Cardiac Glucose and Fatty Acid Transport After Experimental Mono- and Polytrauma

Lackner, Ina; Weber, Birte; Knecht, Deborah; Horst, Klemens; Relja, Borna; Gebhard, Florian; Pape, Hans-Christoph; Huber-Lang, Markus; Hildebrand, Frank; Kalbitz, Miriam

doi:10.1097/SHK.0000000000001400

by Ina Lackner, Birte Weber, Deborah Knecht, Klemens Horst, Borna Relja, Florian Gebhard, Hans-Christoph Pape, Markus Huber-Lang, Frank Hildebrand, Miriam Kalbitz

Abstract:

OBJECTIVE: The aim of this study was to define the influence of trauma on cardiac glucose and fatty acid transport. The effects were investigated in vivo in a porcine mono- and polytrauma model and in vitro in human cardiomyocytes, which were treated simultaneously with different inflammatory substances, mimicking posttraumatic inflammatory conditions. METHODS AND RESULTS: In the porcine fracture- and polytrauma model, blood glucose concentrations were measured by blood gas analysis during an observation period of 72 h. The expression of cardiac glucose and fatty acid transporters in the left ventricle was determined by RT-qPCR and immunofluorescence. Cardiac and hepatic glycogen storage was examined. Furthermore, human cardiomyocytes were exposed to a defined trauma-cocktail and the expression levels of glucose- and fatty acid transporters were determined. Early after polytrauma, hyperglycemia was observed. After 48 and 72 h, pigs with fracture- and polytrauma developed hypoglycemia. The propofol demand significantly increased posttrauma. The hepatic glycogen concentration was reduced 72 h after trauma. Cardiac glucose and fatty acid transporters changed in both trauma models in vivo as well as in vitro in human cardiomyocytes in presence of proinflammatory mediators. CONCLUSIONS: Monotrauma as well as polytrauma changed the cardiac energy transport by altering the expression of glucose and fatty acid transporters. In vitro data suggest that human cardiomyocytes shift to a state alike myocardial hibernation preferring glucose as primary energy source to maintain cardiac function.

Reference:

Cardiac Glucose and Fatty Acid Transport After Experimental Mono- and Polytrauma (Ina Lackner, Birte Weber, Deborah Knecht, Klemens Horst, Borna Relja, Florian Gebhard, Hans-Christoph Pape, Markus Huber-Lang, Frank Hildebrand, Miriam Kalbitz), In Shock (Augusta, Ga.), volume 53, 2020.

Bibtex Entry:

@article{lackner_cardiac_2020,
	title = {Cardiac {Glucose} and {Fatty} {Acid} {Transport} {After} {Experimental} {Mono}- and {Polytrauma}},
	volume = {53},
	issn = {1540-0514 1073-2322},
	doi = {10.1097/SHK.0000000000001400},
	abstract = {OBJECTIVE: The aim of this study was to define the influence of trauma on cardiac  glucose and fatty acid transport. The effects were investigated in vivo in a porcine  mono- and polytrauma model and in vitro in human cardiomyocytes, which were treated  simultaneously with different inflammatory substances, mimicking posttraumatic  inflammatory conditions. METHODS AND RESULTS: In the porcine fracture- and  polytrauma model, blood glucose concentrations were measured by blood gas analysis  during an observation period of 72 h. The expression of cardiac glucose and fatty  acid transporters in the left ventricle was determined by RT-qPCR and  immunofluorescence. Cardiac and hepatic glycogen storage was examined. Furthermore,  human cardiomyocytes were exposed to a defined trauma-cocktail and the expression  levels of glucose- and fatty acid transporters were determined. Early after  polytrauma, hyperglycemia was observed. After 48 and 72 h, pigs with fracture- and  polytrauma developed hypoglycemia. The propofol demand significantly increased  posttrauma. The hepatic glycogen concentration was reduced 72 h after trauma.  Cardiac glucose and fatty acid transporters changed in both trauma models in vivo as  well as in vitro in human cardiomyocytes in presence of proinflammatory mediators.  CONCLUSIONS: Monotrauma as well as polytrauma changed the cardiac energy transport  by altering the expression of glucose and fatty acid transporters. In vitro data  suggest that human cardiomyocytes shift to a state alike myocardial hibernation  preferring glucose as primary energy source to maintain cardiac function.},
	language = {eng},
	number = {5},
	journal = {Shock (Augusta, Ga.)},
	author = {Lackner, Ina and Weber, Birte and Knecht, Deborah and Horst, Klemens and Relja, Borna and Gebhard, Florian and Pape, Hans-Christoph and Huber-Lang, Markus and Hildebrand, Frank and Kalbitz, Miriam},
	month = may,
	year = {2020},
	pmid = {31313740},
	pages = {620--629}
}