AI Article Synopsis

  • The study investigates how caloric restriction (CR) affects protein synthesis, proposing it may not increase in all tissues.
  • Researchers found no significant short-term increase in protein synthesis from feeding in CR mice compared to those on a regular diet (AL).
  • They discovered that CR suppresses mTOR signaling in the liver and heart, suggesting this may lead to lower protein synthesis despite sustained overall levels.

Article Abstract

Increased protein synthesis is proposed as a mechanism of life-span extension during caloric restriction (CR). We hypothesized that CR does not increase protein synthesis in all tissues and protein fractions and that any increased protein synthesis with CR would be due to an increased anabolic effect of feeding. We used short- (4 hours) and long-term (6 weeks) methods to measure in vivo protein synthesis in lifelong ad libitum (AL) and CR mice. We did not detect an acute effect of feeding on protein synthesis while liver mitochondrial protein synthesis was lower in CR mice versus AL mice. Mammalian target of rapamycin (mTOR) signaling was repressed in liver and heart from CR mice indicative of energetic stress and suppression of growth. Our main findings were that CR did not increase rates of mixed protein synthesis over the long term or in response to acute feeding, and protein synthesis was maintained despite decreased mTOR signaling.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3693598PMC
http://dx.doi.org/10.1093/gerona/gls219DOI Listing

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