Alcohol‐Induced Reductions in Cardiac Protein Synthesis In Vivo Are Not Ameliorated by Treatment With the Dihydropyridine Calcium Channel Blocker Amlodipine

Patel, Vinood B.; Siddiq, Tahir; Richardson, Peter J.; Preedy, Victor R.

doi:10.1111/j.1530-0277.2000.tb02045.x

Cited by 3 publications

(1 citation statement)

References 36 publications

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“…Acute alcohol intoxication also decreases global protein synthesis in heart as well as the synthetic rate for cardiac myofibrillar, non-myofibrillar and mitochondrial proteins (50, 79, 97, 111). However, in contrast to skeletal muscle, animals must often ingest alcohol for extended periods of time (at least 12–14 weeks) before decreases in myocardial protein synthesis are detected (112, 116).…”

Section: Alcoholic Myopathymentioning

confidence: 99%

Mechanisms Underlying Muscle Protein Imbalance Induced by Alcohol

Kimball¹,

Lang

2018

Annu. Rev. Nutr.

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Both acute intoxication and longer-term cumulative ingestion of alcohol negatively impact the metabolic phenotype of both skeletal and cardiac muscle, independent of overt protein calorie malnutrition, resulting in loss of skeletal muscle strength and cardiac contractility. In large part, these alcohol-induced changes are mediated by a decrease in protein synthesis that in turn is governed by impaired activity of a protein kinase, the mechanistic target of rapamycin (mTOR). Herein, we summarize recent advances in understanding mTOR signal transduction, similarities and differences between the effects of alcohol on this central metabolic controller in skeletal muscle and in the heart, and the effects of acute versus chronic alcohol intake. While alcohol-induced alterations in global proteolysis via activation of the ubiquitin-proteasome pathway are equivocal, emerging data suggest alcohol increases autophagy in muscle. Further studies are necessary to define the relative contributions of these bidirectional changes in protein synthesis and autophagy in the etiology of alcoholic myopathy in skeletal muscle and the heart.

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Section: Alcoholic Myopathymentioning

confidence: 99%

Mechanisms Underlying Muscle Protein Imbalance Induced by Alcohol

Kimball¹,

Lang

2018

Annu. Rev. Nutr.

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Cardiac-specific overexpression of catalase rescues ventricular myocytes from ethanol-induced cardiac contractile defect

Zhang

Klein

Alberle

et al. 2003

Journal of Molecular and Cellular Cardiology

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Fatty acid profile in skeletal muscle of the rat in response to acute (2.5 hours) and prolonged (6 weeks) ethanol‐dosage

et al. 2003

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We tested the hypothesis that phospholipids are altered in skeletal muscles of rats exposed to ethanol for either acute (2.5 hours) or prolonged (6 weeks) periods. In acute studies, rats were dosed with saline (0.15 mmol/l; controls) or ethanol (75 mmol/kg body weight; treated). There were four groups: (A) saline (control); (B) cyanamide (an aldehyde dehydrogenase inhibitor); (C) ethanol; and (D) cyanamide + ethanol. In prolonged studies, two groups of rats were fed liquid diets containing 35% of total dietary energy as either glucose [group (E)] or ethanol [group (F)]. At the end of the treatments, membrane phospholipids were measured in soleus (Type I fibre-predominant) and plantaris (Type II fibre-predominant) muscle. In acute studies, ethanol alone [(A) vs. (C)] and cyanamide + ethanol [(A) vs. (D)] significantly increased 18 : 2 in plantaris (p < 0.05), whereas in soleus none of the treatments had any effect on the phospholipids. In prolonged studies [(E) vs. (F)], there were decreases in 16 : 0 (p < 0.05) and 18 : 1 (p < 0.01) and increases in 18 : 2 (p < 0.001) in plantaris. In soleus, decreases in 18 : 1 (p < 0.05) and increases in 18 : 2 (p < 0.01) occurred. In conclusion, alterations in the proportions of 16 : 0, 18 : 1 and 18 : 2 provide evidence of an altered membrane domain which may contribute to the pathogenesis of alcohol-induced muscle disease. Changes due to prolonged exposure are more profound than those in acute exposure and the preferential effects in Type II plantaris may reflect the greater susceptibility of this muscle to alcohol.

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Alcohol‐Induced Reductions in Cardiac Protein Synthesis In Vivo Are Not Ameliorated by Treatment With the Dihydropyridine Calcium Channel Blocker Amlodipine

Abstract: Ethanol may affect cardiac protein synthesis independently of altered calcium entry.

Cited by 3 publications

References 36 publications

Mechanisms Underlying Muscle Protein Imbalance Induced by Alcohol

Mechanisms Underlying Muscle Protein Imbalance Induced by Alcohol

Cardiac-specific overexpression of catalase rescues ventricular myocytes from ethanol-induced cardiac contractile defect

Fatty acid profile in skeletal muscle of the rat in response to acute (2.5 hours) and prolonged (6 weeks) ethanol‐dosage

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