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Response to: Correspondence on “Sodium-glucose co-transporter 2 inhibitor therapy: mechanisms of action in heart failure” by Yalta et al
  1. Shruti S Joshi1,
  2. Trisha Singh1,
  3. Jagdeep Singh2,
  4. David E Newby1
  1. 1 Centre for Cardiovascular Science, University of Edinburgh Division of Clinical and Surgical Sciences, Edinburgh, UK
  2. 2 Department of Cardiology, NHS Lothian, Edinburgh, UK
  1. Correspondence to Dr Shruti S Joshi, Centre for Cardiovascular Sciences, University of Edinburgh Division of Clinical and Surgical Sciences, Edinburgh, UK; sjoshi{at}ed.ac.uk

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The Authors’ reply

We would like to thank Yalta et al 1 for their interest in our review. We share their enthusiasm for the potential metabolic benefits of sodium-glucose co-transporter 2 (SGLT-2) inhibition.

We agree with Yalta et al that in patients with type 2 diabetes or heart failure, there is dysregulated fatty acid oxidation and impaired glucose uptake causing myocardial dysfunction. In this setting of restricted fuel selection and low energetic reserve, ketone bodies are a super-fuel producing Adenosine triphosphate (ATP) more efficiently than free fatty acids or glucose, which usually serve as fuels for …

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Footnotes

  • Contributors SSJ drafted the initial manuscript with contributions from all authors.

  • Funding The authors are supported by British Heart Foundation (SJ, RE/18/5/3 and FS/CRTF/20/24087; TS RE/18/5/3; DEN, CH/09/002, RG16/10/3, RE18/5/3), Medical Research Council (TS, MR/T029153/1), Wellcome Trust (DEN, WT103782AIA) and an investigator initiated award from AstraZeneca (SJ, SER-19-20118)

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Commissioned; internally peer reviewed.

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