ArticleJournal of the American Society of Nephrology : JASN2011
The Sweet Pee model for Sglt2 mutation.
Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 73 citations in OpenAlex.
- Interaction Between the Sodium-Glucose-Linked Transporter 2 Inhibitor Dapagliflozin and the Loop Diuretic Bumetanide in Normal Human Subjects.Journal of the American Heart Association · 2018Trial
- SGLT2 inhibition protects kidney function by SAM-dependent epigenetic repression of inflammatory genes under metabolic stress.The Journal of clinical investigation · 2025Article
- Megalin Knockout Reduces SGLT2 Expression and Sensitizes to Western Diet-induced Kidney Injury.Function (Oxford, England) · 2024Article
- Mouse Models with SGLT2 Mutations: Toward Understanding the Role of SGLT2 beyond Glucose Reabsorption.International journal of molecular sciences · 2023Review
- Sodium Glucose Cotransporter-2 Inhibitors: Spotlight on Favorable Effects on Clinical Outcomes beyond Diabetes.International journal of molecular sciences · 2022Review
- Article
- Impact of an SGLT2-loss of function mutation on renal architecture, histology, and glucose homeostasis.Cell and tissue research · 2021Article
- Article
- Hypomagnesaemia and its determinants in a contemporary primary care cohort of persons with type 2 diabetes.Endocrine · 2020Observational
- Mineral and Electrolyte Disorders With SGLT2i Therapy.JBMR plus · 2019Review
- Tubular Deficiency of Heterogeneous Nuclear Ribonucleoprotein F Elevates Systolic Blood Pressure and Induces Glycosuria in Mice.Scientific reports · 2019Article
- Diabetes pharmacotherapy and effects on the musculoskeletal system.Diabetes/metabolism research and reviews · 2019Review
- A model of calcium transport and regulation in the proximal tubule.American journal of physiology. Renal physiology · 2018Article
- Urine: Waste product or biologically active tissue?Neurourology and urodynamics · 2018Article
- Modelling diabetic nephropathy in mice.Nature reviews. Nephrology · 2018Review
- The next generation of therapeutics for chronic kidney disease.Nature reviews. Drug discovery · 2016Review
- A comprehensive review of the pharmacodynamics of the SGLT2 inhibitor empagliflozin in animals and humans.Naunyn-Schmiedeberg's archives of pharmacology · 2015 · on this mapReview
- Probing SGLT2 as a therapeutic target for diabetes: basic physiology and consequences.Diabetes & vascular disease research · 2015 · on this mapReview
- SGLT2 inhibitor empagliflozin reduces renal growth and albuminuria in proportion to hyperglycemia and prevents glomerular hyperfiltration in diabetic Akita mice.American journal of physiology. Renal physiology · 2014 · on this mapArticle
- Increase in SGLT1-mediated transport explains renal glucose reabsorption during genetic and pharmacological SGLT2 inhibition in euglycemia.American journal of physiology. Renal physiology · 2014Article
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15 authors at 6 institutions in 2 countries.
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Abstract
Inhibiting renal glucose transport is a potential pharmacologic approach to treat diabetes. The renal tubular sodium-glucose transporter 2 (SGLT2) reabsorbs approximately 90% of the filtered glucose load. An animal model with sglt2 dysfunction could provide information regarding the potential long-term safety and efficacy of SGLT2 inhibitors, which are currently under clinical investigation. Here, we describe Sweet Pee, a mouse model that carries a nonsense mutation in the Slc5a2 gene, which results in the loss of sglt2 protein function. The phenotype of Sweet Pee mutants was remarkably similar to patients with mutations in the Scl5a2 gene. The Sweet Pee mutants had improved glucose tolerance, higher urinary excretion of calcium and magnesium, and growth retardation. Renal physiologic studies demonstrated a prominent distal osmotic diuresis without enhanced natriuresis. Sweet Pee mutants did not exhibit increased KIM-1 or NGAL, markers of acute tubular injury. After induction of diabetes, Sweet Pee mice had better overall glycemic control than wild-type control mice, but had a higher risk for infection and an increased mortality rate (70% in homozygous mutants versus 10% in controls at 20 weeks). In summary, the Sweet Pee model allows study of the long-term benefits and risks associated with inhibition of SGLT2 for the management of diabetes. Our model suggests that inhibiting SGLT2 may improve glucose control but may confer increased risks for infection, malnutrition, volume contraction, and mortality.
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