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Moderate ethanol administration accentuates cardiomyocyte contractile dysfunction and mitochondrial injury in high fat diet-induced obesity.
Toxicol Lett. 2015 Mar 18; 233(3):267-77.TL

Abstract

Light to moderate drinking confers cardioprotection although it remains unclear with regards to the role of moderate drinking on cardiac function in obesity. This study was designed to examine the impact of moderate ethanol intake on myocardial function in high fat diet intake-induced obesity and the mechanism(s) involved with a focus on mitochondrial integrity. C57BL/6 mice were fed low or high fat diet for 16 weeks prior to ethanol challenge (1g/kg/d for 3 days). Cardiac contractile function, intracellular Ca(2+) homeostasis, myocardial histology, and mitochondrial integrity [aconitase activity and the mitochondrial proteins SOD1, UCP-2 and PPARγ coactivator 1α (PGC-1α)] were assessed 24h after the final ethanol challenge. Fat diet intake compromised cardiomyocyte contractile and intracellular Ca(2+) properties (depressed peak shortening and maximal velocities of shortening/relengthening, prolonged duration of relengthening, dampened intracellular Ca(2+) rise and clearance without affecting duration of shortening). Although moderate ethanol challenge failed to alter cardiomyocyte mechanical property under low fat diet intake, it accentuated high fat diet intake-induced changes in cardiomyocyte contractile function and intracellular Ca(2+) handling. Moderate ethanol challenge failed to affect fat diet intake-induced cardiac hypertrophy as evidenced by H&E staining. High fat diet intake reduced myocardial aconitase activity, downregulated levels of mitochondrial protein UCP-2, PGC-1α, SOD1 and interrupted intracellular Ca(2+) regulatory proteins, the effect of which was augmented by moderate ethanol challenge. Neither high fat diet intake nor moderate ethanol challenge affected protein or mRNA levels as well as phosphorylation of Akt and GSK3β in mouse hearts. Taken together, our data revealed that moderate ethanol challenge accentuated high fat diet-induced cardiac contractile and intracellular Ca(2+) anomalies as well as mitochondrial injury.

Authors+Show Affiliations

Department of Orthopedics, Chinese PLA General Hospital, Beijing 100853, PR China.Wound Healing and Cell Biology Laboratory, The First Affiliated Hospital, Chinese PLA General Hospital, Beijing 100853, PR China.School of Pharmacy, University of Wyoming, Laramie, WY 82071, USA.University of North Dakota School of Medicine, Grand Forks, ND 58201, USA.Department of Civil and Architectural Engineering, University of Wyoming, Laramie, WY 82071, USA.University of North Dakota School of Medicine, Grand Forks, ND 58201, USA.Cardiology Department, Tang Du Hospital, Xi'an, Shaanxi 710038, PR China. Electronic address: lxhlyh@126.com.School of Pharmacy, University of Wyoming, Laramie, WY 82071, USA. Electronic address: jren@uwyo.edu.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

25549548

Citation

Yuan, Fang, et al. "Moderate Ethanol Administration Accentuates Cardiomyocyte Contractile Dysfunction and Mitochondrial Injury in High Fat Diet-induced Obesity." Toxicology Letters, vol. 233, no. 3, 2015, pp. 267-77.
Yuan F, Lei Y, Wang Q, et al. Moderate ethanol administration accentuates cardiomyocyte contractile dysfunction and mitochondrial injury in high fat diet-induced obesity. Toxicol Lett. 2015;233(3):267-77.
Yuan, F., Lei, Y., Wang, Q., Esberg, L. B., Huang, Z., Scott, G. I., Li, X., & Ren, J. (2015). Moderate ethanol administration accentuates cardiomyocyte contractile dysfunction and mitochondrial injury in high fat diet-induced obesity. Toxicology Letters, 233(3), 267-77. https://doi.org/10.1016/j.toxlet.2014.12.018
Yuan F, et al. Moderate Ethanol Administration Accentuates Cardiomyocyte Contractile Dysfunction and Mitochondrial Injury in High Fat Diet-induced Obesity. Toxicol Lett. 2015 Mar 18;233(3):267-77. PubMed PMID: 25549548.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Moderate ethanol administration accentuates cardiomyocyte contractile dysfunction and mitochondrial injury in high fat diet-induced obesity. AU - Yuan,Fang, AU - Lei,Yonghong, AU - Wang,Qiurong, AU - Esberg,Lucy B, AU - Huang,Zaixing, AU - Scott,Glenda I, AU - Li,Xue, AU - Ren,Jun, Y1 - 2014/12/27/ PY - 2014/06/24/received PY - 2014/12/15/revised PY - 2014/12/23/accepted PY - 2015/1/1/entrez PY - 2015/1/1/pubmed PY - 2015/4/24/medline KW - Cardiomyocyte shortening KW - Ethanol KW - Intracellular Ca(2+) transient KW - Mitochondria KW - Obesity SP - 267 EP - 77 JF - Toxicology letters JO - Toxicol. Lett. VL - 233 IS - 3 N2 - Light to moderate drinking confers cardioprotection although it remains unclear with regards to the role of moderate drinking on cardiac function in obesity. This study was designed to examine the impact of moderate ethanol intake on myocardial function in high fat diet intake-induced obesity and the mechanism(s) involved with a focus on mitochondrial integrity. C57BL/6 mice were fed low or high fat diet for 16 weeks prior to ethanol challenge (1g/kg/d for 3 days). Cardiac contractile function, intracellular Ca(2+) homeostasis, myocardial histology, and mitochondrial integrity [aconitase activity and the mitochondrial proteins SOD1, UCP-2 and PPARγ coactivator 1α (PGC-1α)] were assessed 24h after the final ethanol challenge. Fat diet intake compromised cardiomyocyte contractile and intracellular Ca(2+) properties (depressed peak shortening and maximal velocities of shortening/relengthening, prolonged duration of relengthening, dampened intracellular Ca(2+) rise and clearance without affecting duration of shortening). Although moderate ethanol challenge failed to alter cardiomyocyte mechanical property under low fat diet intake, it accentuated high fat diet intake-induced changes in cardiomyocyte contractile function and intracellular Ca(2+) handling. Moderate ethanol challenge failed to affect fat diet intake-induced cardiac hypertrophy as evidenced by H&E staining. High fat diet intake reduced myocardial aconitase activity, downregulated levels of mitochondrial protein UCP-2, PGC-1α, SOD1 and interrupted intracellular Ca(2+) regulatory proteins, the effect of which was augmented by moderate ethanol challenge. Neither high fat diet intake nor moderate ethanol challenge affected protein or mRNA levels as well as phosphorylation of Akt and GSK3β in mouse hearts. Taken together, our data revealed that moderate ethanol challenge accentuated high fat diet-induced cardiac contractile and intracellular Ca(2+) anomalies as well as mitochondrial injury. SN - 1879-3169 UR - https://www.unboundmedicine.com/medline/citation/25549548/Moderate_ethanol_administration_accentuates_cardiomyocyte_contractile_dysfunction_and_mitochondrial_injury_in_high_fat_diet_induced_obesity_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0378-4274(14)01525-2 DB - PRIME DP - Unbound Medicine ER -