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Article ; Online: Cholesterol Availability and Adrenal Steroidogenesis.

Gomez-Sanchez, Celso E / Gomez-Sanchez, Elise P

2024 Volume 165, Issue 4

MeSH term(s)	Cholesterol ; Adrenal Glands ; Lipogenesis
Chemical Substances	Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2024-03-18
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqae032
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Article ; Online: Aldosterone Synthase Inhibitors and the Treatment of Essential Hypertension.

Gomez-Sanchez, Celso E / Gomez-Sanchez, Elise P

The Journal of clinical endocrinology and metabolism

2023 Volume 108, Issue 8, Page(s) e638–e639

MeSH term(s)	Humans ; Aldosterone ; Cytochrome P-450 CYP11B2 ; Mineralocorticoid Receptor Antagonists ; Hypertension/drug therapy ; Essential Hypertension/drug therapy ; Hyperaldosteronism/therapy ; Renin
Chemical Substances	Aldosterone (4964P6T9RB) ; Cytochrome P-450 CYP11B2 (EC 1.14.15.4) ; Mineralocorticoid Receptor Antagonists ; Renin (EC 3.4.23.15)
Language	English
Publishing date	2023-02-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgad071
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Article ; Online: 18-Oxocortisol: A journey.

Gomez-Sanchez, Celso E / Gomez-Sanchez, Elise P

The Journal of steroid biochemistry and molecular biology

2023 Volume 230, Page(s) 106291

Abstract: The search for mineralocorticoids to explain some cases of low renin hypertension with suppressed aldosterone levels led to the isolation of the abundant steroid 18-hydroxycortisol in human urine. 18-Hydroxycortisol proved to be inactive, but because of ... ...

Abstract	The search for mineralocorticoids to explain some cases of low renin hypertension with suppressed aldosterone levels led to the isolation of the abundant steroid 18-hydroxycortisol in human urine. 18-Hydroxycortisol proved to be inactive, but because of its similarity to precursors for the synthesis of aldosterone, bullfrog adrenals were incubated with cortisol, resulting in the discovery of 18-oxocortisol which is structurally similar to aldosterone, but with a 17α-hydroxy group like cortisol. 18-Oxocortisol is a weak mineralocorticoid. Its synthesis occurs primarily in the zona glomerulosa where co-expression of the CYP11B2 (aldosterone synthase) and the CYP17A1 (17α-hydroxylase) occurs in a variable number of cells. The clinical value of the measurement of 18-oxocortisol is that it serves to distinguish subtypes of primary aldosteronism. It is significantly elevated in patients with aldosterone-producing adenomas in comparison to those with idiopathic bilateral hyperaldosteronism and helps predict the type of somatic mutation in the aldosterone-producing adenomas, as it is higher in those with KCNJ5 mutations compared to other gene mutations.
MeSH term(s)	Humans ; Hydrocortisone ; Aldosterone ; Hyperaldosteronism/genetics ; Mineralocorticoids ; Cytochrome P-450 CYP11B2/genetics ; Cytochrome P-450 CYP11B2/metabolism ; Adenoma ; G Protein-Coupled Inwardly-Rectifying Potassium Channels/genetics
Chemical Substances	18-oxocortisol (2410-60-8) ; Hydrocortisone (WI4X0X7BPJ) ; Aldosterone (4964P6T9RB) ; Mineralocorticoids ; Cytochrome P-450 CYP11B2 (EC 1.14.15.4) ; KCNJ5 protein, human ; G Protein-Coupled Inwardly-Rectifying Potassium Channels
Language	English
Publishing date	2023-03-13
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	1049188-0
ISSN	1879-1220 ; 0960-0760
ISSN (online)	1879-1220
ISSN	0960-0760
DOI	10.1016/j.jsbmb.2023.106291
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: An Abbreviated History of Aldosterone Metabolism, Current and Future Challenges.

Gomez-Sanchez, Celso E / Gomez-Sanchez, Elise P

Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association

2023 Volume 131, Issue 7-08, Page(s) 386–393

Abstract: The initial isolation of adrenal steroids from large quantities of animal adrenals resulted in an amorphous fraction resistant to crystallization and identification and had potent effects on electrolyte transport. Aldosterone was eventually isolated and ... ...

Abstract	The initial isolation of adrenal steroids from large quantities of animal adrenals resulted in an amorphous fraction resistant to crystallization and identification and had potent effects on electrolyte transport. Aldosterone was eventually isolated and identified in the fraction and was soon shown to cause hypertension when in excess. The autonomous and excessive production of aldosterone, primary aldosteronism, is the most common cause of secondary hypertension. Aldosterone is metabolized in the liver and kidney, and its metabolites are conjugated with glucuronic acid for excretion. The most common liver metabolite is 3α,5β-tetrahydroaldosterone-3-glucuronide, while that of the kidney is aldosterone-18-oxo-glucuronide. In terms of their value, especially the aldosterone-18-oxo-glucuronide, is commonly used for the diagnosis of primary aldosteronism because they provide an integrated value of the total daily production of aldosterone. Conversion of aldosterone to 18-oxo-glucuronide is impeded by drugs, like some common non-steroidal anti-inflammatory drugs that compete for UDP-glucuronosyltransferase-2B7, the most important glucuronosyltransferase for aldosterone metabolism. Tetrahydroaldosterone is the most abundant metabolite and the most reliable for the diagnosis of primary aldosteronism, but it is not commonly measured.
MeSH term(s)	Animals ; Aldosterone/metabolism ; Glucuronides ; Hypertension/etiology ; Hyperaldosteronism/diagnosis ; Hyperaldosteronism/metabolism ; Glucuronosyltransferase
Chemical Substances	Aldosterone (4964P6T9RB) ; Glucuronides ; Glucuronosyltransferase (EC 2.4.1.17)
Language	English
Publishing date	2023-03-14
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1225416-2
ISSN	1439-3646 ; 0947-7349
ISSN (online)	1439-3646
ISSN	0947-7349
DOI	10.1055/a-2054-1062
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Article ; Online: Extra-adrenal Glucocorticoid and Mineralocorticoid Biosynthesis.

Gomez-Sanchez, Celso E / Gomez-Sanchez, Elise P

Endocrinology

2022 Volume 163, Issue 4

MeSH term(s)	Aldosterone ; Glucocorticoids ; Mineralocorticoids ; Receptors, Mineralocorticoid
Chemical Substances	Glucocorticoids ; Mineralocorticoids ; Receptors, Mineralocorticoid ; Aldosterone (4964P6T9RB)
Language	English
Publishing date	2022-02-11
Publishing country	United States
Document type	Editorial ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqac016
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Article ; Online: The Mineralocorticoid Receptor and the Heart.

Gomez-Sanchez, Celso E / Gomez-Sanchez, Elise P

Endocrinology

2021 Volume 162, Issue 11

MeSH term(s)	Heart ; Mineralocorticoid Receptor Antagonists ; Receptors, Mineralocorticoid/genetics
Chemical Substances	Mineralocorticoid Receptor Antagonists ; Receptors, Mineralocorticoid
Language	English
Publishing date	2021-06-26
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqab131
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Article: [No title information]

Gomez-Sanchez, Celso E / Gomez-Sanchez, Elise P

Experimental and Clinical Endocrinology & Diabetes

2023 Volume 131, Issue 07/08, Page(s) 386–393

Abstract	The initial isolation of adrenal steroids from large quantities of animal adrenals resulted in an amorphous fraction resistant to crystallization and identification and had potent effects on electrolyte transport. Aldosterone was eventually isolated and identified in the fraction and was soon shown to cause hypertension when in excess. The autonomous and excessive production of aldosterone, primary aldosteronism, is the most common cause of secondary hypertension. Aldosterone is metabolized in the liver and kidney, and its metabolites are conjugated with glucuronic acid for excretion. The most common liver metabolite is 3α,5β-tetrahydroaldosterone-3-glucuronide, while that of the kidney is aldosterone-18-oxo-glucuronide. In terms of their value, especially the aldosterone-18-oxo-glucuronide, is commonly used for the diagnosis of primary aldosteronism because they provide an integrated value of the total daily production of aldosterone. Conversion of aldosterone to 18-oxo-glucuronide is impeded by drugs, like some common non-steroidal anti-inflammatory drugs that compete for UDP-glucuronosyltransferase-2B7, the most important glucuronosyltransferase for aldosterone metabolism. Tetrahydroaldosterone is the most abundant metabolite and the most reliable for the diagnosis of primary aldosteronism, but it is not commonly measured.
Keywords	GH Adrenal gland ; Hormones ; aldosterone ; primary aldosteronism
Language	English
Publishing date	2023-03-14
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	1225416-2
ISSN	1439-3646 ; 0947-7349
ISSN (online)	1439-3646
ISSN	0947-7349
DOI	10.1055/a-2054-1062
Database	Thieme publisher's database

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Article ; Online: 11β-hydroxysteroid dehydrogenases: A growing multi-tasking family.

Gomez-Sanchez, Elise P / Gomez-Sanchez, Celso E

Molecular and cellular endocrinology

2021 Volume 526, Page(s) 111210

Abstract: This review briefly addresses the history of the discovery and elucidation of the three cloned 11β-hydroxysteroid dehydrogenase (11βHSD) enzymes in the human, 11βHSD1, 11βHSD2 and 11βHSD3, an ... ...

Abstract	This review briefly addresses the history of the discovery and elucidation of the three cloned 11β-hydroxysteroid dehydrogenase (11βHSD) enzymes in the human, 11βHSD1, 11βHSD2 and 11βHSD3, an NADP
MeSH term(s)	11-beta-Hydroxysteroid Dehydrogenases/antagonists & inhibitors ; 11-beta-Hydroxysteroid Dehydrogenases/chemistry ; 11-beta-Hydroxysteroid Dehydrogenases/genetics ; 11-beta-Hydroxysteroid Dehydrogenases/metabolism ; Animals ; Cytokines/metabolism ; Enzyme Inhibitors/pharmacology ; Humans ; Reproduction/drug effects ; Transcription, Genetic/drug effects
Chemical Substances	Cytokines ; Enzyme Inhibitors ; 11-beta-Hydroxysteroid Dehydrogenases (EC 1.1.1.146)
Language	English
Publishing date	2021-02-17
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2021.111210
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Article ; Online: mTOR Regulates Mineralocorticoid Receptor Transcriptional Activity by ULK1-Dependent and -Independent Mechanisms.

Ali, Yusuf / Gomez-Sanchez, Celso E / Plonczynski, Maria / Naray-Fejes-Toth, Aniko / Fejes-Toth, Geza / Gomez-Sanchez, Elise P

Endocrinology

2024 Volume 165, Issue 4

Abstract: The mineralocorticoid receptor (MR) is a transcription factor for genes mediating diverse, cell-specific functions, including trophic effects as well as promoting fluid/electrolyte homeostasis. It was reported that in intercalated cells, phosphorylation ... ...

Abstract	The mineralocorticoid receptor (MR) is a transcription factor for genes mediating diverse, cell-specific functions, including trophic effects as well as promoting fluid/electrolyte homeostasis. It was reported that in intercalated cells, phosphorylation of the MR at serine 843 (S843) by Unc-51-like kinase (ULK1) inhibits MR activation and that phosphorylation of ULK1 by mechanistic target of rapamycin (mTOR) inactivates ULK1, and thereby prevents MR inactivation. We extended these findings with studies in M1 mouse cortical collecting duct cells stably expressing the rat MR and a reporter gene. Pharmacological inhibition of ULK1 dose-dependently increased ligand-induced MR transactivation, while ULK1 activation had no effect. Pharmacological inhibition of mTOR and CRISPR/gRNA gene knockdown of rapamycin-sensitive adapter protein of mTOR (Raptor) or rapamycin-insensitive companion of mTOR (Rictor) decreased phosphorylated ULK1 and ligand-induced activation of the MR reporter gene, as well as transcription of endogenous MR-target genes. As predicted, ULK1 inhibition had no effect on aldosterone-mediated transcription in M1 cells with the mutated MR-S843A (alanine cannot be phosphorylated). In contrast, mTOR inhibition dose-dependently decreased transcription in the MR-S843A cells, though not as completely as in cells with the wild-type MR-S843. mTOR, Raptor, and Rictor coprecipitated with the MR and addition of aldosterone increased their phosphorylated, active state. These results suggest that mTOR significantly regulates MR activity in at least 2 ways: by suppressing MR inactivation by ULK1, and by a yet ill-defined mechanism that involves direct association with MR. They also provide new insights into the diverse functions of ULK1 and mTOR, 2 key enzymes that monitor the cell's energy status.
MeSH term(s)	Animals ; Mice ; Rats ; Aldosterone ; Autophagy-Related Protein-1 Homolog/genetics ; Autophagy-Related Protein-1 Homolog/metabolism ; Ligands ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Multiprotein Complexes/metabolism ; Phosphorylation ; Rapamycin-Insensitive Companion of mTOR Protein/metabolism ; Receptors, Mineralocorticoid/genetics ; Receptors, Mineralocorticoid/metabolism ; Regulatory-Associated Protein of mTOR ; RNA, Guide, CRISPR-Cas Systems ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases/metabolism ; Transcription Factors/metabolism
Chemical Substances	Aldosterone (4964P6T9RB) ; Autophagy-Related Protein-1 Homolog (EC 2.7.11.1) ; Ligands ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; mTOR protein, rat (EC 2.7.1.1) ; Multiprotein Complexes ; Rapamycin-Insensitive Companion of mTOR Protein ; Receptors, Mineralocorticoid ; Regulatory-Associated Protein of mTOR ; RNA, Guide, CRISPR-Cas Systems ; Sirolimus (W36ZG6FT64) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Transcription Factors ; ULK1 protein, rat (EC 2.7.11.1) ; Ulk1 protein, mouse (EC 2.7.11.1) ; mTOR protein, mouse (EC 2.7.1.1)
Language	English
Publishing date	2024-02-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqae015
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Article ; Online: Mammalian Target of Rapamycin Inhibition Decreases Angiotensin II-Induced Steroidogenesis in HAC15 Human Adrenocortical Carcinoma Cells.

Ali, Yusuf / Gomez-Sanchez, Elise P / Gomez-Sanchez, Celso E

Endocrinology

2022 Volume 164, Issue 1

Abstract: Background: Mammalian target of rapamycin (mTOR) inhibitors suppress adrenal cortical carcinoma cell proliferation and cortisol production; the relationship between mTOR and aldosterone production has not been examined.: Methods: HAC15 cells were ... ...

Abstract	Background: Mammalian target of rapamycin (mTOR) inhibitors suppress adrenal cortical carcinoma cell proliferation and cortisol production; the relationship between mTOR and aldosterone production has not been examined. Methods: HAC15 cells were incubated with an mTOR activator and several inhibitors including AZD8055 (AZD) in the presence and absence of angiotensin II (AngII). The expression of rapamycin-sensitive adapter protein of mTOR (Raptor) and rapamycin-insensitive companion of mTOR (Rictor), adaptor proteins of mTOR complex 1 and 2, respectively, were studied in the HAC15 cells and deleted by CRISPR/gRNA. Results: The mTOR inhibitors decreased aldosterone induced by AngII. Inhibition of mTOR by AZD significantly suppressed AngII-induced aldosterone and cortisol formation in a dose-dependent manner, whereas the mTOR activator MHY had no effect. AZD did not alter forskolin-induced aldosterone production showing that it is specific to the AngII signaling pathway. AngII-mediated ERK and mTOR activation were suppressed by AZD, along with a concomitant dose-dependent reduction of AngII-induced steroidogenic enzymes including steroidogenic acute regulatory protein, 3β-hydroxysteroid dehydrogenase-type 2, CYP17A1, and aldosterone synthase protein. Furthermore, mTOR components ribosomal protein S6 kinase (P70S6K) and protein kinase B phosphorylation levels were decreased by AZD. As mTOR exerts its main effects by forming complexes with adaptor proteins Raptor and Rictor, the roles of these individual complexes were studied. We found an increase in the phosphorylation of Raptor and Rictor by AngII and that their CRISPR/gRNA-mediated knockdown significantly attenuated AngII-induced aldosterone and cortisol production. Conclusion: mTOR signaling has a critical role in transducing the AngII signal initiating aldosterone and cortisol synthesis in HAC15 cells and that inhibition of mTOR could be a therapeutic option for conditions associated with excessive renin-angiotensin system-mediated steroid synthesis.
MeSH term(s)	Humans ; Angiotensin II/pharmacology ; Angiotensin II/metabolism ; Aldosterone/metabolism ; Adrenocortical Carcinoma ; Hydrocortisone/metabolism ; Sirolimus/pharmacology ; RNA, Guide, CRISPR-Cas Systems ; Adrenal Cortex Neoplasms/drug therapy ; TOR Serine-Threonine Kinases
Chemical Substances	Angiotensin II (11128-99-7) ; Aldosterone (4964P6T9RB) ; Hydrocortisone (WI4X0X7BPJ) ; Sirolimus (W36ZG6FT64) ; RNA, Guide, CRISPR-Cas Systems ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2022-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqac185
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