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Article ; Online: New functions and roles of the Na

Dominguez Rieg, Jessica A / Rieg, Timo

Pflugers Archiv : European journal of physiology

2024 Volume 476, Issue 4, Page(s) 505–516

Abstract: The sodium/proton exchanger isoform 3 (NHE3) is expressed in the intestine and the kidney, where it contributes to hydrogen secretion and sodium (re)absorption. The roles of this transporter have been studied by the use of the respective knockout mice ... ...

Abstract	The sodium/proton exchanger isoform 3 (NHE3) is expressed in the intestine and the kidney, where it contributes to hydrogen secretion and sodium (re)absorption. The roles of this transporter have been studied by the use of the respective knockout mice and by using pharmacological inhibitors. Whole-body NHE3 knockout mice suffer from a high mortality rate (with only ∼30% of mice surviving into adulthood), and based on the expression of NHE3 in both intestine and kidney, some conclusions that were originally derived were based on this rather complex phenotype. In the last decade, more refined models have been developed that added temporal and spatial control of NHE3 expression. For example, novel mouse models have been developed with a knockout of NHE3 in intestinal epithelial cells, tubule/collecting duct of the kidney, proximal tubule of the kidney, and thick ascending limb of the kidney. These refined models have significantly contributed to our understanding of the role of NHE3 in a tissue/cell type-specific manner. In addition, tenapanor was developed, which is a non-absorbable, intestine-specific NHE3 inhibitor. In rat and human studies, tenapanor lowered intestinal P
MeSH term(s)	Animals ; Humans ; Mice ; Rats ; Isoquinolines ; Mice, Knockout ; Sodium/metabolism ; Sodium-Hydrogen Exchanger 3/metabolism ; Sodium-Hydrogen Exchangers/genetics ; Sodium-Hydrogen Exchangers/metabolism ; Sulfonamides
Chemical Substances	Isoquinolines ; Sodium (9NEZ333N27) ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers ; Sulfonamides ; tenapanor (WYD79216A6) ; SLC9A3 protein, human
Language	English
Publishing date	2024-03-07
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-024-02938-9
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Article ; Online: Npt2a as a target for treating hyperphosphatemia.

Thomas, Linto / Dominguez Rieg, Jessica A / Rieg, Timo

Biochemical Society transactions

2022 Volume 50, Issue 1, Page(s) 439–446

Abstract: Hyperphosphatemia results from an imbalance in phosphate (Pi) homeostasis. In patients with and without reduced kidney function, hyperphosphatemia is associated with cardiovascular complications. The current mainstays in the management of ... ...

Abstract	Hyperphosphatemia results from an imbalance in phosphate (Pi) homeostasis. In patients with and without reduced kidney function, hyperphosphatemia is associated with cardiovascular complications. The current mainstays in the management of hyperphosphatemia are oral Pi binder and dietary Pi restriction. Although these options are employed in patients with chronic kidney disease (CKD), they seem inadequate to correct elevated plasma Pi levels. In addition, a paradoxical increase in expression of intestinal Pi transporter and uptake may occur. Recently, studies in rodents targeting the renal Na+/Pi cotransporter 2a (Npt2a), responsible for ∼70% of Pi reabsorption, have been proposed as a potential treatment option. Two compounds (PF-06869206 and BAY-767) have been developed which are selective for Npt2a. These Npt2a inhibitors significantly increased urinary Pi excretion consequently lowering plasma Pi and PTH levels. Additionally, increases in urinary excretions of Na+, Cl- and Ca2+ have been observed. Some of these results are also seen in models of reduced kidney function. Responses of FGF23, a phosphaturic hormone that has been linked to the development of left ventricular hypertrophy in CKD, are ambiguous. In this review, we discuss the recent advances on the role of Npt2a inhibition on Pi homeostasis as well as other pleiotropic effects observed with Npt2a inhibition.
MeSH term(s)	Animals ; Female ; Humans ; Hyperphosphatemia/drug therapy ; Male ; Mice ; Mice, Knockout ; Parathyroid Hormone/metabolism ; Phosphates/metabolism ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/metabolism ; Sodium-Phosphate Cotransporter Proteins, Type IIa/metabolism
Chemical Substances	Parathyroid Hormone ; Phosphates ; Sodium-Phosphate Cotransporter Proteins, Type IIa
Language	English
Publishing date	2022-01-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	184237-7
ISSN	1470-8752 ; 0300-5127
ISSN (online)	1470-8752
ISSN	0300-5127
DOI	10.1042/BST20211005
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Zs.A 944: Show issues

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Article ; Online: Intravenous ferric carboxymaltose and ferric derisomaltose alter the intestinal microbiome in female iron-deficient anemic mice.

Rieg, Timo / Xue, Jianxiang / Stevens, Monica / Thomas, Linto / White, James R / Dominguez Rieg, Jessica A

Bioscience reports

2023 Volume 43, Issue 9

Abstract: Iron deficiency anemia (IDA) is a leading global health concern affecting approximately 30% of the population. Treatment for IDA consists of replenishment of iron stores, either by oral or intravenous (IV) supplementation. There is a complex ... ...

Abstract	Iron deficiency anemia (IDA) is a leading global health concern affecting approximately 30% of the population. Treatment for IDA consists of replenishment of iron stores, either by oral or intravenous (IV) supplementation. There is a complex bidirectional interplay between the gut microbiota, the host's iron status, and dietary iron availability. Dietary iron deficiency and supplementation can influence the gut microbiome; however, the effect of IV iron on the gut microbiome is unknown. We studied how commonly used IV iron preparations, ferric carboxymaltose (FCM) and ferric derisomaltose (FDI), affected the gut microbiome in female iron-deficient anemic mice. At the phylum level, vehicle-treated mice showed an expansion in Verrucomicrobia, mostly because of the increased abundance of Akkermansia muciniphila, along with contraction in Firmicutes, resulting in a lower Firmicutes/Bacteroidetes ratio (indicator of dysbiosis). Treatment with either FCM or FDI restored the microbiome such that Firmicutes and Bacteroidetes were the dominant phyla. Interestingly, the phyla Proteobacteria and several members of Bacteroidetes (e.g., Alistipes) were expanded in mice treated with FCM compared with those treated with FDI. In contrast, several Clostridia class members were expanded in mice treated with FDI compared with FCM (e.g., Dorea spp., Eubacterium). Our data demonstrate that IV iron increases gut microbiome diversity independently of the iron preparation used; however, differences exist between FCM and FDI treatments. In conclusion, replenishing iron stores with IV iron preparations in clinical conditions, such as inflammatory bowel disease or chronic kidney disease, could affect gut microbiome composition and consequently contribute to an altered disease outcome.
MeSH term(s)	Female ; Animals ; Mice ; Iron ; Gastrointestinal Microbiome ; Disaccharides ; Iron, Dietary ; Bacteroidetes ; Firmicutes
Chemical Substances	ferric derisomaltose (AHU547PI9H) ; ferric carboxymaltose (6897GXD6OE) ; Iron (E1UOL152H7) ; Disaccharides ; Iron, Dietary
Language	English
Publishing date	2023-09-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	764946-0
ISSN	1573-4935 ; 0144-8463
ISSN (online)	1573-4935
ISSN	0144-8463
DOI	10.1042/BSR20231217
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Zs.A 1676: Show issues

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Article ; Online: Sodium phosphate cotransporter 2a inhibitors: potential therapeutic uses.

Xue, Jianxiang / Thomas, Linto / Dominguez Rieg, Jessica A / Rieg, Timo

Current opinion in nephrology and hypertension

2022 Volume 31, Issue 5, Page(s) 486–492

Abstract: Purpose of review: Targeting sodium phosphate cotransporter 2a (Npt2a) offers a novel strategy for treating hyperphosphatemia in chronic kidney disease (CKD). Here we review recent studies on the efficacy of Npt2a inhibition, its plasma phosphate (Pi)- ... ...

Abstract	Purpose of review: Targeting sodium phosphate cotransporter 2a (Npt2a) offers a novel strategy for treating hyperphosphatemia in chronic kidney disease (CKD). Here we review recent studies on the efficacy of Npt2a inhibition, its plasma phosphate (Pi)-lowering effects, as well as potential "off-target" beneficial effects on cardiovascular consequences. Recent findings: Two novel Npt2a-selective inhibitors (PF-06869206 and BAY-767) have been developed. Pharmacological Npt2a inhibition shows a significant phosphaturic effect and consequently lowers plasma Pi and parathyroid hormone (PTH) levels regardless of CKD. However, plasma fibroblast growth factor 23 (FGF23), a master regulator of Pi homeostasis, shows inconsistent responses between these two inhibitors (no effect by PF-06869206 vs. reduction by BAY-767). In addition to the effects on Pi homeostasis, Npt2a inhibition also enhances urinary excretions of Na+, Cl-, and Ca2+, which is recapitulated in animal models with reduced kidney function. The effect of Npt2a inhibition by BAY-767 on vascular calcification has been studied, with positive results showing that oral treatment with BAY-767 (10 mg kg-1) attenuated the increases in plasma Pi and Ca2+ content in the aorta under the setting of vascular calcification induced by a pan-FGF receptor inhibitor. Together, Npt2a inhibition offers a promising therapeutic approach for treating hyperphosphatemia and reducing cardiovascular complications in CKD. Summary: Npt2a inhibition significantly increases urinary Pi excretion and lowers plasma Pi and PTH levels; moreover, it exerts pleiotropic "off-target" effects, providing a novel treatment for hyperphosphatemia and exhibiting beneficial potential for cardiovascular complications in CKD.
MeSH term(s)	Animals ; Calcium/metabolism ; Fibroblast Growth Factors/metabolism ; Humans ; Hyperphosphatemia/drug therapy ; Hyperphosphatemia/etiology ; Parathyroid Hormone/metabolism ; Phosphates/metabolism ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/drug therapy ; Sodium-Phosphate Cotransporter Proteins, Type IIa/antagonists & inhibitors ; Vascular Calcification
Chemical Substances	Parathyroid Hormone ; Phosphates ; Sodium-Phosphate Cotransporter Proteins, Type IIa ; Fibroblast Growth Factors (62031-54-3) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-07-18
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000828
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Zs.A 3686: Show issues

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Article: Epac induces ryanodine receptor-dependent intracellular and inter-organellar calcium mobilization in mpkCCD cells.

Yip, Kay-Pong / Ribeiro-Silva, Luisa / Cha, Byeong / Rieg, Timo / Sham, James S K

Frontiers in physiology

2023 Volume 14, Page(s) 1250273

Abstract: Arginine vasopressin (AVP) induces an increase in intracellular ... ...

Abstract	Arginine vasopressin (AVP) induces an increase in intracellular Ca
Language	English
Publishing date	2023-08-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2023.1250273
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Book: Über Leichen zum Examen?

Rieg, Timo

Tierversuche im Studium ; ein Diskussions- und Arbeitsbuch

(Tierschutz aktiv ; 1)

1996

Institution	Bundesverband Studentischer Arbeitsgruppen gegen Tiermissbrauch im Studium
Author's details	Bundesverband SATIS e.V. (Hrsg.). Von Timo Rieg
Series title	Tierschutz aktiv ; 1
Collection
Keywords	Education, Medical ; Biology / education ; Ethics, Institutional ; Animals, Laboratory ; Animal Testing Alternatives ; Animal Welfare ; Medizinstudium ; Tierversuch
Subject	Experiment ; Tierexperiment ; Medizin ; Medizinisches Studium
Language	German
Size	458 S. : Ill.
Edition	2., überarb. Aufl.
Publisher	Timona-Verl
Publishing place	Bochum
Publishing country	Germany
Document type	Book
HBZ-ID	HT007341464
ISBN	3-928781-32-4 ; 978-3-928781-32-9
Database	Catalogue ZB MED Medicine, Health

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Shelf mark	Loan status	Location
1997 A 5352	order for loan	Magazin

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Article ; Online: Intestine-Specific NHE3 Deletion in Adulthood Causes Microbial Dysbiosis.

Xue, Jianxiang / Dominguez Rieg, Jessica A / Thomas, Linto / White, James R / Rieg, Timo

Frontiers in cellular and infection microbiology

2022 Volume 12, Page(s) 896309

Abstract: In the intestine, the ... ...

Abstract	In the intestine, the Na
MeSH term(s)	Adult ; Animals ; Bacteroidetes ; Dysbiosis/microbiology ; Firmicutes ; Gastrointestinal Microbiome ; Humans ; Inflammatory Bowel Diseases/microbiology ; Intestines/microbiology ; Mice ; Sodium-Hydrogen Exchanger 3/genetics
Chemical Substances	SLC9A3 protein, human ; Slc9a3 protein, mouse ; Sodium-Hydrogen Exchanger 3
Language	English
Publishing date	2022-05-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2022.896309
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: NHE3 in the thick ascending limb is required for sustained but not acute furosemide-induced urinary acidification.

Xue, Jianxiang / Thomas, Linto / Dominguez Rieg, Jessica A / Fenton, Robert A / Rieg, Timo

American journal of physiology. Renal physiology

2022 Volume 323, Issue 2, Page(s) F141–F155

Abstract: ... ...

Abstract	Na
MeSH term(s)	Alkalosis ; Animals ; Furosemide/pharmacology ; Hydrogen-Ion Concentration ; Mice ; Sodium/metabolism ; Sodium-Hydrogen Exchanger 3/genetics ; Sodium-Hydrogen Exchangers/genetics ; Sodium-Hydrogen Exchangers/metabolism
Chemical Substances	Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers ; Furosemide (7LXU5N7ZO5) ; Sodium (9NEZ333N27)
Language	English
Publishing date	2022-05-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00013.2022
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Article: Die rechtlichen Regelungen von Eingriffen und Behandlungen an Tieren zur Aus-, Fort- und Weiterbildung 123 128 DE Rieg Timo D-Bochum Löblein Claus-M. The German constitution (1948) states that University professors have the complete freedom in the choice of aims and means for their teaching, and that no other law of regulation may restrict this freedom. This unconditional academic freedom ("akademische Lehrfreiheit") comes into conflict with the more recent Animal Rights Law ("Tierschutzgesetz) which e.g. restricts the use of animals for demonstration purposes. The following dissertation explains the regulations concerning animal experiments in education, the question of the protection of animals as guaranteed in the constitution, and possible ethical limits of the academic freedom. Very recently an Animal Protection Authority has issued an order to forestall animal experiments in teaching. This official attempt has now been annulled by a temporary injunction of the administrative Court, Kassel.

Rieg, Timo / Löblein, Claus-M.

ALTEX

1995 Volume 12, Issue 3, Page(s) 123–128

Abstract: The German constitution (1948) states that University professors have the complete freedom in the choice of aims and means for their teaching, and that no other law of regulation may restrict this freedom. This unconditional academic freedom (" ... ...

Title translation	The regulations concerning animal experiments in education by the German Animal Rights Law
Abstract	The German constitution (1948) states that University professors have the complete freedom in the choice of aims and means for their teaching, and that no other law of regulation may restrict this freedom. This unconditional academic freedom ("akademische Lehrfreiheit") comes into conflict with the more recent Animal Rights Law ("Tierschutzgesetz) which e.g. restricts the use of animals for demonstration purposes. The following dissertation explains the regulations concerning animal experiments in education, the question of the protection of animals as guaranteed in the constitution, and possible ethical limits of the academic freedom. Very recently an Animal Protection Authority has issued an order to forestall animal experiments in teaching. This official attempt has now been annulled by a temporary injunction of the administrative Court, Kassel.
Language	English
Publishing date	1995
Publishing country	Germany
Document type	Journal Article
ZDB-ID	165707-0
ISSN	1868-596X ; 1018-4562 ; 0946-7785
ISSN	1868-596X ; 1018-4562 ; 0946-7785
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.B 2971: Show issues

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Article ; Online: Tubular effects of sodium-glucose cotransporter 2 inhibitors: intended and unintended consequences.

Dominguez Rieg, Jessica A / Xue, Jianxiang / Rieg, Timo

Current opinion in nephrology and hypertension

2020 Volume 29, Issue 5, Page(s) 523–530

Abstract: Purpose of review: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are antihyperglycemic drugs that act by inhibiting renal sodium-glucose cotransport. Here we present new insights into 'off target', or indirect, effects of SGLT2 inhibitors.: Recent ...

Abstract	Purpose of review: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are antihyperglycemic drugs that act by inhibiting renal sodium-glucose cotransport. Here we present new insights into 'off target', or indirect, effects of SGLT2 inhibitors. Recent findings: SGLT2 inhibition causes an acute increase in urinary glucose excretion. In addition to lowering blood glucose, there are several other effects that contribute to the overall beneficial renal and cardiovascular effects. Reabsorption of about 66% of sodium is accomplished in the proximal tubule and dependent on the sodium-hydrogen exchanger isoform 3 (NHE3). SGLT2 colocalizes with NHE3, and high glucose levels reduce NHE3 activity. The proximal tubule is also responsible for the majority of phosphate (Pi) reabsorption. SGLT2 inhibition is associated with increases in plasma Pi, fibroblast growth factor 23 and parathyroid hormone levels in nondiabetics and type 2 diabetes mellitus. Studies in humans identified a urate-lowering effect by SGLT2 inhibition which is possibly mediated by urate transporter 1 (URAT1) and/or glucose transporter member 9 in the proximal tubule. Of note, magnesium levels were also found to increase under SGLT2 inhibition, an effect that was preserved in nondiabetic patients with hypomagnesemia. Summary: Cardiorenal effects of SGLT2 inhibition might involve, in addition to direct effects on glucose homeostasis, effects on NHE3, phosphate, urate, and magnesium homeostasis.
MeSH term(s)	Humans ; Hypoglycemic Agents/pharmacology ; Kidney Tubules, Proximal/drug effects ; Kidney Tubules, Proximal/metabolism ; Magnesium/metabolism ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Sodium-Hydrogen Exchanger 3/metabolism
Chemical Substances	Hypoglycemic Agents ; Sodium-Glucose Transporter 2 Inhibitors ; Sodium-Hydrogen Exchanger 3 ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2020-07-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000632
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