Correspondence  |   March 2019
Metabolite Palmitoylcarnitine Mediates Intralipid Cardioprotection Rather Than Membrane Receptors
Author Notes
  • University of Alberta, Edmonton, Alberta, Canada (M.Z.). michael.zaugg@ualberta.ca
  • (Accepted for publication November 16, 2018.)
    (Accepted for publication November 16, 2018.)×
Article Information
Correspondence
Correspondence   |   March 2019
Metabolite Palmitoylcarnitine Mediates Intralipid Cardioprotection Rather Than Membrane Receptors
Anesthesiology 3 2019, Vol.130, 518-519. doi:10.1097/ALN.0000000000002565
Anesthesiology 3 2019, Vol.130, 518-519. doi:10.1097/ALN.0000000000002565
We read with interest the article by Umar et al.1  on Intralipid-induced cardioprotection and the potential mechanistic involvement of the G-protein-coupled receptor 40 (GPCR40), now officially named Free Fatty Acid Receptor 1 (FFA1).2  Based on the abolished Intralipid-induced postischemic functional recovery in Langendorff-perfused mouse hearts subjected to ischemia-reperfusion and treated with Intralipid postconditioning in the presence of GW1100 (a noncompetitive FFA1 antagonist), the authors concluded that activation of FFA1 mediates Intralipid-induced cardioprotection against ischemia-reperfusion injury. We have concerns with their conclusions because of several limitations in their experimental design and methodologic approach.
First, immunoblots and immunostaining as presented do not show positive and negative controls. Although FFA1 messenger RNA has been previously detected in both murine3  and human4  cardiac tissue, its expression levels are very low. Thus, positive and negative controls are required to ultimately prove the presence of the FFA1 protein in cardiomyocytes. Moreover, no data demonstrate that FFA1 is functional in cardiomyocytes and activated by agonists.