Is it time to think about the sodium glucose co‐transporter 2 sympathetically?
Open accessAbstract
Disturbances in glucose homeostasis are a key feature of the metabolic syndrome and type 2 diabetes. Renal glucose reabsorption is an important factor in glycaemic control. Glucose reabsorption in the proximal tubules is mediated by the sodium glucose co‐transporter 2. The capacity for glucose reabsorption is increased in type 2 diabetes and contributes significantly to hyperglycaemia and impaired glucose control. Understanding the mechanisms underpinning the regulation of the sodium glucose co‐transporter 2 is therefore of high clinical relevance. However, despite recent advances in the field and the availability of pharmacological inhibitors of this glucose transporter for the treatment of type 2 diabetes, the mechanisms that regulate sodium glucose co‐transporter 2 expression are not fully understood. The sympathetic nervous system is an important modulator of glucose homeostasis, and sympathetic hyperactivity is a characteristic feature of obesity, the metabolic syndrome and type 2 diabetes. Sympathetic inhibition either achieved pharmacologically or by renal sympathetic denervation has been associated with improved glucose control. Importantly, sympathetic nerves innervate the proximal tubules of the kidney where they have been shown to regulate the expression of other transporters such as the sodium hydrogen exchanger 3. This review aims to explore the evidence for the regulation of sodium glucose co‐transporter 2‐mediated glucose reabsorption by the sympathetic nervous system.
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Inflammation in CNS tissues enhances sympathetic outflow, increases blood pressure and SGLT-2 expression in kidney, causing hypertension or metabolic syndrome.
“Evidence from recent studies show that inflammation in the CNS tissues enhances sympathetic outflow, increases BP and SGLT-2 expression in kidney, causing hypertension or metabolic syndrome.60,61”
From <p>Dapagliflozin Activates Neurons in the Central Nervous System and Regulates Cardiovascular Activity by Inhibiting SGLT-2 in Mice</p> (2020) · cites this paper as [61]
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- Authors
- Elliott, R. H., Matthews, V. B., Rudnicka, C., & Schlaich, M. P.
- Affiliations
- The University of Western Australia (AU)
- Royal Perth Hospital (AU)
- Corresponding author
- Matthews, Vance B
- Venue
- Nephrology
- Publisher
- Wiley
- Published
- 2016-03-30
- Volume
- 21
- Issue
- 4
- Pages
- 286-294
- ISSN
- 1320-5358 (ISSN-L)
- 1440-1797
- OpenAlex
- W1878249378
- Cited by
- 23
- References
- 66
- Citations by year
- 2025: 2 · 2023: 1 · 2022: 5 · 2021: 3 · 2020: 5 · 2019: 1 · 2018: 3 · 2017: 2 · 2016: 1
- FWCI
- 0.30
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Nephrology (publishedVersion)
- PubMed (publishedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion)
- Funders
- University of Western Australia, Royal Perth Hospital (RPH)
- RPH Medical Research Foundation
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Keywords
- SGLT2, renal glucose reabsorption, proximal tubule, sympathetic nervous system, glucose homeostasis, type 2 diabetes, metabolic syndrome, obesity, renal denervation, SGLT2 inhibitors, sodium-hydrogen exchanger 3, hyperglycemia
- MeSH terms
- Sodium-Glucose Transporter 2 Inhibitors, Animals, Blood Glucose, Diabetes Mellitus, Type 2, Humans, Hypoglycemic Agents, Kidney, Sympathectomy, Sympathetic Nervous System, Sympatholytics, Sodium-Glucose Transporter 2, Renal Reabsorption
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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