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Sodium-glucose cotransport
Open accessAbstract
PURPOSE OF REVIEW: Sodium-glucose cotransporters (SGLTs) are important mediators of glucose uptake across apical cell membranes. SGLT1 mediates almost all sodium-dependent glucose uptake in the small intestine, while in the kidney SGLT2, and to a lesser extent SGLT1, account for more than 90% and nearly 3%, respectively, of glucose reabsorption from the glomerular ultrafiltrate. Although the recent availability of SGLT2 inhibitors for the treatment of diabetes mellitus has increased the number of clinical studies, this review has a focus on mechanisms contributing to the cellular regulation of SGLTs. RECENT FINDINGS: Studies have focused on the regulation of SGLT expression under different physiological/pathophysiological conditions, for example diet, age or diabetes mellitus. Several studies provide evidence of SGLT regulation via cyclic adenosine monophosphate/protein kinase A, protein kinase C, glucagon-like peptide 2, insulin, leptin, signal transducer and activator of transcription-3 (STAT3), phosphoinositide-3 kinase (PI3K)/Akt, mitogen-activated protein kinases (MAPKs), nuclear factor-kappaB (NF-kappaB), with-no-K[Lys] kinases/STE20/SPS1-related proline/alanine-rich kinase (Wnk/SPAK) and regulatory solute carrier protein 1 (RS1) pathways. SUMMARY: SGLT inhibitors are important drugs for glycemic control in diabetes mellitus. Although the contribution of SGLT1 for absorption of glucose from the intestine as well as SGLT2/SGLT1 for renal glucose reabsorption has been comprehensively defined, this review provides an up-to-date outline for the mechanistic regulation of SGLT1/SGLT2.
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“In a similar collective with canagliflozin treatment, all MASH components including fibrosis stage improved at one year of treatment compared to pre-treatment without improvement in BMI and these effects were largely maintained over a follow-up period of five years [159].”
From Obesity and MASLD: Is weight loss the (only) key to treat metabolic liver disease? (2024) · cites this paper as [159]
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Abnormal splicing of the leptin receptor in diabetic mice
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Cited by
Sorted by citations
Obesity and MASLD: Is weight loss the (only) key to treat metabolic liver disease?
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Metadata
- Authors
- Poulsen, S. B., Fenton, R. A., & Rieg, T.
- Affiliations
- Aarhus University (DK)
- University of California San Diego (US)
- Corresponding author
- Rieg, Timo
- Venue
- Current Opinion in Nephrology and Hypertension
- Published
- 2015-09
- Volume
- 24
- Issue
- 5
- Pages
- 463-469
- ISSN
- 1062-4821 (ISSN-L)
- PMC
- PMC5364028
- OpenAlex
- W2397061303
- Cited by
- 164
- References
- 4
- Citations by year
- 2026: 6 · 2025: 20 · 2024: 18 · 2023: 23 · 2022: 16 · 2021: 33 · 2020: 10 · 2019: 14 · 2018: 8 · 2017: 7 · 2016: 6 · 2015: 3
- FWCI
- 1.21
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Nephrology & Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK063491)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- sodium-glucose cotransporter, SGLT1, SGLT2, glucose reabsorption, renal glucose reabsorption, intestinal glucose absorption, SGLT2 inhibitors, diabetes mellitus, protein kinase C, glucagon-like peptide-2, insulin, leptin, STAT3, PI3K/Akt, mitogen-activated protein kinase, NF-κB, RS1, glycemic control
- MeSH terms
- Animals, Blood Glucose, Glucose, Humans, Hypoglycemic Agents, Kidney, Sodium, Sodium-Glucose Transport Proteins
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