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Interaction Between High‐Fat Diet and Alcohol Dehydrogenase on Ethanol‐Elicited Cardiac Depression in Murine Myocytes

Interaction Between High‐Fat Diet and Alcohol Dehydrogenase on Ethanol‐Elicited Cardiac... Objective: Consumption of high‐fat diet and alcohol is associated with obesity, leading to enhanced morbidity and mortality. This study was designed to examine the interaction between high‐fat diet and the alcohol metabolizing enzyme alcohol dehydrogenase (ADH) on ethanol‐induced cardiac depression. Research Methods and Procedures: Mechanical and intracellular Ca2+ properties were measured in cardiomyocytes from ADH transgenic and Friend Virus‐B type (FVB) mice fed a low‐ or high‐fat diet for 16 weeks. Expression of protein kinase B (Akt) and Foxo3a, two proteins essential for cardiac survival, was evaluated by Western blot. Cardiac damage was determined by carbonyl formation. Results: High fat but not ADH induced obesity without hyperglycemia or hypertension, prolonged time‐to‐90% relengthening (TR90), and depressed peak shortening (PS) and maximal velocity of shortening/relengthening (± dL/dt) without affecting intracellular Ca2+ properties. Ethanol suppressed PS and intracellular Ca2+ rise in low‐fat‐fed FVB mouse cardiomyocytes. ADH but not high‐fat diet shifted the threshold of ethanol‐induced inhibition of PS and ± dL/dt to lower levels. The amplitude of ethanol‐induced cardiac depression was greater in the high‐fat but not the ADH group without additive effects. Ethanol down‐ and up‐regulated Akt and Foxo3a expression, respectively, and depressed intracellular Ca2+ rise, the effects of which were exaggerated by ADH, high‐fat, or both. High‐fat diet, but not ADH, enhanced Foxo3a expression and carbonyl content in non‐ethanol‐treated mice. Ethanol challenge significantly enhanced protein carbonyl formation, with the response being augmented by ADH, high‐fat, or both. Discussion: Our data suggest that high‐fat diet and ADH transgene may exaggerate ethanol‐induced cardiac depression and protein damage in response to ethanol. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Obesity Wiley

Interaction Between High‐Fat Diet and Alcohol Dehydrogenase on Ethanol‐Elicited Cardiac Depression in Murine Myocytes

Ren, Jun
Obesity , Volume 15 (12) – Dec 1, 2007
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References (37)

Publisher
Wiley
Copyright
2007 North American Association for the Study of Obesity (NAASO)
ISSN
1930-7381
eISSN
1930-739X
DOI
10.1038/oby.2007.350
pmid
18198301
Publisher site
See Article on Publisher Site

Abstract

Objective: Consumption of high‐fat diet and alcohol is associated with obesity, leading to enhanced morbidity and mortality. This study was designed to examine the interaction between high‐fat diet and the alcohol metabolizing enzyme alcohol dehydrogenase (ADH) on ethanol‐induced cardiac depression. Research Methods and Procedures: Mechanical and intracellular Ca2+ properties were measured in cardiomyocytes from ADH transgenic and Friend Virus‐B type (FVB) mice fed a low‐ or high‐fat diet for 16 weeks. Expression of protein kinase B (Akt) and Foxo3a, two proteins essential for cardiac survival, was evaluated by Western blot. Cardiac damage was determined by carbonyl formation. Results: High fat but not ADH induced obesity without hyperglycemia or hypertension, prolonged time‐to‐90% relengthening (TR90), and depressed peak shortening (PS) and maximal velocity of shortening/relengthening (± dL/dt) without affecting intracellular Ca2+ properties. Ethanol suppressed PS and intracellular Ca2+ rise in low‐fat‐fed FVB mouse cardiomyocytes. ADH but not high‐fat diet shifted the threshold of ethanol‐induced inhibition of PS and ± dL/dt to lower levels. The amplitude of ethanol‐induced cardiac depression was greater in the high‐fat but not the ADH group without additive effects. Ethanol down‐ and up‐regulated Akt and Foxo3a expression, respectively, and depressed intracellular Ca2+ rise, the effects of which were exaggerated by ADH, high‐fat, or both. High‐fat diet, but not ADH, enhanced Foxo3a expression and carbonyl content in non‐ethanol‐treated mice. Ethanol challenge significantly enhanced protein carbonyl formation, with the response being augmented by ADH, high‐fat, or both. Discussion: Our data suggest that high‐fat diet and ADH transgene may exaggerate ethanol‐induced cardiac depression and protein damage in response to ethanol.

Journal

Obesity – Wiley

Published: Dec 1, 2007

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