Comment on: “High released lactate by epicardial fat from coronary artery disease patients is reduced by dapagliflozin treatment”

Abstract

We read with interest the article by Couselo-Seijas et al. “High released lactate by epicardial fat from coronary artery disease patients is reduced by dapagliflozin treatment” [ [1] Couselo-Seijas M. Agra-Bermejo R.M. Fernandez A.L. Martinez-Cereijo J.M. Sierra J. Soto-Perez M. Rozados-Luis A. Gonzalez-Juanatey ., J.R. Eiras S. High released lactate by epicardial fat from coronary artery disease patients is reduced by dapagliflozin treatment. Atherosclerosis. 2020; 292: 60-69 Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar ]. The use of sodium-glucose cotransporter-2 (SGLT-2) inhibitors (SGLT-2i) is gradually increasing in diabetes mellitus (DM) and heart failure treatment. Increasing pieces of novel information are added to the literature on these drugs. We strongly agree with the authors' findings. The article has led us to consider lactate levels in euglycemic (E) diabetic ketoacidosis (DKA) due to SGLT2i use, and the usefulness of metformin and SGLT-2i combination. We would like to draw attention on a few important points in this regard. High released lactate by epicardial fat from coronary artery disease patients is reduced by dapagliflozin treatmentAtherosclerosisVol. 292PreviewDapagliflozin, a sodium-glucose co-transporter 2 inhibitor, improves glucose uptake by epicardial adipose tissue (EAT). However, its metabolism might raise the lactate production and acidosis under hypoxia conditions, i.e. coronary artery disease (CAD), or lipogenesis and, in consequence, expand adipose tissue. Since lactate secreted by adipose tissue is correlated with tissue stress and inflammation, our aim was to study glucose metabolism by epicardial fat in CAD and its regulation by dapagliflozin. Full-Text PDF