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PubMed1987

Pancreatic acinar cell amylase gene expression: selective effects of adrenalectomy and corticosterone replacement.

To examine the role of glucocorticoids in the regulation of the acinar pancreas, adult male rats were adrenalectomized (Adx) and replaced with no corticosterone (B), normal B, or high B. Plasma B concentration, body weight gain, and thymus weight were used as independent measures of treatment efficacy. Compared to controls, Adx animals had a 75 +/- 0.5% (n = 30) reduction in pancreatic amylase content; a 50% decrease occurred within 1 day and the maximal 75% decrease was observed after 5 days. In Adx animals, amylase content was normalized by normal B replacement and was increased to 235 +/- 39% (n = 30) of control by high B replacement. Furthermore, in all Adx rats, pancreatic content of amylase and plasma B concentration was significantly correlated (r = 0.81, n = 30). The effect of adrenalectomy was selective for amylase; contents of ribonuclease, chymotrypsin, and elastase were not altered. However, the effects of high B replacement were not selective, and increased the content of all digestive enzymes. To determine whether the changes in enzyme content were associated with changes in messenger RNA (mRNA), pancreatic RNA was probed with 32P-labeled complementary DNAs for amylase, ribonuclease, and chymotrypsin. After adrenalectomy and B replacement there was a significant correlation only between amylase mRNA (r = 0.87, n = 13) and plasma B concentration. These data indicate that physiological levels of B have a selective effect on pancreatic amylase gene expression. In contrast, high levels of B have the separate, nonselective effect of increasing the content of all digestive enzymes without increasing corresponding mRNA levels.

Adrenalectomy↗
PubMed1975

Modification of stress-induced prolactin release by dexamethasone or adrenalectomy.

A study was conducted to determine the influence of conditions known to alter ACTH secretion on prolactin release by the pituitary. Dexamethasone or 0.9% NaCl was injected subcutaneously into intact male rats 4 hr before a 2-min ether stress. Other rats were submitted to the ether stress 2 weeks following adrenalectomy. Five min following exposure to the ether stress, the rats were decapitated and trunk blood was collected. Dexamethasone (31, 125 or 500 mug/kg) blocked the stress-induced prolactin release in a dosage dependent manner with the highest dose decreasing plasma prolactin to levels similar to those observed in rats not exposed to the ether stress. Conversely, adrenalectomy was found to potentiate prolactin release due to ether stress. The results indicate that the adrenal may play a regulatory role in stress-induced prolactin release. The are also consistent with the suggestion that a common pathway or mechanism may be involved in pituitary release.

Adrenal Glands↗
PubMed1996

Adrenocorticotropin secretion by fetal sheep anterior and intermediate lobe pituitary cells in vitro: effects of gestation and adrenalectomy.

Immunoreactive (ir) ACTH is present in the fetal sheep intermediate lobe (IL) as well as the anterior pituitary (AP). It is not clear whether fetal IL cells can secrete irACTH and if gestational age and glucocorticoids influence the secretion of ACTH from these tissues in a similar fashion. Therefore, we examined the control of irACTH secretion by IL cells, whether the responsiveness of AP and IL cells to arginine vasopressin (AVP) and CRH changes during gestation, and whether withdrawal of adrenal steroids by adrenalectomy influences AP and IL responses. Cultured pituitary cells were studied from intact fetuses at an immature (n = 5; 108 +/- 5 days) and a mature (n = 8; 139 +/- 0 days) stage, from mature fetuses 3 weeks after bilateral adrenalectomy (n = 6), and from neonatal lambs within 16 h of birth (n = 6). Secretion of irACTH was determined by RIA of incubation medium obtained during 3-h exposure of cells to vehicle, AVP, CRH, or both. In all cases, IL cells secreted measurable irACTH. The IL cells of immature fetuses responded to CRH (133 +/- 8% increase over basal secretion), AVP (52 +/- 6%), and CRH plus AVP (244 +/- 8%). In contrast, IL cells from mature fetuses responded only to CRH (160 +/- 20%) or CRH plus AVP (259 +/- 44%), as did cells from mature adrenalectomized fetuses (CRH, 356 +/- 70%; CRH plus AVP, 627 +/- 100%). Secretion from neonatal IL cells was not significantly increased above basal rates by CRH and/or AVP. The AP cells from immature fetuses responded significantly to CRH (406 +/- 16%), AVP (114 +/- 8%), and CRH plus AVP (559 +/- 38%), whereas cells from mature fetuses responded only to AVP (249 +/- 40%) or to CRH plus AVP (570 +/- 146%). In AP cells from mature adrenalectomized fetuses, the response pattern resembled that of immature intact fetal sheep (CRH, 429 +/- 76%; AVP, 146 +/- 15%; CRH plus AVP, 541 +/- 94%). Neonatal AP cells responded to CRH (196 +/- 25%), AVP (442 +/- 71%), and CRH plus AVP (646 +/- 93%). Further characterization of IL cells (n = 6 fetal and 2 neonatal) indicated that they were inhibited by dopamine (basal ACTH secretion decreased by 25 +/- 4%; ACTH secretory response to CRH decreased by 32 +/- 10%). These results show that fetal neurointermediate lobe cells secrete irACTH under basal and stimulated conditions. Moreover, the pattern of response of AP and neurointermediate lobe cells to secretagogues is influenced by gestational age and, possibly, cortisol.

Adrenalectomy↗
PubMed1997

Adrenalectomy after weaning restores beta3-adrenergic receptor expression in white adipocytes from C57BL/6J-ob/ob mice.

The role of hypercorticism in the development of compromised beta-adrenergic signaling in adipose tissue was assessed in ob/ob mice adrenalectomized at 4 weeks of age and studied 1 and 3 weeks thereafter. Adrenalectomy prevented the rapid increase in body weight and fat deposition between 4 and 5 weeks of age in ob/ob mice and produced a phenotype indistinguishable from that of lean mice. However, adrenalectomized ob/ob mice became intermediate between lean and ob/ob mice by 7 weeks of age. Adipocyte beta3-adrenergic receptor (AR) messenger RNA levels were similar between lean and adrenalectomized ob/ob mice at both time points and were 4- to 8-fold higher than messenger RNA levels in ob/ob mice. As judged by maximal activation of adenylyl cyclase by a beta3-AR-selective agonist, adrenalectomy also restored functional activity of the beta3-AR to levels above or equivalent to those seen in lean mice at both time points. The present results suggest that development of hypercorticism at or before weaning in ob/ob mice represses expression of the beta3-AR and prevents the normal postweaning development of this signaling system in the adipocyte.

Adipocytes↗
PubMed1998

Regulation of pituitary corticotropin-releasing hormone-binding protein messenger ribonucleic acid levels by restraint stress and adrenalectomy.

CRH is the primary hypothalamic regulator of the stress response in higher organisms, where it acts as the key mediator of ACTH release in the hypothalamus-pituitary-adrenal axis. The 37-kDa CRH-binding protein (CRH-BP) is known to bind CRH and antagonize CRH-induced ACTH release in vitro. The expression of this protein in anterior pituitary corticotrophs suggests a role for CRH-BP in modulation of the stress response. To investigate the in vivo role of rat CRH-BP, the regulation of pituitary CRH-BP gene expression by acute restraint stress and/or adrenalectomy was examined using ribonuclease protection assays. After restraint stress, steady-state levels of CRH-BP transcripts increase two to three times over basal level and remain significantly higher than basal levels for 120 min after the start of restraint. Adrenalectomy decreases CRH-BP messenger RNA steady-state levels to 8% of control levels. These results demonstrate that pituitary CRH-BP messenger RNA levels are increased in response to acute restraint stress and that glucocorticoids play a significant role in this positive regulation. These data also suggest that increased CRH-BP levels, in response to stress, may modulate the endocrine stress response by providing an additional feedback mechanism to maintain homeostasis of the hypothalamus-pituitary-adrenal axis.

Adrenalectomy↗
PubMed2003

Improvement of insulin sensitivity after adrenalectomy in patients with pheochromocytoma.

OBJECTIVE: Decreased insulin secretion is considered to be the main cause for pheochromocytoma-associated diabetes mellitus. Data from animal and evidence from clinical studies suggest that catecholamines can induce insulin resistance. However, there is no study investigating the effect of catecholamine excess on insulin resistance in patients with pheochromocytopma by the euglycemic hyperinsulinaemic clamp technique. RESEARCH DESIGN AND METHODS: We characterized the effect of high catecholamine plasma concentrations on glucose metabolism and insulin resistance. Euglycemic hyperinsulinemic clamps were performed in 10 patients with pheochromocytoma with and without diabetes mellitus before and 5 wk after adrenalectomy. RESULTS: In five patients with diabetes mellitus, glucose infusion rate required to maintain euglycemia during the clamp (mean +/- SEM) significantly improved from 27.5 +/- 6.5 micro mol/kg.min before surgery to 44.6 +/- 12.3 micro mol/kg.min 5 wk after adrenalectomy (P < 0.05). In five individuals without diabetes, total glucose disposal improved from 105 +/- 13.6 to 130 +/- 11.2 (P < 0.05). Improved insulin sensitivity after surgery was confirmed by a decrease of fasting hyperinsulinemia from 210 +/- 74 pmol/liter (diabetes mellitus) and 69 +/- 9 pmol/liter (no diabetes) before to 134 +/- 56 pmol/liter and 54 +/- 8 after surgery respectively (P < 0.01). In three patients, diabetes and hyperinsulinemia were reversed by the surgical removal of the pheochromocytoma. CONCLUSION: Our data provide evidence that endogenous catecholamine excess in patients with pheochromocytoma can induce or aggravate insulin resistance both in patients with type 2 diabetes and patients with normal glucose tolerance.

Adrenal Gland Neoplasms↗
PubMed1980

Complete remission of Cushing's disease by total bilateral adrenalectomy and adrenal autotransplantation.

A 15-yr-old girl was diagnosed as suffering from Cushing's disease. She was treated by bilateral adrenalectomy and autotransplantation of one third of each adrenal to the corresponding thigh. The adrenal that was embedded in the right satorius muscle started functioning after about 1 yr, as proven by significant differences in cortisol levels in both femoral veins (82.5 and 17.5 micrograms/100 ml). 19-[131I]Cholesterol scanning showed adrenal tissue in the right thigh, while no adrenal remnant was demonstrated. Eleven years after surgery, the patient is symptom free and does not require replacement therapy. We find that adrenal autotransplantation, which is a simple and nonrisky procedure, should be considered whenever bilateral adrenalectomy is chosen as a treatment for Cushing's disease.

17-Ketosteroids↗
PubMed1997

Prophylactic adrenalectomy of a three-year-old girl with congenital adrenal hyperplasia: pre- and postoperative studies.

Long term follow-up studies of children with congenital adrenal hyperplasia have documented less than desirable outcomes, including reduction in final adult height, obesity, virilism, and decreased fertility. We have proposed that children with the most severe forms of congenital adrenal hyperplasia would be better off if their adrenals were removed at an early age. We report here on our experience with prophylactic bilateral adrenalectomy in a 3-yr-old girl with a double null mutation of the CYP21 gene. The results of sodium balance studies, performed preoperatively on our patient and her unaffected fraternal twin sister, and hormonal data are presented as well. In contrast to her twin, who markedly increased her sodium retention in response to ACTH, our patient showed increased natriuresis, suggesting a deleterious effect of her adrenals on sodium homeostasis. Adrenalectomy was carried out at the time of necessary genital repair. No surgical or postsurgical complications were encountered.

17-alpha-Hydroxyprogesterone↗
PubMed2000

Bilateral laparoscopic adrenalectomy for congenital adrenal hyperplasia with severe hypertension, resulting from two novel mutations in splice donor sites of CYP11B1.

We present an in vivo and in vitro study of congenital adrenal hyperplasia in a patient with 11beta-hydroxylase deficiency. Sequencing of the CYP11B1 gene showed two new base substitutions, a conservative 954 G-->C transversion at the last base of exon 5 (T318T), and a IVS8 + 4A-->G transition in intron 8. In addition, two polymorphisms were found in exons 1 and 2. The genetically female patient was raised as a male because of severe pseudohermaphroditism. Glucocorticoid-suppressive treatment encountered difficulties in equilibration and compliance, resulting in uncontrolled hypertension with pronounced hypertrophic cardiomyopathy. At 42 yr of age the occurrence of central retinal vein occlusion with permanent loss of left eye vision led to the decision to perform bilateral laparoscopic adrenalectomy. Surgery was followed by normalization of blood pressure and good compliance with glucocorticoid and androgen substitutive therapies. In vitro, adrenal cells in culture and isolated mitochondria showed extremely low 11beta-hydroxylase activity. Analysis of adrenal CYP11B1 messenger ribonucleic acid (mRNA) by RT-PCR and sequencing showed the expression of a shorter mRNA that lacked exon 8 and did not contain either the exon 5 mutation or the exon 1 and 2 polymorphisms. This suggested that one CYP11B1 allele carried the intron 8 mutation, responsible for skipping exon 8. The other allele carried the exon 5 mutation, and its mRNA was not detectable. Western blot analysis showed weak expression of a shorter CYP11B immunoreactive band of 43 kDa, consistent with truncation of exon 8. Thus, bilateral adrenalectomy in this patient allowed effective treatment of severe hypertension and helped in understanding the mechanisms and physiopathological consequences of two novel mutations of CYP11B1.

Adrenal Glands↗
PubMed2003

Effects of insulin and adrenalectomy on elevation of serum leptin levels induced by 5-hydroxytryptophan in mice.

We previously reported that a serotonin precursor 5-hydroxytryptophan (5-HTP) increases serum leptin levels in mice. In this study, we studied the effects of insulin and adrenalectomy on hyperleptinemia induced by 5-HTP. Co-administration of insulin significantly increased hyperleptinemia elicited by 5-HTP. 5-HTP itself increased serum insulin levels. Adrenalectomy, which depletes corticosterone, did not abolish hyperleptinemic effects of 5-HTP. These results suggest that insulin may participate in hyperleptinemic effects of 5-HTP and that the involvement of corticosterone in effects of 5-HTP may be probably small.

5-Hydroxytryptophan↗
PubMed1990

The acetylcholine-hypersensitive model of diabetic KK-CA(y) mice analyzed with pulse rate, and modified by repeated cold stress and by adrenalectomy.

The effects of acetylcholine on pulse rate were examined in the conscious state of diabetic KK-CA(y) male mice. By subcutaneously-administered acetylcholine at 3 and 10 mg/kg the pulse rate was increased in the prediabetic state, whereas it was decreased in the diabetic state. The acetylcholine-induced responses in pulse rate were significantly and multiply correlated with both the blood glucose level and the dose of acetylcholine in KK-CA(y) mice (r = 0.47, p less than 0.01). The diabetic state and adrenalectomy produced an acetylcholine-hypersensitive syndrome, respectively. The hypersensitivity to acetylcholine in a whole body of diabetic mice was attenuated by repeated cold stress producing acetylcholine-subsensitivity, and was enhanced by adrenalectomy. The diabetic KK-CA(y) mice are an acetylcholine-hypersensitive animal model.

Acetylcholine↗
PubMed1987

Effects of adrenalectomy and chronic guanethidine treatment on tissue adrenaline concentrations in swimming-exposed rats.

Adrenaline is known to increase in extra-adrenal peripheral organs as well as urine and plasma in the rat after swimming stress. In order to clarify the physiological significance of adrenaline in stress responses, the origin and location of adrenaline in the peripheral organs were examined by measuring adrenaline in the heart, spleen, submaxillary gland and some other organs after adrenalectomy or guanethidine treatment. After bilateral adrenalectomy, adrenaline in the peripheral organs mostly disappeared. Swimming stress caused no increase in the adrenaline content of the organs in the adrenalectomized rats, while a marked increase was observed in the sham-operated animals. In guanethidine-treated rats, the adrenaline content of the peripheral organs was extremely low as compared to that in the saline-treated animals, and the swimming-induced increase in adrenaline level in the organs was greatly suppressed. These observations suggest that the organ adrenaline, which exists in sympathetic nerve endings, is mostly derived from the adrenal gland. It is considered that adrenaline would be involved in sympathetic neurotransmission, especially under stressful conditions.

Adrenalectomy↗
PubMed2006

Laparoscopic left adrenalectomy during Roux-en-Y gastric bypass using a supragastric approach.

A 54-year-old female had a BMI of 44 kg/m(2), biliary colic, gastro-eophageal reflux disease, joint pain, hyperlipidemia, and diabetes type 2. Her medical history included complete remission of non-Hodgkin's lymphoma and prolactinoma since 1999. An abdominal CT scan demonstrated an incidental left adrenal tumor, which had increased in diameter from 2 cm to 3 cm in 6 months. A laparoscopic Roux-en-Y gastric bypass with ultrasonography and supragastric left adrenalectomy were performed successfully. Combined surgical procedures appear to be suitable for treatment of coexisting abdominal pathologic findings with minimally invasive surgery. A supragastric approach should be considered when planning a simultaneous gastric bypass and left adrenalectomy.

Adenoma↗
PubMed2001

Adrenalectomy regulates apoptotic-associated genes in rat hippocampus.

Morphological studies of granular neurons of the hippocampus have shown that adrenalectomy (ADX) induces the cell death of granular neurons, an effect prevented by corticosterone replacement. We addressed the hypothesis that corticosterone regulates the expression of the apoptotic bcl-2 gene family. Five days after adrenalectomy, we observed morphological changes related to hippocampal granule cell apoptosis that was accompanied by terminal dUTP nick and labeling (TUNEL) labeling in nuclei located in the hilus region. Corticosterone replacement prevented the cell death induced by ADX. Using RT-PCR we found a reduction in mRNA levels of the antiapoptotic gene bcl-2 in whole hippocampus, an effect which was prevented by corticosterone administration to ADX rats. However, Bcl-2 protein levels were not altered by this treatment. We did not observe modifications in the level of bcl-X(L) mRNA however, we did find a 40% reduction in Bcl-X(L) protein levels, an effect not reversed by corticosterone. In contrast, we found a reduction in the mRNA of the antiapoptotic gene bax and Bax levels after ADX; both effects were prevented by corticosterone. The reduction in proapoptotic bax and in antiapoptotic bcl-2 mRNA levels in the whole hippocampus, suggests that local variations in these molecules could account for both neuronal viability of the CA1-CA3 and granular cell death detected by morphological means and observed after ADX.

Adrenalectomy↗
PubMed1994

Adrenal autotransplantation after total adrenalectomy: delayed determined function.

Adrenal autotransplantation after bilateral total adrenalectomy has been utilized to eliminate the need for replacement therapy and to prevent the late occurrence of Nelson's syndrome in some patients with Cushing's disease. It is possible to follow these cases up closely today, owing to the highly developed hormonal evaluation and imaging techniques. In this study, two patients who underwent bilateral total adrenalectomy and cortex autotransplantation are presented. The autografts were found functional and the patients had not required any steroid replacement therapy.

Adrenal Cortex↗
PubMed2002

Twenty-four hour 17-hydroxyprogesterone response to adrenocorticotropine in adrenal incidentalomas: augmented response after adrenalectomy in two patients.

The current study aimed to investigate the midterm (24 hour) response of 17-hydroxyprogesterone (17-OHP) and dehydroepiandrosterone sulphate (DHEA-S) to synthetic high-dose adrenocorticotropin (ACTH) in adrenal incidentalomas (Al). Seventeen patients with Al and 40 age- and sex-matched controls received synthetic ACTH (tetracosactide, 1000 microg, IM). Plasma, 17-OHP and DHEA-S were collected in basal conditions and after 1, 4, 6, 8 and 24 hours. (HPA) axis was also evaluated using circadian serum cortisol, urinary free cortisol and over-night 2 mg dexamethasone suppression. Basal plasma 17-OHP levels did not differ among the groups. However, the increment in plasma 17-OHP in patients both in terms of peak [13.76 +/- 2.52, 4.77 +/- 0.30ng/ml, mean +/- S.E.M, p < 0.001] and area under the curve [190 +/- 46, 96.75 +/- 32 ng/ml/h, p < 0.001] were significantly higher than that of the controls. Stimulated 17OH-P levels never reached 9.1 ng/ml in controls. Sixty-five (11/17) % of the patients were found to have exaggerated response. Three of the patients were found to have subclinical Cushing's syndrome and interestingly, two augmented their 17-OHP response to ACTH after unilateral adrenalectomy and normalisation of their HPA axis. Basal DHEA-S levels of the patients were significantly lower [99.21 +/- 45, 230.18 +/- 34 microg/dl, p < 0.01] and stayed persistently lower than that of the controls. Evidence of a heterozygous 21 hydroxylase deficiency, as indicated by the exaggerated 17-OHP response to ACTH, has been widely reported in Al patients. However, to our knowledge to date there is no report on augmented 17-OHP response to ACTH after adrenalectomy. Possible reasons for the augmentation were discussed.

17-alpha-Hydroxyprogesterone↗
PubMed1975

Effects of ACTH, dexamethasone, adrenalectomy and stress on cAMP content of adenohypophysis and adrenals in rats.

The effects of adrenalectomy, ether-laparotomy stress and in vivo administration of either ACTH or dexamethasone on the cAMP levels in the anterior pituitary and the adrenal glands were investigated in male rats. After adrenalectomy or ether-laparotomy stress, an increase of the pituitary cAMP levels was observed. A prior administration of dexamethasone failed to inhibit the increase of the pituitary cAMP levels. Acute administration of dexamethasone increased the cAMP levels in the pituitary. Chronic administration of dexamethasone decreased the cAMP levels in the pituitary, but ACTH did not. These data suggest that cAMP might be involved in the mediation of the hypothalamo-pituitary-adrenal axis.

Adrenal Glands↗
PubMed1992

Adrenalectomy enhances the susceptibility of pancreatic islets to interleukin-1 beta: immunohistochemical study.

To determine the importance of adrenal steroid in the effects of interleukin-1, we investigated changes in the number of islet cells reactive toward antiserum to insulin (anti-Ins) by intraperitoneal administration of recombinant human interleukin-1 beta (IL-1) in intact and adrenalectomized (ADX) rats. IL-1 significantly reduced serum insulin levels in ADX rats only, while it similarly decreased plasma glucose levels. In intact rats, IL-1 did not affect the number of islet cells reactive to anti-Ins, although cytoplasmic immunostaining tended to be reduced by IL-1 treatment. Only adrenalectomy decreased the number of islet cells immunostained by anti-Ins. Furthermore, IL-1 treatment significantly reduced the number of islet cells reactive to anti-Ins in ADX rats. The present study immunohistochemically supported our working hypothesis that the withdrawal of adrenal steroids by adrenalectomy enhances the islet cell sensitivity to exogenous administration of IL-1.

Adrenal Glands↗