Difference between revisions of "Lou 2014b PLoS One"
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{{Publication | {{Publication | ||
|title=Lou PH, Lucchinetti E, Zhang L, Affolter A, Gandhi M, Hersberger M, Warren BE, Lemieux H, Sobhi HF, Clanachan AS, Zaugg M (2014) Loss of IntralipidĀ®- but not sevoflurane-mediated cardioprotection in early type-2 diabetic hearts of fructose-fed rats: importance of ROS signaling. PLoS One 9: e104971. | |title=Lou PH, Lucchinetti E, Zhang L, Affolter A, Gandhi M, Hersberger M, Warren BE, Lemieux H, Sobhi HF, Clanachan AS, Zaugg M (2014) Loss of IntralipidĀ®- but not sevoflurane-mediated cardioprotection in early type-2 diabetic hearts of fructose-fed rats: importance of ROS signaling. PLoS One 9:e104971. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/25127027 PMID:25127027] | |||
|authors=Lou PH, Lucchinetti E, Zhang L, Affolter A, Gandhi M, Hersberger M, Warren BE, Lemieux H, Sobhi HF, Clanachan AS, Zaugg M | |authors=Lou PH, Lucchinetti E, Zhang L, Affolter A, Gandhi M, Hersberger M, Warren BE, Lemieux H, Sobhi HF, Clanachan AS, Zaugg M | ||
|year=2014 | |year=2014 | ||
|journal=PLoS One | |journal=PLoS One | ||
|abstract= | |abstract=Insulin resistance and early type-2 diabetes are highly prevalent. However, it is unknown whether IntralipidĀ® and sevoflurane protect the early diabetic heart against ischemia-reperfusion injury. | ||
Insulin resistance and early type-2 diabetes are highly prevalent. However, it is unknown whether IntralipidĀ® and sevoflurane protect the early diabetic heart against ischemia-reperfusion injury. | |||
Early type-2 diabetic hearts from Sprague-Dawley rats fed for 6 weeks with fructose were exposed to 15 min of ischemia and 30 min of reperfusion. IntralipidĀ® (1%) was administered at the onset of reperfusion. Peri-ischemic sevoflurane (2 vol.-%) served as alternative protection strategy. Recovery of left ventricular function was recorded and the activation of Akt and ERK 1/2 was monitored. Mitochondrial function was assessed by high-resolution respirometry and mitochondrial ROS production was measured by Amplex Red and aconitase activity assays. Acylcarnitine tissue content was measured and concentration-response curves of complex IV inhibition by palmitoylcarnitine were obtained. | Early type-2 diabetic hearts from Sprague-Dawley rats fed for 6 weeks with fructose were exposed to 15 min of ischemia and 30 min of reperfusion. IntralipidĀ® (1%) was administered at the onset of reperfusion. Peri-ischemic sevoflurane (2 vol.-%) served as alternative protection strategy. Recovery of left ventricular function was recorded and the activation of Akt and ERK 1/2 was monitored. Mitochondrial function was assessed by high-resolution respirometry and mitochondrial ROS production was measured by Amplex Red and aconitase activity assays. Acylcarnitine tissue content was measured and concentration-response curves of complex IV inhibition by palmitoylcarnitine were obtained. | ||
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Early type-2 diabetic hearts lose complex IV-mediated protection by IntralipidĀ® potentially due to a switch in complex IV subunit expression and increased mitochondrial uncoupling, but are amenable to complex I-mediated sevoflurane protection. | Early type-2 diabetic hearts lose complex IV-mediated protection by IntralipidĀ® potentially due to a switch in complex IV subunit expression and increased mitochondrial uncoupling, but are amenable to complex I-mediated sevoflurane protection. | ||
|keywords=Amplex Red | |||
|mipnetlab=CA Edmonton Lemieux H, CA Edmonton Zaugg M | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration, Pharmacology;toxicology | ||
|diseases=Diabetes | |||
|injuries=Ischemia-reperfusion | |||
|organism=Rat | |||
|tissues=Heart | |||
|preparations=Permeabilized tissue | |||
|couplingstates=LEAK | |||
|pathways=F, N, S, CIV | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Latest revision as of 16:49, 27 March 2018
| Lou PH, Lucchinetti E, Zhang L, Affolter A, Gandhi M, Hersberger M, Warren BE, Lemieux H, Sobhi HF, Clanachan AS, Zaugg M (2014) Loss of IntralipidĀ®- but not sevoflurane-mediated cardioprotection in early type-2 diabetic hearts of fructose-fed rats: importance of ROS signaling. PLoS One 9:e104971. |
Lou PH, Lucchinetti E, Zhang L, Affolter A, Gandhi M, Hersberger M, Warren BE, Lemieux H, Sobhi HF, Clanachan AS, Zaugg M (2014) PLoS One
Abstract: Insulin resistance and early type-2 diabetes are highly prevalent. However, it is unknown whether IntralipidĀ® and sevoflurane protect the early diabetic heart against ischemia-reperfusion injury.
Early type-2 diabetic hearts from Sprague-Dawley rats fed for 6 weeks with fructose were exposed to 15 min of ischemia and 30 min of reperfusion. IntralipidĀ® (1%) was administered at the onset of reperfusion. Peri-ischemic sevoflurane (2 vol.-%) served as alternative protection strategy. Recovery of left ventricular function was recorded and the activation of Akt and ERK 1/2 was monitored. Mitochondrial function was assessed by high-resolution respirometry and mitochondrial ROS production was measured by Amplex Red and aconitase activity assays. Acylcarnitine tissue content was measured and concentration-response curves of complex IV inhibition by palmitoylcarnitine were obtained.
IntralipidĀ® did not exert protection in early diabetic hearts, while sevoflurane improved functional recovery. Sevoflurane protection was abolished by concomitant administration of the ROS scavenger N-2-mercaptopropionyl glycine. Sevoflurane, but not IntralipidĀ® produced protective ROS during reperfusion, which activated Akt. IntralipidĀ® failed to inhibit respiratory complex IV, while sevoflurane inhibited complex I. Early diabetic hearts exhibited reduced carnitine-palmitoyl-transferase-1 activity, but palmitoylcarnitine could not rescue protection and enhance postischemic functional recovery. Cardiac mitochondria from early diabetic rats exhibited an increased content of subunit IV-2 of respiratory complex IV and of uncoupling protein-3.
Early type-2 diabetic hearts lose complex IV-mediated protection by IntralipidĀ® potentially due to a switch in complex IV subunit expression and increased mitochondrial uncoupling, but are amenable to complex I-mediated sevoflurane protection. ā¢ Keywords: Amplex Red
ā¢ O2k-Network Lab: CA Edmonton Lemieux H, CA Edmonton Zaugg M
Labels: MiParea: Respiration, Pharmacology;toxicology
Pathology: Diabetes
Stress:Ischemia-reperfusion
Organism: Rat
Tissue;cell: Heart
Preparation: Permeabilized tissue
Coupling state: LEAK
Pathway: F, N, S, CIV
HRR: Oxygraph-2k
