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Perspectives in Diabetes

Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans

  1. Muhammad A. Abdul-Ghani⇑,
  2. Ralph A. DeFronzo and
  3. Luke Norton
  1. Division of Diabetes, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
  1. Corresponding author: Muhammad A. Abdul-Ghani, abdulghani{at}uthscsa.edu.
Diabetes 2013 Oct; 62(10): 3324-3328. https://doi.org/10.2337/db13-0604
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    FIG. 1.

    Renal glucose reabsorption in the proximal tubule in NGT individuals under physiologic conditions.

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    FIG. 2.

    Relationship between glucose filtration load (GFL) and UGE and the plasma glucose concentration under physiologic conditions and during maximal inhibition of SGLT2.

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    FIG. 3.

    Renal glucose reabsorption in the proximal tubule in NGT individuals under complete SGLT2 inhibition.

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    FIG. 4.

    Predicted relationship between the fraction of filtered glucose excreted in the urine and the plasma glucose concentration during maximal inhibition of SGLT2. The maximal SGLT1 transport capacity was estimated at 120 g/day (see text for details). GFL, glucose filtration load.

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    FIG. 5.

    Predicted fold increase in the level of glucosuria produced by SGLT2 inhibitors in relation to the percent inhibition of SGLT1 activity.

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October 2013, 62(10)
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Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans
Muhammad A. Abdul-Ghani, Ralph A. DeFronzo, Luke Norton
Diabetes Oct 2013, 62 (10) 3324-3328; DOI: 10.2337/db13-0604

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Novel Hypothesis to Explain Why SGLT2 Inhibitors Inhibit Only 30–50% of Filtered Glucose Load in Humans
Muhammad A. Abdul-Ghani, Ralph A. DeFronzo, Luke Norton
Diabetes Oct 2013, 62 (10) 3324-3328; DOI: 10.2337/db13-0604
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