marmoset, however, had no adrenal reticular zone and no evidence of adrenal DHA secretion; DHA levels in castrate adults were undetectable (less than 25 ng/dl). Thus, the marmoset represents the first example of a primate that has a regressing, DHA- and DHAS-secreting fetal adrenal zone but that does not subsequently develop a DHA-secreting adrenal reticular zone.

Adrenal Glands↗
PubMed2003

Diagnosis of adrenal insufficiency: Evaluation of the corticotropin-releasing hormone test and Basal serum cortisol in comparison to the insulin tolerance test in patients with hypothalamic-pituitary-adrenal disease.

The aim of the study was to evaluate the diagnostic value of the human CRH test and the basal morning serum cortisol for the diagnosis of adrenal insufficiency. Putative peak cortisol cut points for the CRH test and basal cortisol cut points were determined by receiver operating characteristic (ROC) analysis with the insulin tolerance test as reference test. Fifty-four patients with suspected hypothalamic-pituitary-adrenal disease were tested. In 20 healthy controls, CRH led to a mean peak cortisol of 594.8 +/- 21.7 nmol/liter. The lower limit of a normal response was calculated as 400 nmol/liter. ROC analysis of peak cortisol levels during CRH testing of patients with suspected hypothalamic-pituitary-adrenal disease suggested an optimal peak cortisol cut point of < or 377 nmol/liter for the diagnosis of adrenal insufficiency and a 96% specificity but poor sensitivity of 76%. The baseline cortisol in the healthy control group showed a mean of 439.3 +/- 24.9 nmol/liter, resulting in a lower limit of 267 nmol/liter. ROC analysis of patients suggested the highest accuracy for basal cortisol levels of 285 nmol/liter or more for the diagnosis of adrenal insufficiency (100% sensitivity and 61% specificity). Within this patient group, a cortisol of more than 98 nmol/liter excluded adrenal insufficiency among those without the disorder, yielding 100% specificity. Using these criteria of upper (285 nmol/liter) and lower (98 nmol/liter) cut-off points with high sensitivity and specificity can reduce the number of individuals who need provocative tests. Basal cortisol is less expensive, and we therefore suggest to use it as a first-line test of adrenal insufficiency. Because of the low sensitivity of the human CRH test, we do not recommend it as a second test.

Adrenal Gland Diseases↗
PubMed1990

Adrenal autoantibodies bind to adrenal subcellular fractions enriched in cytochrome-c reductase and 5'-nucleotidase.

A quantitative assay for human adrenal autoantibodies has been developed to aid in the detection and isolation of human adrenal antigens. To define the subcellular location(s) of the antigen(s) capable of binding with these antibodies, we have quantitated both antibody binding to various adrenal subcellular fractions and the adrenal autoantibody binding inhibition caused by each subcellular fraction. To further define the subcellular location of the autoantibody binding, each fraction was assayed for organelle-specific marker enzyme activities. Enzyme activities were correlated to adrenal autoantibody binding to each fraction by linear regression. Of the materials tested, both antibody binding and inhibition of binding were most highly correlated with adrenal subcellular fractions enriched with cytochrome-c reductase and 5'-nucleotidase (r = 0.98; P less than 0.05). Thus, our data support the localization of adrenal autoantigen(s) in the microsomes, plasma membrane, or both.

5'-Nucleotidase↗
PubMed1992

Preclinical Cushing's syndrome in adrenal "incidentalomas": comparison with adrenal Cushing's syndrome.

Adrenal tumors are usually diagnosed by clinical symptoms of hormone excess. The increasing use of ultrasound and computed tomography results in the detection of a substantial number of incidentally discovered adrenal tumors. Most of these tumors are nonfunctional adrenocortical adenomas, but a few cases of subclinical cortisol production in "incidentalomas" have been reported. We investigated prospectively the prevalence of autonomous cortisol production in 68 patients (44 females and 24 males, aged 25-90 yr) with adrenal incidentalomas at our institution. As a screening procedure all patients with incidentalomas underwent an overnight dexamethasone suppression test (1 mg). Patients who failed to suppress serum cortisol below 140 nmol/L (5 micrograms/dL) underwent more comprehensive studies (prolonged dexamethasone suppression test, determination of the diurnal rhythm of cortisol secretion in saliva, and CRH stimulation test). Eight patients (12% of all patients with incidentalomas; 5 females and 3 males, aged 25-71 yr) were finally identified as having cortisol-producing tumors, and the findings in these patients were compared with those of overt Cushing's syndrome in 8 patients (8 females, aged 26-50 yr) suffering from cortisol-producing adrenal adenomas. The tumor size of patients with cortisol-producing incidentalomas ranged from 2-5 cm. No specific signs and symptoms of hypercortisolism were present, but arterial hypertension (seven of eight subjects), diffuse obesity (four of eight subjects), and noninsulin-dependent diabetes mellitus (NIDDM; two of eight subjects) were frequently observed. Baseline cortisol levels were in the normal to upper normal range, whereas baseline ACTH levels were suppressed in five of the eight patients. In none of the patients was serum cortisol suppressible by low dose or high dose dexamethasone. The ACTH and cortisol responses to CRH were normal in two, blunted in one, and suppressed in four patients. Unilateral adrenalectomy was performed in seven patients and resulted in temporary adrenal insufficiency in four of them. After surgery, improvement of arterial hypertension, a permanent weight loss in obese subjects, and a better metabolic control of NIDDM were noted in the majority of patients. The following conclusions were reached. Incidentally diagnosed adrenal tumors with pathological cortisol secretion in otherwise clinically asymptomatic patients are more frequently observed than previously assumed. Adrenocortical insufficiency is a major risk in these patients after adrenalectomy. After surgery, hypertension, obesity, and NIDDM may improve. Patients with asymptomatic adrenal incidentalomas, therefore, should be screened for cortisol production by means of an overnight dexamethasone suppression test.

Adrenal Gland Neoplasms↗
PubMed2001

Expression of orexin-A and functional orexin type 2 receptors in the human adult adrenals: implications for adrenal function and energy homeostasis.

The hypothalamic peptides, orexin-A and orexin-B, have been implicated in the regulation of feeding behavior. In starved rats catabolic activity quickly predominates, reinforced by elevated corticosterone, independent of ACTH, implicating adrenal activity as a metabolic regulator. In view of these findings, we investigated whether orexin and orexin receptors are present in human adult adrenals and might therefore be implicated in hormonal regulation and energy homeostasis outside the central nervous system. RT-PCR, fluorescent in situ hybridization, immunoblotting, and immunostaining analysis confirmed the expression of the orexin type 2 receptor, but not of orexin type 1 receptor, in the adrenal cortex. Immunoblotting analysis also detected the presence of the prepro-orexin and its cleaved product orexin-A. Treatment of adult adrenal membranes with orexin-A increased the labeling of G(s), G(q), and, to a lesser degree, G(i), but not G(o). Stimulation with orexin-A induced cAMP and IP3 production in a dose-dependent manner. The data presented here provide conclusive evidence for the presence of orexin-A and orexin type 2 receptors in human adult adrenal glands. At the moment the functional relevance of this is uncertain. However, it is known that both orexin-A and orexin-B can induce corticosterone production in dispersed rat adrenocortical cells. Our data provide further evidence for a functional link between orexogenic signals and adrenal function. The concept that the peptide acting via these receptors in the adult adrenal is responsible for steroidogenesis and energy balance is attractive.

Adrenal Glands↗