Preserved protein synthesis in the heart in response to acute fasting and chronic food restriction despite reductions in liver and skeletal muscle. Am J Physiol 295:E216-E222

Department of Nutrition, Case Western Reserve University School of Medicine, 10900 Euclid Ave., Cleveland, OH 44106, USA.
AJP Endocrinology and Metabolism (Impact Factor: 4.09). 08/2008; 295(1):E216-22. DOI: 10.1152/ajpendo.00545.2007
Source: PubMed

ABSTRACT Whole body protein synthesis is reduced during the fed-to-fasted transition and in cases of chronic dietary restriction; however, less is known about tissue-specific alterations. We have assessed the extent to which protein synthesis in cardiac muscle responds to dietary perturbations compared with liver and skeletal muscle by applying a novel (2)H(2)O tracer method to quantify tissue-specific responses of protein synthesis in vivo. We hypothesized that protein synthesis in cardiac muscle would be unaffected by acute fasting or food restriction, whereas protein synthesis in the liver and gastrocnemius muscle would be reduced when there is a protein-energy deficit. We found that, although protein synthesis in liver and gastrocnemius muscle was significantly reduced by acute fasting, there were no changes in protein synthesis in the left ventricle of the heart for either the total protein pool or in isolated mitochondrial or cytosolic compartments. Likewise, a chronic reduction in calorie intake, induced by food restriction, did not affect protein synthesis in the heart, whereas protein synthesis in skeletal muscle and liver was decreased. The later observations are supported by changes in the phosphorylation state of two critical mediators of protein synthesis (4E-BP1 and eIF2alpha) in the respective tissues. We conclude that cardiac protein synthesis is maintained in cases of nutritional perturbations, in strong contrast to liver and gastrocnemius muscle, where protein synthesis is decreased by acute fasting or chronic food restriction.

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Available from: Yi Li, May 14, 2015
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    • "Liver and myocardium tissues have different rate of protein synthesis, being higher in hepatocytes, which are able to produce elevated levels of secretory proteins, than in myocardium. However, while the liver can regulate protein synthesis and inhibition according to its own physiological needs and energy demands, the myocardium is resistant to suppression of protein synthesis [35]. The upregulation of the UPR markers along the PERK-eIF2α axis as CHOP, GADD34 and ATF4, although significant, is low when compared with in vitro studies where cell cultures were exposed to anoxia or severe hypoxia. "
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