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Article ; Online: How can inhibition of glucose and sodium transport in the early proximal tubule protect the cardiorenal system?

Vallon, Volker

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2024

Abstract: What mechanisms can link the inhibition of SGLT2-mediated Na+-coupled glucose reabsorption in early proximal tubules to kidney and heart protection in patients with and without type 2 diabetes? Due to physical and functional coupling of SGLT2 to other ... ...

Abstract	What mechanisms can link the inhibition of SGLT2-mediated Na+-coupled glucose reabsorption in early proximal tubules to kidney and heart protection in patients with and without type 2 diabetes? Due to physical and functional coupling of SGLT2 to other sodium and metabolite transporters in the early proximal tubule (including NHE3, URAT1), inhibitors of SGLT2 (SGLT2i) reduce reabsorption not only of glucose, inducing osmotic diuresis, but of other metabolites plus of a larger amount of sodium than expected based on SGLT2 inhibition alone, thereby reducing volume retention, hypertension, and hyperuricemia. Metabolic adaptations to SGLT2i include a fasting-like response, with enhanced lipolysis and formation of ketone bodies that serve as additional fuel for kidneys and heart. Making use of the physiology of tubulo-glomerular communication, SGLT2i functionally lower glomerular capillary pressure and filtration rate, thereby reducing physical stress on the glomerular filtration barrier, tubular exposure to albumin and nephrotoxic compounds, and the oxygen demand for reabsorbing the filtered load. Together with reduced gluco-toxicity in the early proximal tubule and better distribution of transport work along the nephron, SGLT2i can preserve tubular integrity and transport function and, thereby, GFR in the long-term. By shifting transport downstream, SGLT2 inhibitors may simulate systemic hypoxia at the oxygen sensors in the deep cortex/outer medulla, which stimulates erythropoiesis and, together with osmotic diuresis, enhances hematocrit and thereby improves oxygen delivery to all organs. The described SGLT2-dependent effects may be complemented by off-target effects of SGLT2i on the heart itself and on the microbiome formation of cardiovascular-effective uremic toxins.
Language	English
Publishing date	2024-03-04
Publishing country	England
Document type	Journal Article
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfae060
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Zs.MO 329: Show issues

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Article: Renoprotective Effects of SGLT2 Inhibitors.

Vallon, Volker

Heart failure clinics

2022 Volume 18, Issue 4, Page(s) 539–549

Abstract: SGLT2 inhibitors can protect the kidneys of patients with and without type 2 diabetes from failing. This includes blood glucose dependent and independent mechanisms. SGLT2 inhibitors lower glomerular pressure and filtration, thereby reducing the physical ...

Abstract	SGLT2 inhibitors can protect the kidneys of patients with and without type 2 diabetes from failing. This includes blood glucose dependent and independent mechanisms. SGLT2 inhibitors lower glomerular pressure and filtration, thereby reducing the physical stress on the filtration barrier and the oxygen demand for tubular reabsorption. This improves cortical oxygenation, which, together with lesser tubular glucotoxicity and improved mitochondrial function and autophagy, can reduce proinflammatory and profibrotic signaling and preserve tubular function and GFR in long term. By shifting transport downstream, SGLT2 inhibitors may mimic systemic hypoxia and stimulate erythropoiesis, which improves oxygen delivery to the kidney and other organs.
MeSH term(s)	Blood Glucose ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Diabetic Nephropathies/prevention & control ; Glomerular Filtration Rate ; Humans ; Oxygen/pharmacology ; Sodium-Glucose Transporter 2/pharmacology ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use
Chemical Substances	Blood Glucose ; Sodium-Glucose Transporter 2 ; Sodium-Glucose Transporter 2 Inhibitors ; Oxygen (S88TT14065)
Language	English
Publishing date	2022-10-01
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2212019-1
ISSN	1551-7136
ISSN	1551-7136
DOI	10.1016/j.hfc.2022.03.005
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Article ; Online: Did you know how SGLT2 inhibitors protect the kidney?

Layton, Anita T / Vallon, Volker

Acta physiologica (Oxford, England)

2023 Volume 238, Issue 4, Page(s) e14011

MeSH term(s)	Humans ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use ; Kidney ; Hypoglycemic Agents ; Diabetes Mellitus, Type 2/drug therapy
Chemical Substances	Sodium-Glucose Transporter 2 Inhibitors ; Hypoglycemic Agents
Language	English
Publishing date	2023-06-18
Publishing country	England
Document type	Editorial
ZDB-ID	2218636-0
ISSN	1748-1716 ; 1748-1708
ISSN (online)	1748-1716
ISSN	1748-1708
DOI	10.1111/apha.14011
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Article ; Online: Glucose transporters in the kidney in health and disease.

Vallon, Volker

Pflugers Archiv : European journal of physiology

2020 Volume 472, Issue 9, Page(s) 1345–1370

Abstract: The kidneys filter large amounts of glucose. To prevent the loss of this valuable fuel, the tubular system of the kidney, particularly the proximal tubule, has been programmed to reabsorb all filtered glucose. The machinery involves the sodium-glucose ... ...

Abstract	The kidneys filter large amounts of glucose. To prevent the loss of this valuable fuel, the tubular system of the kidney, particularly the proximal tubule, has been programmed to reabsorb all filtered glucose. The machinery involves the sodium-glucose cotransporters SGLT2 and SGLT1 on the apical membrane and the facilitative glucose transporter GLUT2 on the basolateral membrane. The proximal tubule also generates new glucose, particularly in the post-absorptive phase but also to enhance bicarbonate formation and maintain acid-base balance. The glucose reabsorbed or formed by the proximal tubule is primarily taken up into peritubular capillaries and returned to the systemic circulation or provided as an energy source to further distal tubular segments that take up glucose by basolateral GLUT1. Recent studies provided insights on the coordination of renal glucose reabsorption, formation, and usage. Moreover, a better understanding of renal glucose transport in disease states is emerging. This includes the kidney in diabetes mellitus, when renal glucose retention becomes maladaptive and contributes to hyperglycemia. Furthermore, enhanced glucose reabsorption is coupled to sodium retention through the sodium-glucose cotransporter SGLT2, which induces secondary deleterious effects. As a consequence, SGLT2 inhibitors are new anti-hyperglycemic drugs that can protect the kidneys and heart from failing. Recent studies discovered unique roles for SGLT1 with implications in acute kidney injury and glucose sensing at the macula densa. This review discusses established and emerging concepts of renal glucose transport, and outlines the need for a better understanding of renal glucose handling in health and disease.
MeSH term(s)	Acute Kidney Injury/drug therapy ; Acute Kidney Injury/metabolism ; Animals ; Humans ; Kidney/metabolism ; Renal Reabsorption ; Sodium-Glucose Transporter 2/metabolism ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use
Chemical Substances	Sodium-Glucose Transporter 2 ; Sodium-Glucose Transporter 2 Inhibitors
Language	English
Publishing date	2020-03-06
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	6380-0
ISSN	1432-2013 ; 0031-6768
ISSN (online)	1432-2013
ISSN	0031-6768
DOI	10.1007/s00424-020-02361-w
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Article ; Online: CRRT 2023 Meeting: Targeting Amino Acid Transport to Improve Acute Kidney Injury Outcome.

Oe, Yuji / Vallon, Volker

Nephron

2023 Volume 147, Issue 12, Page(s) 774–777

Abstract: Background: In acute kidney injury (AKI), proximal tubules are a primary site of injury, resulting in significant alterations in amino acid transport and metabolism. However, little is known about the therapeutic potential of targeting amino acid ... ...

Abstract	Background: In acute kidney injury (AKI), proximal tubules are a primary site of injury, resulting in significant alterations in amino acid transport and metabolism. However, little is known about the therapeutic potential of targeting amino acid transporters. Here, we briefly review the first experimental evidence that targeting the sodium-coupled amino acid transporter SLC6A19 (B0AT1) can improve AKI outcome. Summary: SLC6A19 is expressed in the small intestine and early proximal tubules, where it absorbs and reabsorbs most of the ingested and filtered neutral amino acids, respectively. Systemic SLC6A19 deficiency alleviates renal cellular senescence and suppresses subsequent inflammation and fibrosis in a murine model of aristolochic acid-induced nephropathy, which targets the proximal tubule. The underlying mechanisms remain to be determined, but potentially may include reduced tubular workload, an inhibitory effect on SGLT2, downstream shift in transport and preconditioning of late proximal tubules, and induction of a fasting-like phenotype and lowering tubular accumulation of branched-chain amino acids, which all can promote tubular health.
MeSH term(s)	Humans ; Mice ; Animals ; Amino Acids/metabolism ; Kidney/metabolism ; Kidney Tubules, Proximal/metabolism ; Acute Kidney Injury/therapy ; Acute Kidney Injury/metabolism ; Amino Acid Transport Systems, Neutral
Chemical Substances	Amino Acids ; SLC6A19 protein, mouse ; Amino Acid Transport Systems, Neutral
Language	English
Publishing date	2023-07-25
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	207121-6
ISSN	2235-3186 ; 1423-0186 ; 1660-8151 ; 0028-2766
ISSN (online)	2235-3186 ; 1423-0186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000531918
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Article ; Online: Protecting the Kidney: The Unexpected Logic of Inhibiting a Glucose Transporter.

Vallon, Volker / Kim, Young Chul

Clinical pharmacology and therapeutics

2022 Volume 112, Issue 3, Page(s) 434–438

MeSH term(s)	Diabetes Mellitus, Type 2 ; Glucose ; Glucose Transport Proteins, Facilitative ; Humans ; Kidney ; Logic ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use
Chemical Substances	Glucose Transport Proteins, Facilitative ; Sodium-Glucose Transporter 2 Inhibitors ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	123793-7
ISSN	1532-6535 ; 0009-9236
ISSN (online)	1532-6535
ISSN	0009-9236
DOI	10.1002/cpt.2651
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Article: The Pathophysiological Basis of Diabetic Kidney Protection by Inhibition of SGLT2 and SGLT1.

Oe, Yuji / Vallon, Volker

Kidney and dialysis

2022 Volume 2, Issue 2, Page(s) 349–368

Abstract: SGLT2 inhibitors can protect the kidneys of patients with and without type 2 diabetes mellitus and slow the progression towards end-stage kidney disease. Blocking tubular SGLT2 and spilling glucose into the urine, which triggers a metabolic counter- ... ...

Abstract	SGLT2 inhibitors can protect the kidneys of patients with and without type 2 diabetes mellitus and slow the progression towards end-stage kidney disease. Blocking tubular SGLT2 and spilling glucose into the urine, which triggers a metabolic counter-regulation similar to fasting, provides unique benefits, not only as an anti-hyperglycemic strategy. These include a low hypoglycemia risk and a shift from carbohydrate to lipid utilization and mild ketogenesis, thereby reducing body weight and providing an additional energy source. SGLT2 inhibitors counteract hyperreabsorption in the early proximal tubule, which acutely lowers glomerular pressure and filtration and thereby reduces the physical stress on the filtration barrier, the filtration of tubule-toxic compounds, and the oxygen demand for tubular reabsorption. This improves cortical oxygenation, which, together with lesser tubular gluco-toxicity and improved mitochondrial function and autophagy, can reduce pro-inflammatory, pro-senescence, and pro-fibrotic signaling and preserve tubular function and GFR in the long-term. By shifting transport downstream, SGLT2 inhibitors more equally distribute the transport burden along the nephron and may mimic systemic hypoxia to stimulate erythropoiesis, which improves oxygen delivery to the kidney and other organs. SGLT1 inhibition improves glucose homeostasis by delaying intestinal glucose absorption and by increasing the release of gastrointestinal incretins. Combined SGLT1 and SGLT2 inhibition has additive effects on renal glucose excretion and blood glucose control. SGLT1 in the macula densa senses luminal glucose, which affects glomerular hemodynamics and has implications for blood pressure control. More studies are needed to better define the therapeutic potential of SGLT1 inhibition to protect the kidney, alone or in combination with SGLT2 inhibition.
Language	English
Publishing date	2022-06-18
Publishing country	Switzerland
Document type	Journal Article
ISSN	2673-8236
ISSN	2673-8236
DOI	10.3390/kidneydial2020032
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Book ; Online: Extracellular Nucleotides in the Regulation of Kidney Functions

Vallon, Volker / Unwin, Robert John / Kishore, Bellamkonda K / Praetorius, Helle

2015

Abstract: ATP is normally regarded as the major source of fuel for the energy-demanding processes within cells; however, ATP and other nucleotides (such as ADP, UTP, UDP) can be released from cells, where they act as autocrine or paracrine signaling molecules to ... ...

Abstract	ATP is normally regarded as the major source of fuel for the energy-demanding processes within cells; however, ATP and other nucleotides (such as ADP, UTP, UDP) can be released from cells, where they act as autocrine or paracrine signaling molecules to affect cellular and tissue functions. In response to various stimuli, ATP and other nucleotides are released from cells in a regulated fashion, either by exocytosis of nucleotide-containing vesicles, or through channels in the plasma membrane. This process occurs in virtually every organ or cell in the body. The cellular effects of these extracellular nucleotides are mediated through specific membrane receptors (P2X and P2Y). These nucleotide signals can be terminated by rapid degradation of the ligand molecules by ecto-nucleotidases (e.g., NTPDases and NPPs). Many of the molecular components essential to nucleotide signaling have been cloned and characterized in detail, and their crystal structures are beginning to emerge.- The collected data on extracellular nucleotides suggest a vivid and dynamic signaling system that is modulated by the expression and sensitivity of specific receptors on cells, and by the regulated release and extracellular degradation of ATP and other nucleotides; thus creating a microenvironment of highly regulated paracrine or autocrine control mechanisms. Within the kidney, extracellular nucleotides have emerged as potent modulators of glomerular, tubular, and microvascular functions. These functions include, but are not limited to, tubular transport of water and sodium, tubuloglomerular feedback and auto-regulation, regulation of blood pressure and the microcirculation, oxidative stress, and cell proliferation/ necrosis/apoptosis. Moreover, studies have also uncovered the interaction of nucleotide signaling with other mediators of renal function, such as vasopressin, aldosterone, nitric oxide, prostaglandins, angiotensin II, and the ATP-break down product adenosine.- These insights have provided a more comprehensive and cohesive picture of the role of extracellular nucleotides in the regulation of renal function in health and disease. The availability of transgenic mouse models of the key proteins involved in nucleotide signaling has markedly enhanced our understanding of the physiological and pathophysiological roles of the different components of the system in the kidney. Although at a preliminary stage, the pathophysiological significance of this system in the kidney holds the key for the development of an entirely new class of drugs for the treatment of disease conditions, including disorders of water and/or sodium homeostasis, hypertension, acute kidney injury, etc. Thus, the regulation of renal function by extracellular nucleotides is clearly emerging as a distinct field and discipline in renal physiology and pathophysiology that has the potential to develop new drug treatments.-
Keywords	Physiology ; Science (General)
Size	1 electronic resource (77 p.)
Publisher	Frontiers Media SA
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT020090111
ISBN	9782889195046 ; 288919504X
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Deletion of the Sodium Glucose Cotransporter 1 (Sglt-1) impairs mouse sperm movement.

Numata, September / Oishee, Mumtarin Jannat / McDermott, Jeffrey / Koepsell, Hermann / Vallon, Volker / Blanco, Gustavo

Molecular reproduction and development

2024 Volume 91, Issue 1, Page(s) e23723

Abstract: The Sodium Glucose Cotransporter Isoform 1 (Sglt-1) is a symporter that moves ... ...

Abstract	The Sodium Glucose Cotransporter Isoform 1 (Sglt-1) is a symporter that moves Na
MeSH term(s)	Animals ; Male ; Mice ; Glucose/metabolism ; Mice, Knockout ; Semen/metabolism ; Sodium-Glucose Transporter 1/genetics ; Sodium-Glucose Transporter 1/metabolism ; Sperm Capacitation/physiology ; Sperm Motility/physiology ; Spermatozoa/metabolism
Chemical Substances	Glucose (IY9XDZ35W2) ; Sodium-Glucose Transporter 1 ; Slc5a1 protein, mouse
Language	English
Publishing date	2024-01-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	20321-x
ISSN	1098-2795 ; 1040-452X
ISSN (online)	1098-2795
ISSN	1040-452X
DOI	10.1002/mrd.23723
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Article ; Online: Effects of SGLT2 inhibitor and dietary NaCl on glomerular hemodynamics assessed by micropuncture in diabetic rats.

Thomson, Scott Culver / Vallon, Volker

American journal of physiology. Renal physiology

2021 Volume 320, Issue 5, Page(s) F761–F771

Abstract: Inhibitors of the main proximal tubular Na-glucose cotransporter (SGLT2) mitigate diabetic glomerular hyperfiltration and have been approved by the United States Food and Drug Administration for slowing the progression of diabetic kidney disease. It has ... ...

Abstract	Inhibitors of the main proximal tubular Na-glucose cotransporter (SGLT2) mitigate diabetic glomerular hyperfiltration and have been approved by the United States Food and Drug Administration for slowing the progression of diabetic kidney disease. It has been proposed that SGLT2 inhibitors improve hard renal outcomes by reducing glomerular capillary pressure (PGC) via a tubuloglomerular feedback (TGF) response to a decrease in proximal reabsorption (J
MeSH term(s)	Animals ; Bridged Bicyclo Compounds, Heterocyclic/pharmacology ; Diabetes Mellitus, Experimental/chemically induced ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/physiopathology ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/physiopathology ; Diabetic Nephropathies/prevention & control ; Diet, Sodium-Restricted ; Disease Progression ; Glomerular Filtration Rate/drug effects ; Hemodynamics/drug effects ; Kidney Glomerulus/blood supply ; Male ; Punctures ; Rats, Wistar ; Renal Circulation/drug effects ; Renal Reabsorption/drug effects ; Sodium Chloride, Dietary/administration & dosage ; Sodium Chloride, Dietary/metabolism ; Sodium Chloride, Dietary/toxicity ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Streptozocin ; Rats
Chemical Substances	Bridged Bicyclo Compounds, Heterocyclic ; Sodium Chloride, Dietary ; Sodium-Glucose Transporter 2 Inhibitors ; Streptozocin (5W494URQ81) ; ertugliflozin (6C282481IP)
Language	English
Publishing date	2021-03-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00552.2020
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