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Corrigendum Free access | 10.1172/JCI76184

Dapagliflozin improves muscle insulin sensitivity but enhances endogenous glucose production

Aurora Merovci, Carolina Solis-Herrera, Giuseppe Daniele, Roy Eldor, Teresa Vanessa Fiorentino, Devjit Tripathy, Juan Xiong, Zandra Perez, Luke Norton, Muhammad A. Abdul-Ghani, and Ralph A. DeFronzo

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Published May 1, 2014 - More info

Published in Volume 124, Issue 5 on May 1, 2014
J Clin Invest. 2014;124(5):2287–2287. https://doi.org/10.1172/JCI76184.
© 2014 The American Society for Clinical Investigation
Published May 1, 2014 - Version history
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Related article:

Dapagliflozin improves muscle insulin sensitivity but enhances endogenous glucose production
Aurora Merovci, … , Muhammad A. Abdul-Ghani, Ralph A. DeFronzo
Aurora Merovci, … , Muhammad A. Abdul-Ghani, Ralph A. DeFronzo
Research Article

Dapagliflozin improves muscle insulin sensitivity but enhances endogenous glucose production

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Abstract

Chronic hyperglycemia impairs insulin action, resulting in glucotoxicity, which can be ameliorated in animal models by inducing glucosuria with renal glucose transport inhibitors. Here, we examined whether reduction of plasma glucose with a sodium-glucose cotransporter 2 (SGLT2) inhibitor could improve insulin-mediated tissue glucose disposal in patients with type 2 diabetes. Eighteen diabetic men were randomized to receive either dapagliflozin (n = 12) or placebo (n = 6) for 2 weeks. We measured insulin-mediated whole body glucose uptake and endogenous glucose production (EGP) at baseline and 2 weeks after treatment using the euglycemic hyperinsulinemic clamp technique. Dapagliflozin treatment induced glucosuria and markedly lowered fasting plasma glucose. Insulin-mediated tissue glucose disposal increased by approximately 18% after 2 weeks of dapagliflozin treatment, while placebo-treated subjects had no change in insulin sensitivity. Surprisingly, following dapagliflozin treatment, EGP increased substantially and was accompanied by an increase in fasting plasma glucagon concentration. Together, our data indicate that reduction of plasma glucose with an agent that works specifically on the kidney to induce glucosuria improves muscle insulin sensitivity. However, glucosuria induction following SGLT2 inhibition is associated with a paradoxical increase in EGP. These results provide support for the glucotoxicity hypothesis, which suggests that chronic hyperglycemia impairs insulin action in individuals with type 2 diabetes.

Authors

Aurora Merovci, Carolina Solis-Herrera, Giuseppe Daniele, Roy Eldor, Teresa Vanessa Fiorentino, Devjit Tripathy, Juan Xiong, Zandra Perez, Luke Norton, Muhammad A. Abdul-Ghani, Ralph A. DeFronzo

×

Original citation: J Clin Invest. 2014;124(2):509–514. doi:10.1172/JCI70704.

Citation for this corrigendum: J Clin Invest. 2014;124(5):2287. doi:10.1172/JCI76184.

An authorship note and a sentence in the Acknowledgments were inadvertently omitted. The correct sentences are below.

Authorship note: Aurora Merovci and Carolina Solis-Herrera contributed equally to this work.

Acknowledgments: Ralph A. DeFronzo and Devjit Tripathy are supported by the South Texas Veterans Health Care System — Audie Murphy Division.

The authors regret the error.

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