Manoj Gandhi

Edmonton, AB, Canada

Last Updated: 09/26/2026

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Found 14 publications

The GLP-1 Receptor Agonist Liraglutide Increases Myocardial Glucose Oxidation Rates via Indirect Mechanisms and Mitigates Experimental Diabetic Cardiomyopathy.

The GLP-1 Receptor Agonist Liraglutide Increases Myocardial Glucose Oxidation Rates via Indirect Mechanisms and Mitigates Experimental Diabetic Cardiomyopathy.

Journal: The Canadian journal of cardiology
Published: July 30, 2019

Cardiac-Specific Deletion of Pyruvate Dehydrogenase Impairs Glucose Oxidation Rates and Induces Diastolic Dysfunction.

Cardiac-Specific Deletion of Pyruvate Dehydrogenase Impairs Glucose Oxidation Rates and Induces Diastolic Dysfunction.

Journal: Frontiers in cardiovascular medicine
Published: January 14, 2018

Differential Effects of Anesthetics and Opioid Receptor Activation on Cardioprotection Elicited by Reactive Oxygen Species-Mediated Postconditioning in Sprague-Dawley Rat Hearts.

Differential Effects of Anesthetics and Opioid Receptor Activation on Cardioprotection Elicited by Reactive Oxygen Species-Mediated Postconditioning in Sprague-Dawley Rat Hearts.

Journal: Anesthesia and analgesia
Published: December 20, 2017

Alterations in fatty acid metabolism and sirtuin signaling characterize early type-2 diabetic hearts of fructose-fed rats.

Alterations in fatty acid metabolism and sirtuin signaling characterize early type-2 diabetic hearts of fructose-fed rats.

Journal: Physiological reports
Published: June 27, 2017

FoxO1 regulates myocardial glucose oxidation rates via transcriptional control of pyruvate dehydrogenase kinase 4 expression.

FoxO1 regulates myocardial glucose oxidation rates via transcriptional control of pyruvate dehydrogenase kinase 4 expression.

Journal: American journal of physiology. Heart and circulatory physiology
Published: March 29, 2017

Postconditioning with Intralipid emulsion protects against reperfusion injury in post-infarct remodeled rat hearts by activation of ROS-Akt/Erk signaling.

Postconditioning with Intralipid emulsion protects against reperfusion injury in post-infarct remodeled rat hearts by activation of ROS-Akt/Erk signaling.

Journal: Translational research : the journal of laboratory and clinical medicine
Published: January 18, 2017

Hearts lacking plasma membrane KATP channels display changes in basal aerobic metabolic substrate preference and AMPK activity.

Hearts lacking plasma membrane KATP channels display changes in basal aerobic metabolic substrate preference and AMPK activity.

Journal: American journal of physiology. Heart and circulatory physiology
Published: September 09, 2016

Myocardial mechanical dysfunction following endotoxemia: role of changes in energy substrate metabolism.

Myocardial mechanical dysfunction following endotoxemia: role of changes in energy substrate metabolism.

Journal: Basic research in cardiology
Published: September 10, 2015

Propofol (Diprivan®) and Intralipid® exacerbate insulin resistance in type-2 diabetic hearts by impairing GLUT4 trafficking.

Propofol (Diprivan®) and Intralipid® exacerbate insulin resistance in type-2 diabetic hearts by impairing GLUT4 trafficking.

Journal: Anesthesia and analgesia
Published: December 02, 2014

Loss of Intralipid®- but not sevoflurane-mediated cardioprotection in early type-2 diabetic hearts of fructose-fed rats: importance of ROS signaling.

Loss of Intralipid®- but not sevoflurane-mediated cardioprotection in early type-2 diabetic hearts of fructose-fed rats: importance of ROS signaling.

Journal: PloS one
Published: May 02, 2014

The mechanism of Intralipid®-mediated cardioprotection complex IV inhibition by the active metabolite, palmitoylcarnitine, generates reactive oxygen species and activates reperfusion injury salvage kinases.

The mechanism of Intralipid®-mediated cardioprotection complex IV inhibition by the active metabolite, palmitoylcarnitine, generates reactive oxygen species and activates reperfusion injury salvage kinases.

Journal: PloS one
Published: November 04, 2013

Pressure-overload-induced heart failure induces a selective reduction in glucose oxidation at physiological afterload.

Pressure-overload-induced heart failure induces a selective reduction in glucose oxidation at physiological afterload.

Journal: Cardiovascular research
Published: December 22, 2012
Showing 1-12 of 14

Last Updated: 09/26/2026