Relevant bibliographies by topics / Adrenal medulla – Metabolism

Academic literature on the topic 'Adrenal medulla – Metabolism'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Adrenal medulla – Metabolism"

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Macdonald, I. A., T. Bennett, and I. W. Fellows. "Catecholamines and the control of metabolism in man." Clinical Science 68, no. 6 (June 1, 1985): 613–19. http://dx.doi.org/10.1042/cs0680613.

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Introduction: The physiological effects of catecholamines can result from a combination of increased activity of the sympathetic nervous system and secretion from the adrenal medulla. However, studies in the rat have revealed circumstances in which adrenal medullary secretion can occur at a time when the activity of the sympathetic nervous system is suppressed [1]; furthermore, in the lamb there may be variations in the relative amounts of noradrenaline and adrenaline secreted from the adrenal medulla [2]. It is not known whether such phenomena occur in man.
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Coulter, C. L., H. M. Mulvogue, I. R. Young, C. A. Browne, and I. C. McMillen. "Effect of fetal hypophysectomy on the localization of the catecholamine biosynthetic enzymes and enkephalins in the adrenal medulla of the fetal sheep." Journal of Endocrinology 121, no. 3 (June 1989): 425—NP. http://dx.doi.org/10.1677/joe.0.1210425.

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ABSTRACT We have investigated the effect of fetal hypophysectomy on the localization of dopamine B-hydroxylase (DBH), phenylethanolamine N-methyltransferase (PNMT) and enkephalin-containing peptides in the fetal sheep adrenal, using immunocytochemical techniques. Staining with anti-DBH was observed throughout the adrenal medulla in the intact (140–146 days of gestation) and hypophysectomized fetal sheep (147–164 days of gestation) and the newborn lamb (10–12 days after birth). In the adrenal medulla of the lategestation intact fetal sheep and newborn lamb, positive staining with anti-PNMT was observed in the peripheral rim of medullary cells adjacent to the adrenal cortex. After hypophysectomy, there was intense positive staining with anti-PNMT in the peripheral adrenal medullary cells and a small and variable proportion of central adrenal medullary cells were stained with anti-PNMT. In the adrenal gland of the intact fetal sheep and the newborn lamb, there was intense staining with anti-enkephalin in the peripheral rim of adrenal medullary cells. Staining with antienkephalin was less intense in the central medullary cells of the adrenal gland of the intact fetal sheep and the 10- to 12-day-old newborn lamb, and many unstained central medullary cells were present. After hypophysectomy, intense positive staining with antienkephalin was observed throughout the entire fetal adrenal medulla. Therefore, the fetal pituitary, either directly or indirectly through the adrenal cortex, plays a role in regulating the pattern of localization of both PNMT and enkephalin in the fetal sheep adrenal. Journal of Endocrinology (1989) 121, 425–430
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Liu, J., AI Kahri, P. Heikkila, and R. Voutilainen. "Adrenomedullin gene expression and its different regulation in human adrenocortical and medullary tumors." Journal of Endocrinology 155, no. 3 (December 1, 1997): 483–90. http://dx.doi.org/10.1677/joe.0.1550483.

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Adrenomedullin (ADM) is a polypeptide originally discovered in a human pheochromocytoma and is also present in normal adrenal medulla. It has been proposed that ADM could be involved in the regulation of adrenal steroidogenesis via paracrine mechanisms. Our aim was to find out if ADM gene is expressed in adrenocortical tumors and how ADM gene expression is regulated in adrenal cells. ADM mRNA was detectable by Northern blotting in most normal and hyperplastic adrenals, adenomas and carcinomas. The average concentration of ADM mRNA in the hormonally active adrenocortical adenomas was about 80% and 7% of that in normal adrenal glands and separated adrenal medulla respectively. In adrenocortical carcinomas, the ADM mRNA concentration was very variable, but on average it was about six times greater than that in normal adrenal glands. In pheochromocytomas, ADM mRNA expression was about ten times greater than that in normal adrenals and three times greater than in separated adrenal medulla. In primary cultures of normal adrenal cells, a protein kinase C inhibitor, staurosporine, reduced ADM mRNA accumulation in a dose- and time-dependent fashion (P < 0.01), whereas it simultaneously increased the expression of human cholesterol side-chain cleavage enzyme (P450 scc) gene (a key gene in steroidogenesis). In cultured Cushing's adenoma cells, adrenocorticotropin, dibutyryl cAMP ((Bu)2cAMP) and staurosporine inhibited the accumulation of ADM mRNA by 40, 50 and 70% respectively (P < 0.05), whereas the protein kinase C activator, 12-O-tetradecanoyl phorbol 13-acetate (TPA), increased it by 50% (P < 0.05). In primary cultures of pheochromocytoma cells, treatment with (Bu)2cAMP for 1 and 3 days increased ADM mRNA accumulation two- to threefold (P < 0.05). Our results show that ADM mRNA is present not only in adrenal medulla and pheochromocytomas, but also in adrenocortical neoplasms. Both protein kinase A- and C-dependent mechanisms regulate ADM mRNA expression in adrenocortical and pheochromocytoma cells supporting the suggested role for ADM as an autocrine or paracrine (or both) regulator of adrenal function.
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Chabot, J. G., P. Walker, and G. Pelletier. "Distribution of epidermal growth factor binding sites in the adult rat adrenal gland by light microscope autoradiography." Acta Endocrinologica 113, no. 3 (November 1986): 391–95. http://dx.doi.org/10.1530/acta.0.1130391.

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Abstract. The distribution of epidermal growth factor (EGF) receptors was studied in the adrenal gland using light microscope autoradiography which was carried out 2 min after intravenous (iv) injection of [125I]EGF into adult rat. At the light microscope level, the labelling was found over the cells of the capsule and adrenal medullary chromaffin cells. No specific labelling of the steroid-secreting cells was observed. Control experiments indicated that the autoradiography reaction was due to specific interaction of [125I]EGF with its receptor. These results clearly indicate that EGF receptors are present in the majority of the adrenal medulla cells. They suggest that EGF may exert a physiological role in the regulation of rat adrenal medulla.
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Liu, J., R. Voutilainen, A. I. Kahri, and P. Heikkilä. "Expression patterns of the c-myc gene in adrenocortical tumors and pheochromocytomas." Journal of Endocrinology 152, no. 2 (February 1997): 175–81. http://dx.doi.org/10.1677/joe.0.1520175.

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Abstract Abundant c-myc gene expression in neoplasms has been often linked to poor prognosis. As c-myc mRNA is expressed and hormonally regulated in human adrenals, we examined the c-myc gene expression in adrenal tumors by RNA analysis and immunohistochemistry to find out the possible role of c-myc in adrenal neoplasms. The abundant expression of the c-myc gene in normal adrenals was localized to the zona fasciculata and zona reticularis, with much lower expression in the zona glomerulosa and adrenal medulla. In hormonally active adrenocortical carcinomas (n=6) and in virilizing adenomas (n=4), c-myc mRNA levels were approximately 10% of those in normal adrenals (n=11). In contrast, adrenal adenomas from patients with Cushing's (n=4) and Conn's (n=9) syndrome, non-functional adenomas (n=2), adrenocortical hyperplasias (bilateral, n=5; nodular, n=4), and non-functional adrenocortical carcinomas (n=3) expressed c-myc mRNA to the same extent as normal adrenals. The c-myc mRNA abundance in benign adrenal pheochromocytomas (n=19) was similar to that in normal adrenal medulla. However, in malignant adrenal pheochromocytomas (n=6), the average c-myc mRNA levels were approximately threefold that in benign adrenal pheochromocytomas. There was a good correlation between c-myc mRNA expression and immunohistochemical reactivity in both normal and pathological adrenal tissues. Southern blot analysis revealed no amplification or rearrangement of the c-myc gene in any of the adrenal tumors. In conclusion, c-myc expression localized to zona fasciculata and reticularis in normal adrenals. Virilizing adenomas and hormonally active adrenocortical carcinomas expressed c-myc mRNA clearly less than the other adrenal neoplasms and normal adrenal tissue. On the other hand, malignant pheochromocytomas contained more c-myc mRNA than benign ones. Further studies are required to clarify the mechanisms and significance for the distinct expression pattern of the c-myc gene in different adrenal neoplasms. Journal of Endocrinology (1997) 152, 175–181
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Fukuda, Tsuyoshi, Kazuhiro Takahashi, Takashi Suzuki, Masayuki Saruta, Mika Watanabe, Taisuke Nakata, and Hironobu Sasano. "Urocortin 1, Urocortin 3/Stresscopin, and Corticotropin-Releasing Factor Receptors in Human Adrenal and Its Disorders." Journal of Clinical Endocrinology & Metabolism 90, no. 8 (August 1, 2005): 4671–78. http://dx.doi.org/10.1210/jc.2005-0090.

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Abstract Context: Urocortin 1 (Ucn1) and urocortin 3 (Ucn3)/stresscopin are new members of the corticotropin-releasing factor (CRF) neuropeptide family. Ucn1 binds to both CRF type 1 (CRF1) and type 2 receptors (CRF2), whereas Ucn3 is a specific agonist for CRF2. Recently, direct involvement of the locally synthesized CRF family in adrenocortical function has been proposed. Objective, Design, and Setting: We examined in situ expression of Ucn and CRF receptors in nonpathological human adrenal gland and its disorders using immunohistochemistry and mRNA in situ hybridization. Results: Ucn immunoreactivity was localized in the cortex and medulla of nonpathological adrenal glands. Ucn1 immunoreactivity was marked in the medulla, whereas Ucn3 was immunostained mostly in the cortex. Both CRF type 1 and CRF2 were expressed in the cortex, particularly in the zonae fasciculata and reticularis but very weakly or undetectably in the medulla. Immunohistochemistry in serial tissue sections with mirror images revealed that both Ucn3 and CRF2 were colocalized in more than 85% of the adrenocortical cells. mRNA in situ hybridization confirmed these findings above. In fetal adrenals, Ucn and CRF receptors were expressed in both fetal and definitive zones of the cortex. Ucn and CRF receptors were all expressed in the tumor cells of pheochromocytomas, adrenocortical adenomas, and carcinomas, but its positivity was less than that in nonpathological adrenal glands, suggesting that Ucn1, Ucn3, and CRF receptors were down-regulated in these adrenal neoplasms. Conclusions: Ucn1, Ucn3, and CRF receptors are all expressed in human adrenal cortex and medulla and may play important roles in physiological adrenal functions.
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McMillen, I. C., H. M. Mulvogue, C. L. Coulter, C. A. Browne, and P. R. C. Howe. "Ontogeny of catecholamine-synthesizing enzymes and enkephalins in the sheep adrenal medulla: an immunocytochemical study." Journal of Endocrinology 118, no. 2 (August 1988): 221—NP. http://dx.doi.org/10.1677/joe.0.1180221.

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ABSTRACT An immunocytochemical staining technique was used to investigate the development of the sheep adrenal medullary cells containing enkephalins and the catecholamine synthetic enzymes dopamine β-hydroxylase (DBH) and phenylethanolamine N-methyl transferase (PNMT). No staining was observed in the adrenocortical cells with any of the antisera used in this study. Positive staining with anti-DBH was observed throughout the medulla in both adult and fetal adrenal glands from 80 days of gestation. Positive staining with anti-PNMT was observed in all glands from as early as 80 days of gestation, and staining with this antiserum was mainly confined to the peripheral medullary cells, which were adjacent to, and interdigitated between, the cells of the adrenal cortex. In the fetus between 80 and 120 days of gestation, staining for the enkephalins was observed in both the peripheral columnar and the central polygonal adrenal medullary cells. After 125 days of gestation and in the adult ewe, the peripheral columnar cells were uniformly stained with anti-enkephalin whereas many unstained cells were present in the central medullary region. Therefore, enkephalin-containing peptides are present in the catecholamine cells of the fetal and adult sheep adrenal and there appears to be a changing pattern in the distribution of the enkephalins in the fetal adrenal in late gestation. J. Endocr. (1988) 118, 221–226
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8

Nussey, S. S., R. A. Prysor-Jones, A. Taylor, V. T. Y. Ang, and J. S. Jenkins. "Arginine vasopressin and oxytocin in the bovine adrenal gland." Journal of Endocrinology 115, no. 1 (October 1987): 141–49. http://dx.doi.org/10.1677/joe.0.1150141.

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ABSTRACT The concentrations of immunoreactive oxytocin and arginine vasopressin (AVP) and their respective neurophysins (NpI and NpII) were compared in bovine adrenal cortex and medulla. While the concentration of AVP was similar in both tissues there was more NpII in the medulla. The medulla also contained much more oxytocin and NpI than the cortex. The extracted AVP and oxytocin had identical retention times to those of the synthetic peptides on high-performance liquid chromatography (HPLC) and were biologically active in assays for antidiuretic and milk-ejection activity (with potencies of 310 units/mg and 340 units/mg respectively). Adrenal NpI and NpII behaved identically to commercially available neurohypophysial proteins on HPLC. Oxytocin, NpI and AVP were assayed in five subcellular fractions of bovine adrenal medulla prepared on discontinuous sucrose gradients. A high proportion of each co-localized with noradrenaline and adrenaline in the chromaffin granule fraction. Binding of [3H]AVP and [3H]oxytocin to crude bovine adrenal medulla membranes was dependent upon both time and temperature. The binding sites were specific and saturable: studies with the V1 AVP antagonist d(CH2)5Tyr(Me)AVP and the V2 agonist 1-deamino-8-d-AVP indicated that the AVP receptor was V1 in specificity. Scatchard plots showed that each ligand interacted with a single high-affinity, low-capacity binding site: oxytocin dissociation constant (Kd) 3·1 ±0·29 nmol/l, maximum binding capacity (Bmax) 89·6 ±18·4 fmol/mg protein (n = 3); AVP Kd 0·73 ±0·02 nmol/l, Bmax 26·5 ±8·3 fmol/mg protein (n = 3). Oxytocin and AVP had no effect on basal catecholamine release from bovine chromaffin cells in primary monolayer culture. However, both peptides inhibited acetylcholine- or nicotine-stimulated noradrenaline and adrenaline release in a dose-related manner. Neither inhibited noradrenaline or adrenaline secretion stimulated by veratridine- or potassium-induced depolarization. We conclude that the bovine adrenal cortex and medulla contain authentic AVP and oxytocin. In the medulla the peptides are packaged in secretory granules. The presence of the related neurophysins and high-affinity receptors in the medulla suggests that the peptides are both synthesized and have their site of action within this tissue. The function of AVP and oxytocin in the medulla may be indicated by the inhibition of acetylcholine-stimulated catecholamine secretion in vitro, although the effect requires high concentrations of either peptide. J. Endocr. (1987) 115, 141–149
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9

Inoue, Aiko, Sachika Inoue, Rui Sawai, Keita Hamamatsu, Kyoko Okazaki, Hitoshi Nishizawa, Yuto Yamazaki, Hironobu Sasano, Hiroyuki Murabe, and Toshihiko Yokota. "Mixed Corticomedullary Tumors of the Adrenal Gland Harboring Both Medullary and Cortical Properties." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A143. http://dx.doi.org/10.1210/jendso/bvab048.289.

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Abstract Adrenal cortex and medulla are derived from mesoderm and ectoderm, respectively. Mixed corticomedullary tumors (MCMTs), comprising an intimately admixed population of both adrenal cortical cells and pheochromocytes in a single adrenal tumor, are extremely rare and its pathogenesis has remained unknown. Here, we report a case of MCMT whose cells co-expressed cortical and medullary antigens in the same tumor cells.[Case description]A 40-year-old woman was referred to our hospital for investigating Takotsubo cardiomyopathy following resection of uterine fibroids. An abdominal CT scan depicted a 24 mm tumor on her left adrenal gland. Her basal serum ACTH, cortisol levels and urinary cortisol were 13.8 pg/mL, 9.5 μg/dL, and 26.5 μg/day respectively. The cortisol level was normally suppressed by an administration of 1 mg dexamethasone (1.4 μg/dL). Plasma renin activity, aldosterone levels and urinary aldosterone were 15.0 ng/mL/h, 122 pg/mL, and 5.0 μg/day, respectively (with administration history of azosemide). On the other hand, her plasma adrenaline and noradrenaline levels were elevated as high as 177 pg/mL and 536 pg/mL, and urinary metanephrine and normetanephrine were 2.12 mg/day and 1.10 mg/day. A 123I-metaiodobenzylguanidine scan revealed high uptake in the tumor. After adequate adrenergic α-receptor blockage, left adrenalectomy was performed. Her postoperative endocrine and clinical findings were normalized without any further complications.[Pathology] Immunohistochemistry (IHC) revealed the presence of MCMT. Cells morphologically consistent with pheochromocytoma and adrenocortical cells were confirmed by immunostaining of chromogranin A and SF-1, respectively. Chromogranin A-positive medullary-derived and SF-1-positive cortical-derived tumor cells were intermixed in the chimeric fashion. In addition, some tumor cells were positive for both proteins, indicating hybrid nature of the cells. Tumor cells of cortical origin expressed CYP11β1, 3β-HSD, p450c21, and p450c17, but not CYP11β2. Non neoplastic adrenal cortex were atrophic, whereas the glomerulosa was hyperplastic positive for CYP11β2, consistent with diffuse hyperplasia and adrenal medullar unremarkable. [Conclusions:]The adrenal tumor was clinically diagnosed as pheochromocytoma, but the pathological findings did reveal cortisol production in the tumor and aldosterone overproduction in the accompanying cortex. This is the first case of MCMT co-expressing adrenal medullary and cortical antigens in the same tumor cells as hybrid cells.
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Breslow, M. J., J. R. Tobin, T. D. Mandrell, L. C. Racusen, H. Raff, and R. J. Traystman. "Changes in adrenal oxygen consumption during catecholamine secretion in anesthetized dogs." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 3 (September 1, 1990): H681—H688. http://dx.doi.org/10.1152/ajpheart.1990.259.3.h681.

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Prior attempts to study adrenal medullary O2 metabolism during catecholamine secretion have been unsuccessful because venous blood from medulla mixes with venous blood from the much larger cortex. To circumvent this problem, eight adult mongrel dogs were pretreated for 5-6 wk with the adrenocorticolytic agent 1,1-dichloro-2-(o-chlorophenyl)-2-(p-chlorophenyl)ethane (o,p'-DDD). Prednisolone (5 mg/day) and fludrocortisone (0.1 mg.10 kg-1.day-1) were administered orally to prevent adrenocortical insufficiency. Animals were then anesthetized with pentobarbital sodium and subjected to splanchnic nerve stimulation (NS) at 20 and 4 Hz to elicit catecholamine secretion. NS at 20 Hz increased epinephrine secretion from 1.6 +/- 0.7 to 1,780 +/- 762 ng.min-1.g medulla-1 but had no effect on medullary O2 consumption. Medullary blood flow (MQ) increased from 216 +/- 63 to 1,522 +/- 182 ml.min-1.100 g-1, and O2 extraction decreased from 2.7 +/- 0.7 to 0.8 +/- 0.2%. NS at 4 Hz increased epinephrine secretion from 3.1 +/- 1.4 to 76 +/- 17 ng.min-1.g medulla-1 and MQ from 226 +/- 66 to 649 +/- 122 ml.min-1.100 g-1 but had no effect on adrenal O2 consumption or extraction. Cortical blood flow was 342 +/- 98 ml.min-1.100 g-1 at baseline and was unaffected by NS. Gross weight of cortex was reduced by 80% in o,p'-DDD-treated animals, and histological examination of glands from three animals showed only rare islands of glomerulosa cells remaining. These data suggest that increases in MQ during NS do not occur in response to changes in O2 consumption.
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Dissertations / Theses on the topic "Adrenal medulla – Metabolism"

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BADER, MARIE-FRANCE. "Contribution a l'etude du mecanisme de la secretion dans les cellules chromaffines." Université Louis Pasteur (Strasbourg) (1971-2008), 1986. http://www.theses.fr/1986STR13086.

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Les cellules chromaffines de la medullosurrenale synthetisent et stockent les catecholamines dans des vesicules membranaires et liberent ces hormones par mecanisme d'exocytose. Mise au point d'une technique d'etude qui fait appel a une toxine staphylococcique. Phenotype neuronal (neurites et neurofilaments) en culture cellulaire. Les proteines du cytosquelette interviennent dans le processus de secretion
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Books on the topic "Adrenal medulla – Metabolism"

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1928-, Takeda Ryōyū, Miyamori Isamu, and Japan Intractable Diseases Research Foundation., eds. Controversies in disorders of adrenal hormones: Proceedings of the Open Symposium of Disorders of Adrenal Hormones, held in Tokyo, Japan, on 20 February 1988. Amsterdam: Excerpta Medica, 1988.

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(Editor), Ryoyu Takeda, and Isamu Miyamori (Editor), eds. Controversies in Disorders of Adrenal Hormones (International Congress). Elsevier, 1988.

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Prout, Jeremy, Tanya Jones, and Daniel Martin. Endocrinology, metabolism, and body temperature. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199609956.003.0005.

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This chapter summarizes endocrine physiology that is of particular relevance to anaesthesia. Disorders of the adrenal cortex and medulla, pituitary and thyroid are described with perioperative management considerations highlighted. Current guidelines in perioperative steroid replacement are included. Diabetes is a particularly common problem encountered in clinical practice. Diabetic complications, pre-assessment and perioperative management aims are included. The surgical stress response is summarized with details of the neuroendocrine changes and their modification with anaesthetic technique. Consequences of perioperative hypothermia and use of therapeutic hypothermia are detailed.
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Cocaine and exercise: Alteration in carbohydrate metabolism in adrenodemedullated rats. 1994.

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Cocaine and exercise: Alteration in carbohydrate metabolism in adrenodemedullated rats. 1994.

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Cocaine and exercise: Alteration in carbohydrate metabolism in adrenodemedullated rats. 1994.

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Book chapters on the topic "Adrenal medulla – Metabolism"

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Vargas, Fernando F., Soledad Calvo, Raul Vinet, and Eduardo Rojas. "Interactions Between Bovine Adrenal Medulla Endothelial and Chromaffin Cells." In Whole Organ Approaches to Cellular Metabolism, 91–107. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4612-2184-5_4.

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Torpy, David J., Michael W. O’Reilly, and Sunita M. C. De Sousa. "Adrenal Disease in Pregnancy." In Oxford Textbook of Endocrinology and Diabetes 3e, edited by John A. H. Wass, Wiebke Arlt, and Robert K. Semple, 1479–88. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198870197.003.0177.

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Diagnosis of adrenal gland dysfunction in pregnancy is complex, and confounded by physiological gestational changes in maternal adrenal hormone metabolism. Management of newly diagnosed or pre-existing adrenal disease in pregnant women requires intensive input from the endocrinologist, and close collaboration with the obstetrician or fetal medicine specialist. Maternal adrenal gland dysfunction during pregnancy encompasses adrenocortical disorders resulting in glucocorticoid and mineralocorticoid deficiency or excess, and medullary disease resulting in catecholamine excess. The aim of this chapter is to review clinical aspects of the most common adrenal disorders in pregnancy, and to discuss approaches to diagnosis and management. Both benign and malignant diseases of the adrenal cortex and medulla will also be discussed.
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Yialamas, Maria A. "Reproductive and Androgenic Disorders." In The Brigham Intensive Review of Internal Medicine, 476–81. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199358274.003.0048.

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The adrenal gland consists of the cortex and medulla. The adrenal cortex secretes three classes of steroid hormones: glucocorticoids, mineralocorticoids, and androgens. The outer zona glomerulosa secretes the mineralocorticoid aldosterone, which performs a key role in the maintenance of blood pressure, vascular volume, and potassium homeostasis. The central zona fasciculata produces cortisol, which is crucial in the stress response and controls intermediary metabolism and immune functions. The inner layer, the zona reticularis, produces androgens, which serve as precursors of testosterone and androstenedione; they play a role in the development of secondary sexual characteristics in females.
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"Adrenal Medulla: I (Catecholamine Biosynthesis and Degradation)." In Metabolic and Endocrine Physiology, 76–77. Teton NewMedia, 2012. http://dx.doi.org/10.1201/b16175-36.

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"Adrenal Medulla: II (Adrenergic Receptors and the Sympathoadrenal Response)." In Metabolic and Endocrine Physiology, 78–79. Teton NewMedia, 2012. http://dx.doi.org/10.1201/b16175-37.

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Feher, Joseph. "The Adrenal Medulla and Integration of Metabolic Control." In Quantitative Human Physiology, 916–23. Elsevier, 2012. http://dx.doi.org/10.1016/b978-0-12-800883-6.00089-6.

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Feher, Joseph. "The Adrenal Medulla and Integration of Metabolic Control." In Quantitative Human Physiology, 820–27. Elsevier, 2012. http://dx.doi.org/10.1016/b978-0-12-382163-8.00089-x.

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Ryan, Richella, and Ruth Casey. "Endocrine and metabolic complications of advanced cancer." In Oxford Textbook of Palliative Medicine, edited by Nathan I. Cherny, Marie T. Fallon, Stein Kaasa, Russell K. Portenoy, and David C. Currow, 890–903. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198821328.003.0084.

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This chapter reviews the epidemiology, pathogenesis, clinical features, and management of endocrine and metabolic complications of advanced cancer. Broadly, these complications may arise in three ways due to (1) direct tumour invasion of organs or tissues; (2) non-metastatic systemic effects resulting from secretion of hormones, cytokines, or growth factors either by the tumour itself or by normal cells in response to tumour invasion (‘paraneoplastic effects’); and (3) treatments targeted at cancer or its symptoms. The chapter is divided into four sections. First, it describes the three most common endocrine manifestations of advanced cancer, including hypercalcaemia, Cushing’s syndrome, and syndrome of inappropriate antidiuresis. Second, it discusses the endocrine manifestations resulting from rare but important secretory endocrine tumours, including hypoglycaemia secondary to islet-cell and non-islet cell tumours, enteropancreatic hormone syndromes, carcinoid syndrome, phaeochromocytoma, adrenocortical carcinoma, and medullary thyroid carcinoma. Third, it briefly describes miscellaneous rare endocrine manifestations of cancer, including gynaecomastia, hypo- and hyperthyroidism, hypothalamic–pituitary dysfunction, and adrenal insufficiency. Finally, it concludes with a brief discussion of metabolic complications that may arise in association with malignancy, including paraneoplastic pyrexia, hyperglycaemia, and metabolic bone disease. Renal failure and hepatic failure are dealt with separately in the volume.
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