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Cited by 395Diabetes Treatment and ManagementDiabetes Management and ResearchChronic Kidney Disease and Diabetes

The DOI matches its Crossref record; 93 of the 93 references it cites were found in a registry or an index.

Probing SGLT2 as a therapeutic target for diabetes: Basic physiology and consequences

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Gallo, Linda A, Wright, Ernest M, Vallon, Volker·2015·Diabetes and Vascular Disease Research
DOI 10.1177/1479164114561992PMC PMC5886707
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Abstract

Traditional treatments for type 1 and type 2 diabetes are often associated with side effects, including weight gain and hypoglycaemia that may offset the benefits of blood glucose lowering. The kidneys filter and reabsorb large amounts of glucose, and urine is almost free of glucose in normoglycaemia. The sodium-dependent glucose transporter (SGLT)-2 in the early proximal tubule reabsorbs the majority of filtered glucose. Remaining glucose is reabsorbed by SGLT1 in the late proximal tubule. Diabetes enhances renal glucose reabsorption by increasing the tubular glucose load and the expression of SGLT2 (as shown in mice), which maintains hyperglycaemia. Inhibitors of SGLT2 enhance urinary glucose excretion and thereby lower blood glucose levels in type 1 and type 2 diabetes. The load-dependent increase in SGLT1-mediated glucose reabsorption explains why SGLT2 inhibitors in normoglycaemic conditions enhance urinary glucose excretion to only ~50% of the filtered glucose. The role of SGLT1 in both renal and intestinal glucose reabsorption provides a rationale for the development of dual SGLT1/2 inhibitors. SGLT2 inhibitors lower blood glucose levels independent of insulin and induce pleiotropic actions that may be relevant in the context of lowering cardiovascular risk. Ongoing long-term clinical studies will determine whether SGLT2 inhibitors have a safety profile and exert cardiovascular benefits that are superior to traditional agents.

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Research works printed but not linked: 6

  1. International Diabetes Federation, 2013, IDF diabetes Atlas
  2. Barfuss DW, 1981, Am J Physiol, 241, F322
  3. Turner RJ, 1982, Am J Physiol, 242, F406
  4. Wells RG, 1992, Am J Physiol, 263, F459
  5. Petersen C., 1835, Annales Académie Science Française, 15, 178
  6. von Mering J., 1886, Centralbl Med Wiss, 531

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Metadata

Authors
Gallo, L. A., Wright, E. M., & Vallon, V.
Affiliations
  • Translational Research Institute (AU)
  • University of California, Los Angeles (US)
  • University of California San Diego (US)
ORCID
Venue
Diabetes and Vascular Disease Research
Publisher
SAGE Publications
Published
2015-01-23
Volume
12
Issue
2
Pages
78-89
ISSN
  • 1479-1641 (ISSN-L)
  • 1752-8984
DOI
10.1177/1479164114561992
PMC
PMC5886707
OpenAlex
W2142065502
Cited by
395
References
92
Citations by year
2026: 15 · 2025: 26 · 2024: 45 · 2023: 33 · 2022: 45 · 2021: 60 · 2020: 47 · 2019: 30 · 2018: 36 · 2017: 20 · 2016: 19 · 2015: 16
FWCI
4.56
Type
journal article
Language
en
Open access
Licence
journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations
  • Diabetes and Vascular Disease Research (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
  • National Heart, Lung, and Blood Institute (R01HL094728)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK19567, R01 DK-56248, R01DK019567, P30DK079337, R01DK056248)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
Keywords
SGLT2 inhibitors, type 1 diabetes, type 2 diabetes, renal glucose reabsorption, proximal tubule, SGLT1, urinary glucose excretion, hyperglycemia, cardiovascular risk, drug safety, insulin-independent glucose lowering
MeSH terms
Sodium-Glucose Transporter 2 Inhibitors, Animals, Blood Glucose, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Humans, Hypoglycemic Agents, Kidney Tubules, Proximal, Treatment Outcome, Sodium-Glucose Transporter 1, Sodium-Glucose Transporter 2, Molecular Targeted Therapy, Renal Reabsorption, Renal Elimination

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