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PubMed1983

Activation of ovine fetal adrenal function by pulsatile or continuous administration of adrenocorticotropin-(1-24). II. Effects on adrenal cell responses in vitro.

We have examined 1) the effects of mode of ACTH administration to fetal sheep in vivo on the pattern of corticosteroid output by dispersed adrenal cells in vitro, and 2) the time course of fetal adrenal activation during pulsatile ACTH administration to the fetus. Fetal sheep received the same amount of ACTH either as a continuous infusion (C-ACTH; 0.5 microgram/h) or as 15-min pulses every 2 h for 72 h (P-ACTH). Other fetuses received P-ACTH until labor occurred (mean, 100 h) or saline for 72 or 100 h. Adrenal cells from fetuses that received C-ACTH for 72 h produced more corticosterone from endogenous precursors after the addition of ACTH in vitro and after the addition of 0.3 microM progesterone (P4) or pregnenolone (P5) than cells from fetuses treated with P-ACTH for 72 h. There was no difference in cortisol (F) response between the two groups, although in both groups F output was greater than in controls. Adrenal cells from control fetuses produced more P4 in vitro during incubation with ACTH plus guanosine-5'-(beta, gamma-imido)triphosphate [Gpp(NH)p] or N6,O2'-dibutyryladenosine 3',5'-cyclic monophosphate [(Bu)2cAMP] than after ACTH alone. There was no significant F response to the agonists, and F output was quantitatively less than that of P4. After 72-h P-ACTH, the mean P4 output after ACTH addition was not significantly different from that after ACTH plus Gpp(NH)p or (Bu)2cAMP. By 100 h of P-ACTH, the output of F exceeded that of P4 and was not different in response to ACTH, ACTH plus Gpp(NH)p, or (Bu)2cAMP. After 72 h of P-ACTH, incorporation of exogenous P4, but not P5, 17 alpha-hydroxyprogesterone, or 17 alpha-hydroxypregnenolone, into F was greater than that in cells from control fetuses. By 100 h of P-ACTH, incorporation of all substrates into F was greater than that after P-ACTH for 72 h. We conclude that 1) both C-ACTH and P-ACTH for 72 h increase fetal adrenal responses, but the pattern of corticosteroid output in vitro is determined by the mode of ACTH administration in vivo; 2) adrenal responsiveness is increased further between 72 and 100 h of P-ACTH, and activation probably involves changes in ACTH receptor-GTP coupling as well as enzyme activities on the pathway to F biosynthesis.

Adrenal Glands↗

PubMed2002

Differential expression of c-fos and tyrosine hydroxylase mRNA in the adrenal gland of the infant rat: evidence for an adrenal hyporesponsive period.

Rats exhibit a stress hyporesponsive period from postnatal day (PND) 4-14 in which the neonate displays a minimal corticosterone response to stress. We used the maternal deprivation model to test whether this adrenocortical hyporesponsiveness to stress results from a decrease in adrenal sensitivity to ACTH. Neonates (PND 6, 9, and 12) were injected ip with dexamethasone to block endogenous ACTH release, and 4 h later injected with graded doses of ACTH and killed. In another experiment, neonates were injected with isotonic saline and adrenal glands were collected at 30, 60, and 120 min post injection to examine c-fos and tyrosine hydroxylase mRNA levels using in situ hybridization. Maternally deprived pups demonstrated elevated corticosterone levels at the two highest ACTH doses and showed a greater magnitude in glucocorticoid secretion compared with the nondeprived pups. Maternally deprived pups given a saline injection exhibited elevated basal and stress-induced levels of corticosterone, in contrast to the nondeprived pups that showed a minimal response. Strikingly, maternally deprived pups exhibited elevated levels of adrenocortical c-fos mRNA, whereas the nondeprived pups did not. In contrast, the pattern of c-fos gene expression in the adrenal medulla in both groups did not display any correlation with glucocorticoid secretion. Tyrosine hydroxylase gene expression in the adrenal medulla was observed in both nondeprived and maternally deprived pups, with the latter exhibiting an earlier response of greater magnitude. These results demonstrate that the suppression of steroidogenesis occurs directly in the adrenal cortex and provide further evidence for an adrenal hyporesponsive period in the rat.

Adrenal Glands↗

PubMed1981

The relationship of adrenal iodocholesterol uptake to adrenal zona glomerulosa function.

Dexamethasone suppression adrenal scintigraphy is routinely used in the clinical assessment of patients with aldosteronism. To determine the relation between adrenal iodocholesterol uptake and aldosterone secretory activity, iodocholesterol uptake in dexamethasone-suppressed dogs was measured during salt loading and salt depletion. Sodium loading resulted in decreases in both serum aldosterone and adrenal iodocholesterol uptake. Sodium depletion was associated with increases in both serum aldosterone and iodocholesterol uptake. From these studies we calculate that under basal conditions, approximately 10% of adrenal iodocholesterol uptake is angiotension dependent, and approximately 50% is ACTH dependent. The administration of dexamethasone results in an increase in the sensitivity of adrenal scintiscanning in the assessment of adrenal zona glomerulosa function.

19-Iodocholesterol↗

PubMed1997

Insulin-like growth factors augment steroid production and expression of steroidogenic enzymes in human fetal adrenal cortical cells: implications for adrenal androgen regulation.

The fetal zone is a unique adrenal cortical compartment that exists only during fetal life in humans and higher primates and produces large amounts of the adrenal androgen dehydroepiandrosterone sulfate (DHEA-S). Growth of the fetal zone is primarily regulated by ACTH, the actions of which are mediated in part by locally produced autocrine/paracrine growth factors. We previously demonstrated that one of these growth factors, insulin-like growth factor II (IGF-II), is mitogenic for cultured fetal zone cells and is produced in high abundance by these cells in response to ACTH. In the present study, we determined whether IGF-II also modulates the differentiated function of fetal zone cells. We examined the effects of recombinant human IGF-II and the closely related peptide, IGF-I, on 1) basal and agonist-stimulated [ACTH-(1-24), forskolin, or 8-bromo-cAMP] cortisol and DHEA-S production, 2) basal and ACTH-stimulated steady state abundance of messenger ribonucleic acids (mRNAs) encoding the steroidogenic enzymes cytochrome P450 side-chain cleavage (P450scc) and cytochrome P450 17alpha-hydroxylase/17,20-lyase (P450c17), and 3) basal and ACTH-stimulated steady state abundance of mRNA encoding the ACTH receptor. Basal cortisol (23.93 +/- 1.20 pmol/10(5) cells x 24 h) and DHEA-S (548.87 +/- 43.17 pmol/10(5) cells x 24 h) productions were significantly (P < 0.05) increased by IGF-I (2.3- and 1.8-fold, respectively) and IGF-II (2.8- and 1.8-fold, respectively). As expected, ACTH, forskolin, and cAMP markedly increased the production of cortisol by 26-, 10-, and 13-fold, respectively, and that of DHEA-S by 5.4-, 4.6-, and 5.5-fold, respectively, compared with basal levels. IGF-II (100 ng/mL) significantly (P < 0.001) increased ACTH-, forskolin-, and cAMP-stimulated production of cortisol by 2.4-, 4.3-, and 3.2-fold, respectively, and that of DHEA-S by 1.4, 1.6-, and 1.4-fold, respectively. IGF-I (100 ng/mL) had similar effects as IGF-II and significantly (P < 0.001) increased ACTH-, forskolin-, and cAMP-stimulated production of cortisol by 2.8-, 3.9-, and 3.1-fold, respectively, and that of DHEA-S by 1.3-, 1.6-, and 1.4-fold, respectively. The similar potencies of IGF-I and IGF-II suggest that the actions of these factors were mediated via a common receptor, most likely the type I IGF receptor. The effects of IGF-II on ACTH-stimulated steroid production were dose-dependent (EC50, 0.5-1.0 nmol/L), and IGF-II markedly increased the steroidogenic responsiveness of fetal zone cells to ACTH. With respect to cortisol production, IGF-II shifted the ACTH dose-response curve to the left by 1 log10 order of magnitude. IGF-II also increased ACTH-stimulated abundance of mRNA encoding P450scc (1.9-fold) and P450c17 (2.2-fold). Basal expression of P450scc was not affected by IGF-II. In contrast, basal expression of P450c17 was increased 2.2-fold by IGF-II and IGF-I in a dose-responsive fashion. Neither IGF-I nor IGF-II affected basal or ACTH-stimulated abundance of mRNA encoding the ACTH receptor, suggesting that the increase in ACTH responsiveness was not mediated by an increase in ACTH-binding capacity. Taken together, these data indicate that activation of the type I IGF receptor increases ACTH responsiveness in fetal zone cells by modulating ACTH signal transduction at some point distal to ACTH receptor activation. These data also indicate that locally produced IGF-II modulates fetal adrenal cortical cell function by increasing responsiveness to ACTH and possibly (based on its direct stimulation of P450c17 expression) augmenting the potential for adrenal androgen synthesis. Thus, activation of the type I IGF receptor on adrenal cortical cells may play a pivotal role in adrenal androgen production, both physiologically in utero and at adrenarche, and in pathophysiological conditions ofhyperandrogenemia, such as the polycystic ovary syndrome.

Adrenal Cortex↗

PubMed2006

Liver X receptors regulate adrenal steroidogenesis and hypothalamic-pituitary-adrenal feedback.

The nuclear hormone receptors liver X receptor alpha (LXRalpha) (NR1H3) and LXRbeta (NR1H2) are established regulators of cholesterol, lipid, and glucose metabolism and are attractive drug targets for the treatment of diabetes and cardiovascular disease. Adrenal steroid hormones including glucocorticoids and mineralocorticoids are known to interfere with glucose metabolism, insulin signaling, and blood pressure regulation. Here we present genome-wide expression profiles of LXR-responsive genes in both the adrenal and the pituitary gland. LXR activation in cultured adrenal cells inhibited expression of multiple steroidogenic genes and consequently decreased adrenal steroid hormone production. In addition, LXR agonist treatment elevated ACTH mRNA expression and hormone secretion from pituitary cells both in vitro and in vivo. Reduced expression of the glucocortioid-activating enzyme 11beta-hydroxysteroid dehydrogenase 1 in pituitary cells upon LXR activation suggests blunting of the negative feedback of glucocorticoids by LXRs. In conclusion, LXRs independently interfere with the hypothalamic-pituitary-adrenal axis regulation at the level of the pituitary and the adrenal gland.

Adrenal Glands↗

PubMed1994

Cushing's disease associated with adrenal myelolipoma, adrenal calcification and thyroid cancer.

A 51-year-old woman with Cushing's disease associated with adrenal myelolipoma is reported. A further characteristic feature was the coexistence of bilateral adrenal calcification and thyroid cancer. Previously several cases of adrenal myelolipoma associated with endocrine dysfunction were reported. The combination of Cushing's disease and adrenal myelolipoma has only been described in two cases of recurrent Cushing's disease but never in an initial occurrence of Cushing's disease. Continued stimulation by excessive adrenocorticotropic hormone (ACTH) not only developed adrenal hyperplasia but also might be involved in the pathogenesis of adrenal myelolipoma.

Adrenal Gland Neoplasms↗

PubMed2005

Investigation of the hypothalamo-pituitary-adrenal axis and changes in the size of adrenal glands in acute brucellosis.

The aim of the study was to investigate the hypothalamo-pituitary-adrenal (HPA) axis by ACTH stimulation test and the changes in adrenal size in acute brucellosis before and after therapy in a prospective study. Sixteen patients with acute brucellosis and 15 healthy subjects were included in the study during the last two years. Cortisol levels were assessed before, 30 and 60 minutes after ACTH (250 microg i.v.) injection and the size of the adrenals was measured in both groups. Mean basal cortisol levels in the patients before the therapy and after the therapy were 22.1 +/- 6.9 microg/dL and 11.3 +/- 6.0 microg/dL, respectively. The difference was statistically significant (p<0.001). There was also statistically significant difference for basal cortisol levels between the healthy subjects (12.2 +/- 4.6 microg/dL) and the patients before the therapy (p<0.001). Peak cortisol responses to ACTH were higher before the therapy in the patients with acute brucellosis (39.3 +/- 10.7 microg/dL) than in the healthy subjects (30.4 +/- 4.8 microg/dL, p = 0.014). However, there was no significant difference for peak cortisol levels in the patients before and after the therapy (32.7 +/- 8.0 microg/dL). Mean basal cortisol levels and peak cortisol responses to ACTH between the patients after the therapy and the healthy controls were similar. Both the maximum width of the adrenal glands and the width of the adrenal limbs were significantly greater before the therapy compared to healthy subjects and post-treatment period. We concluded that the HPA axis is activated and the adrenal glands are enlarged in acute brucellosis, which is reduced after appropriate therapy.

Acute Disease↗

PubMed1992

Disordered expression of adrenal steroidogenic P450 mRNAs in incidentally discovered nonfunctioning adrenal adenoma.

In order to elucidate the steroidogenesis of clinically nonfunctioning adrenocortical adenoma, we studied the aldosterone, cortisol (F) and dehydroepiandrosterone (DHEA) content and the expression of mRNA of cytochrome P450 for side chain cleavage (P450scc), 17 alpha-hydroxylase (P450c17). 21-hydroxylase (P450c21) and 11 beta-hydroxylase (P450c11) in four clinically nonfunctioning adrenocortical adenomas discovered incidentally in asymptomatic patients (Cases 1, 2, 3 and 4). The results were compared with those in normal adrenal glands. In the adenomas from cases 1 and 2, the abundance of steroidogenic P450s mRNA were similar to those in normal adrenal glands, except P450c11 mRNA expression in the adenoma from case 1 which was slightly higher than normal. The steroid content was normal level, except for higher F in the adenoma from case 1 and lower aldosterone in case 2 adenoma than normal. The adenoma from case 3 contained much less P450scc, P450c17 and P450c21 mRNA, while the amount of P450c11 mRNA was slightly greater than in normal adrenals. The adenoma showed normal aldosterone, high F and low DHEA content compared with normal adrenal glands. In the adenoma from case 4, the accumulation of all four P450 mRNAs decreased, whereas aldosterone, F and DHEA content in the adenoma was similar to that of normal adrenal glands. These data indicated that nonfunctioning adrenocortical adenoma showed similar or decreased expression of steroidogenic P450 mRNAs that the normal adrenal gland. This decreased expression of steroidogenic P450 mRNAs may be at least partly concerned with the absence of clinical symptoms in patients with nonfunctioning adenoma.

Adenoma↗

PubMed1989

Blood vascular beds of rat adrenal and accessory adrenal glands, with special reference to the corticomedullary portal system: a further scanning electron microscopic study of corrosion casts and tissue specimens.

Blood vascular casts of the rat adrenal glands were observed with a scanning electron microscope. The cortical capillary plexus drains, through the corticomedullary venous radicles, into the subcortical veins continuous with the medullary collecting veins. The medullary capillary plexus drains into the corticomedullary venous radicles, subcortical veins and medullary collecting veins. No portal vessel was noted between the cortical and medullary capillaries. These findings indicate that the cortical blood rich in glucocorticoids preferentially and continuously flows into the corticomedullary venous radicles, subcortical veins and medullary collecting veins all three of which are fenestrated in type, and also suggest that the vascular route from the cortical capillaries to the medullary collecting veins functions as a substitute for the portal system, controlling the biosynthesis of catecholamines in the adrenal medulla. The vascular bed of the accessory adrenal gland (extra-adrenal cortical or chromaffin body) is sometimes annexed to that of the adrenal gland. On rare occasions, the vascular beds of the extra-adrenal cortical and chromaffin bodies fuse with each other. Additional scanning of tissue samples confirmed the direct drainage of cortical capillaries into the medullary veins and also the endothelial fenestrations of these capillaries and veins.

Adrenal Glands↗

PubMed1992

Phosphoribosyl pyrophosphate formation in the rat adrenal gland in relation to adrenal growth in experimental diabetes.

Adrenal growth occurs in experimental diabetes, and evidence exists for increased adrenal function. The concentration of PPRibP has been examined in the rat adrenal gland at various times after induction of diabetes with STZ, in view of the key role it plays in the synthesis of Purs and Pyrs. The PPRibP level was exceptionally high in the adrenal gland and increased faster than the rate of growth during the initial rapid growth phase--the first 7 days after STZ was given; PPRibP synthetase showed a parallel increase. Formation of R5P via the oxidative and nonoxidative segments of the PPP also was measured. The oxidative enzymes, G-6-PD and 6-PGD, increased in parallel with growth during the early phase, but showed a more marked rise during the secondary, slower, growth phase seen 6 wk after STZ was given, when this may be associated with the known sustained rise in plasma corticosteroids. The nonoxidative enzymes of the PPP, an alternate route for the production of R5P, showed smaller changes. The specifically high adrenal concentration of PPRibP may be related to the high Km for PPRibP (250 microM) of the first enzyme of the de novo pathway of Pur synthesis, as such synthesis may be required in the rat to replace the net loss of ATP associated with catecholamine secretion. Factors controlling PPRibP synthetase and their potential relative importance in the adrenal gland have been considered.

Adrenal Glands↗

PubMed2000

Adrenal function in Angora goats: a comparative study of adrenal steroidogenesis in Angora goats, Boer goats, and Merino sheep.

South African Angora goats (Capra aegagrus) are susceptible to stress conditions, possibly due to adrenal cortex malfunction. Selection for mohair production may reduce adrenal function and decrease cortisol production. Secretion of cortisol by the adrenal cortex is essential for the induction of several gluconeogenic enzymes that enable animals to survive stressful conditions, and adrenocortical insufficiency, therefore, precipitates a vulnerability to stress. In this study, Angora goats were compared with two breeds generally accepted as hardy, Boer goats (Capra hircus) and Merino sheep (Ovis aries). Adrenal steroidogenesis was studied using subcellular fractions prepared from the adrenal glands of freshly slaughtered animals. Adrenal microsomes and mitochondria were incubated with the relevant steroid substrates, and products were analyzed and quantified with TLC, HPLC, or RIA. Subsequently, the activity of individual enzymes involved in this pathway were further investigated. The cytochrome P450 content in the preparations was also compared. The results from these studies indicated that the activity of the cytochrome P450c17 enzyme in Angora goats differed (P < .01) from that of the other species investigated. This difference may contribute to the cause of the observed hypoadrenocorticism in Angora goats.

Adrenal Glands↗

PubMed1980

Cellular and humoral hypersensitivity to adrenal antigen in experimental adrenalitis.

A role for specific cellular, as well as humoral immunity has been suggested in experimental adrenalitis. This study was performed to seek a correlation between cellular and humoral immunity in experimental adrenalitis of the guinea pig. 34 guinea pigs (GP) were arranged into 4 experimental groups. One group (11 GP) was immunized with a single injection of 250 mg homologous adrenal antigen (HAA) in complete Freund's adjuvant (CFA). A second group (6 GP) was similarly immunized at 1 and 14 days. A third group (9 GP) received 3 such injections at 1, 14, and 21 days. The fourth group (8 control GP) received RPMI-1640 in CFA. The following were performed on all groups 10 days after the last injection: lymphocyte response to PHA and HAA; HAA-specific macrophage migration inhibition (MIF); antibody titers to HAA by hemagglutination; and histopathology of adrenal, thyroid and testis. Antibody titers reached a mean level of 500 in each of the 3 HAA-immunized groups. In the single injection group, MIF activity and response to PHA were significantly increased when compared to the other immunized groups and to controls. Histopathologic changes were seen in adrenal glands of all immunized groups, but were most remarkable in the single injection group. Progressively fewer changes were observed in double and triple immunized groups. Antibody titers and histological changes were not found in controls. Histopathology correlated better with cell-mediated immune parameters than with specific antibody titers; this suggests that cell-mediated mechanisms may be the more important factor in pathologic lesions of experimental adrenalitis.

Adrenal Glands↗

PubMed2000

Prognostic value of immunohistochemical expression of topoisomerase alpha II, MIB-1, p53, E-cadherin, retinoblastoma gene protein product, and HER-2/neu in adrenal and extra-adrenal pheochromocytomas.

No reliable pathologic criteria have been identified that predict clinical behavior in adrenal and extra-adrenal pheochromocytomas (PHEOs). Reliable prognostic markers for the prediction of clinical outcome are needed to assign optimal treatment for potentially malignant tumors. In this report, we evaluated several molecular markers (topoisomerase II alpha, E-cadherin, HER-2/neu, and retinoblastoma (RB) gene protein) that have not been previously studied in PHEOs. Paraffin-embedded, formalin-fixed tissue blocks from 50 cases of PHEO (30 benign and 20 malignant, 31 adrenal and 19 extra-adrenal) were obtained from University of Utah Health Sciences Center, Salt Lake City, and the Medical College of Wisconsin, Milwaukee. Gross (tumor size, weight, local extension, cyst formation, hemorrhage, necrosis), microscopic (pleomorphism, hyaline globules, intranuclear inclusion, mitotic count, capsular and vascular invasion, ganglionic/neuronal differentiation), and immunohistochemical features (topoisomerase II alpha, p53, MIB-1, E-cadherin, RB, and HER-2/neu) were studied. With the exception of vascular invasion (P = 0.025), there were no unequivocal gross or microscopic characteristics that distinguished benign from malignant lesions (P approximately = 0.11-0.71). Topoisomerase III and MIB-1 indices in malignant lesions were significantly higher than those observed in benign lesions (P = 0.012 and 0.019). Differences in p53 expression were not statistically significant (P = 0.082). Loss in RB protein product expression was significantly more common in malignant lesions (P = 0.001), E-cadherin loss and HER-2/-neu overexpression were not observed in any of the benign or malignant lesions. We studied the immunohistochemical expression of topoisomerase II alpha, MIB-1, p53, RB gene protein product, E-cadherin, and HER-2/neu in a series of adrenal and extra-adrenal PHEOs. Overexpression of topoisomerase II alpha and MIB-1 and loss of RB protein product were more common in malignant lesions, whereas p53, E-cadherin, and HER-2/neu do not seem to have diagnostic utility in the prediction of biologic behavior in these neoplasms.

Adolescent↗

PubMed2003

Primary adrenal lymphoma manifestating as adrenal incidentaloma.

Although involvement of the adrenals by malignant lymphoma is common, primary adrenal lymphoma is extremely rare. Herein, we report a case of a 59-year-old woman with bilateral adrenal glands enlargement found incidentally on abdominal imaging. Despite of the huge size of the tumor, her adrenal function was intact. Ultrasound-guided biopsy disclosed a picture of malignant lymphoma, diffuse large B cell type. The patient received bilateral adrenalectomy and adjuvant chemotherapy, but succumbed 6 months later. We suggest that, although rare, primary adrenal lymphoma should be considered as a possible cause of bilateral adrenal incidentalomas.

Adrenal Gland Neoplasms↗

PubMedDate not supplied

Role and cost-effectiveness of adrenal imaging and image-guided FNA cytology in the management of incidentally discovered adrenal tumours.

Incidentally discovered adrenal masses (incidentalomas) are relatively frequent and unsuspected incidentalomas (AI) of more than 1 cm in size may be found in 1-5% of patients who have undergone abdominal or chest computed tomography (CT)-scan for unrelated reasons. Once an AI is detected, the two major questions are whether the patient has biochemical evidence of adrenal hyperfunction, and whether the mass is an adrenal metastasis or a malignant adrenal tumour. In most cases (>90%) AI are non-functioning, with a low (<10%) risk of being malignant, and an estimated cumulative risk of malignant transformation of less than 1:1000. However, all patients with non-functioning AI usually undergo several imaging studies, but the impact of imaging techniques and image-guided fine-needle aspiration cytology (FNAC) on the cost-effectiveness in the management of patients is not well established. A single test for disease probabilities is not always more cost-effective than two-test approaches and it has been shown that the cumulative sensitivity and accuracy of both FNAC + magnetic resonance imaging (MRI) and FNAC + norcholesterol adrenal scintigraphy reach 100%, at a similar cost-to-accuracy ratio (7.5 vs. 7.0), whilst the strategy CT-scan + MRI together is less sensitive at a lower cost-to-accuracy ratio. In conclusion, the significance of AI, as well as the optimal management approach to treatment, is still under discussion. However, image-guided FNAC in conjunction with MRI as the exclusive imaging test has the major role and cost-effectiveness in the management of patients with AL, and should be considered the strategy of choice in distinguishing between benign and malignant non-functioning adrenal masses of more than 2 cm in diameter.

Adrenal Gland Neoplasms↗

PubMed1990

Rat insulin-like growth factor-I and -II mRNAs are unchanged during compensatory adrenal growth but decrease during ACTH-induced adrenal growth.

The insulin-like growth factors (IGFs) may be important autocrine and paracrine mediators of organ growth. We used solution-hybridization/ribonuclease protection assays to examine IGF-I and IGF-II mRNA abundance during hypertrophy or the rat adrenal gland induced by unilateral adrenalectomy or by adrenocorticotropic hormone (ACTH) infusion. Adrenal IGF-I mRNA did not change during the period of rapid organ growth at 18 or 66 h after unilateral adrenalectomy. ACTH infusion induced a time- and dose-dependent decrease in adrenal IGF-I mRNA despite significant increases in gland size. IGF-II mRNA also remained unchanged after unilateral adrenalectomy and decreased after ACTH infusion, to a greater extent than IGF-I mRNA. Liver IGF-I mRNA did not change with ACTH exposure, indicating an effect specific to the adrenal. We also measured adrenal P450scc mRNA as a marker of steroidogenic capacity. P450scc mRNA was unchanged after unilateral adrenalectomy and increased with ACTH infusion. Thus IGF-I and IGF-II mRNAs respond in parallel, but in different fashions with different stimuli for adrenal growth. The decrease in IGF mRNA after exposure to ACTH may be a factor in the ACTH-induced inhibition of compensatory hypertrophy after unilateral adrenalectomy.

Adrenal Glands↗

PubMed1986

Characterization of the molecular forms of proenkephalin in bovine adrenal medulla and rat adrenal, brain, and spinal cord with a site-directed antiserum.

An antiserum was generated against a synthetic peptide corresponding to amino acids 95-117 of bovine proenkephalin, and a sensitive radioimmunoassay was developed. Comparison of the reactivities of the synthetic peptide, its specific cleavage products, and other synthetic peptides showed that the important immunological determinant was contained within residues 101-109 of bovine proenkephalin (-Gly-Gly-Glu-Val-Leu-Gly-Lys-Arg-Tyr-). Radioimmunoassay of fractions after gel filtration of bovine adrenal medullary chromaffin granule lysate showed three pools of immunoreactivity: pool 1 (Mr 20,000-30,000), pool 2 (Mr 10,000-20,000), and pool 3 (Mr approximately 5,000). Further characterization by sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by immunoblotting showed that the antiserum recognized 27-, 20.5-, 16.5-, and 5.6-kilodalton enkephalin-containing proteins. The radioimmunoassay was also used to detect proenkephalin-like material in extracts of rat adrenal and regions of rat brain and spinal cord following gel filtration. Immunoreactivity from the rat adrenal chromatographed predominantly as high molecular weight material (Mr 31,500-43,500), whereas material in regions of rat brain showed a broader molecular weight distribution (Mr 4,000-43,500). This indicated differences in the processing of proenkephalin between rat adrenal and brain tissue. Differences were also seen in the molecular weight profile of immunoreactivity in different brain regions, most noticeable in the case of striatum and hypothalamus, suggesting regional differences in processing. Based on quantitation of higher molecular weight immunoreactive proenkephalin-like material and free Met-enkephalin immunoreactivity in different brain regions, it was apparent that extensive processing of proenkephalin occurs in brain. We concluded that antisera against proenkephalin-(95-117) recognize a wide range of intermediates in the processing of proenkephalin in both bovine adrenal medulla and rat adrenal, brain, and spinal cord, making it a useful tool for further studies concerned with the expression and post-translational processing of proenkephalin.

Adrenal Medulla↗

PubMed1999

Adrenal insufficiency caused by primary aggressive non-Hodgkin's lymphoma of bilateral adrenal glands: report of a case and literature review.

A 64-year-old woman was hospitalized because of poor general condition, gastrointestinal upset, unexplained fever, electrolyte imbalances, and an incidental finding of bilateral huge adrenal masses on computerized tomography (CT) of the abdomen. Non-Hodgkin's lymphoma (NHL) of B-cell origin was proven by ultrasound-guided aspiration biopsy of the left adrenal gland. Meanwhile, primary adrenal insufficiency was confirmed by her low serum cortisol level, high ACTH level, and inadequate adrenal response to the rapid ACTH stimulation test. The diagnosis of primary adrenal NHL was supported by detailed physical examinations, bone marrow examination, and such imaging studies as CT scan and sonography. She received three courses of chemotherapy with cyclophosphamide, vincristine, and prednisolone and there was an initial transient response, but she died of sepsis and progression of NHL three and a half months later.

Adrenal Gland Neoplasms↗