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SGLT2 deletion improves glucose homeostasis and preserves pancreatic beta-cell function

Jurczak, Michael J
Lee, Hui-Young
Birkenfeld, Andreas L
Frederick, David W
Pongratz, Rebecca L
Zhao, Xiaoxian
Moeckel, Gilbert W
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Published in Diabetes. 2011, vol. 60, no. 3, p. 890-8
Abstract Inhibition of the Na(+)-glucose cotransporter type 2 (SGLT2) is currently being pursued as an insulin-independent treatment for diabetes; however, the behavioral and metabolic consequences of SGLT2 deletion are unknown. Here, we used a SGLT2 knockout mouse to investigate the effect of increased renal glucose excretion on glucose homeostasis, insulin sensitivity, and pancreatic β-cell function.
Keywords Analysis of VarianceAnimalsApoptosis/geneticsDietary Fats/metabolismGlucose/metabolismHomeostasis/geneticsHyperglycemia/genetics/metabolism/physiopathologyInsulin/bloodInsulin ResistanceInsulin-Secreting Cells/metabolismIslets of Langerhans/metabolism/physiopathologyKidney/metabolismMiceMiceKnockoutObesity/genetics/metabolism/physiopathologySodium-Glucose Transporter 2/genetics/metabolism
PMID: 21357472
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JURCZAK, Michael J et al. SGLT2 deletion improves glucose homeostasis and preserves pancreatic beta-cell function. In: Diabetes, 2011, vol. 60, n° 3, p. 890-8. doi: 10.2337/db10-1328

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Deposited on : 2017-12-21

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