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Nutrients 2016, 8(8), 499; doi:10.3390/nu8080499

Is Cancer Cachexia Attributed to Impairments in Basal or Postprandial Muscle Protein Metabolism?

1
Departments of Human Biology and Movement Sciences, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, P.O. Box 616, Maastricht 6200 MD, The Netherlands
2
Departments of Surgery, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, P.O. Box 616, Maastricht 6200 MD, The Netherlands
3
Respiratory Medicine, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, P.O. Box 616, Maastricht 6200 MD, The Netherlands
*
Author to whom correspondence should be addressed.
Received: 11 June 2016 / Revised: 3 August 2016 / Accepted: 11 August 2016 / Published: 16 August 2016
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Abstract

Cachexia is a significant clinical problem associated with very poor quality of life, reduced treatment tolerance and outcomes, and a high mortality rate. Mechanistically, any sizeable loss of skeletal muscle mass must be underpinned by a structural imbalance between muscle protein synthesis and breakdown rates. Recent data indicate that the loss of muscle mass with aging is, at least partly, attributed to a blunted muscle protein synthetic response to protein feeding. Whether such anabolic resistance is also evident in conditions where cachexia is present remains to be addressed. Only few data are available on muscle protein synthesis and breakdown rates in vivo in cachectic cancer patients. When calculating the theoretical changes in basal or postprandial fractional muscle protein synthesis and breakdown rates that would be required to lose 5% of body weight within a six-month period, we can define the changes that would need to occur to explain the muscle mass loss observed in cachectic patients. If changes in both post-absorptive and postprandial muscle protein synthesis and breakdown rates contribute to the loss of muscle mass, it would take alterations as small as 1%–2% to induce a more than 5% decline in body weight. Therefore, when trying to define impairments in basal and/or postprandial muscle protein synthesis or breakdown rates using contemporary stable isotope methodology in cancer cachexia, we need to select large homogenous groups of cancer patients (>40 patients) to allow us to measure physiological and clinically relevant differences in muscle protein synthesis and/or breakdown rates. Insight into impairments in basal or postprandial muscle protein synthesis and breakdown rates in cancer cachexia is needed to design more targeted nutritional, pharmaceutical and/or physical activity interventions to preserve skeletal muscle mass and, as such, to reduce the risk of complications, improve quality of life, and lower mortality rates during the various stages of the disease. View Full-Text
Keywords: muscle metabolism; lean body mass; nutrition; protein; FSR; FBR; postprandial; anabolic resistance muscle metabolism; lean body mass; nutrition; protein; FSR; FBR; postprandial; anabolic resistance
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Horstman, A.M.H.; Olde Damink, S.W.; Schols, A.M.W.J.; van Loon, L.J.C. Is Cancer Cachexia Attributed to Impairments in Basal or Postprandial Muscle Protein Metabolism? Nutrients 2016, 8, 499.

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