Abstract
Glycine supplementation can protect skeletal muscles of mice from cancer-induced wasting, but the mechanisms underlying this protection are not well-understood. The aim of this study was to determine whether exogenous glycine directly protects skeletal muscle cells from wasting. C2C12 muscle cells were exposed to non-inflammatory catabolic stimuli via two models: serum withdrawal (SF) for 48 h; or incubation in HEPES buffered saline (HBS) for up to 5 h. Cells were supplemented with glycine or equimolar concentrations of L-alanine. SF- and HBS-treated myotubes (with or without L-alanine) were ~20% and ~30% smaller than control myotubes. Glycine-treated myotubes were up to 20% larger (P < 0.01) compared to cells treated with L-alanine in both models of muscle cell atrophy. The mTORC1 inhibitor rapamycin prevented the glycine-stimulated protection of myotube diameter, and glycine-stimulated S6 phosphorylation, suggesting that mTORC1 signaling may be necessary for glycine's protective effects in vitro. Increasing glycine availability may be beneficial for muscle wasting conditions associated with inadequate nutrient intake.
Highlights
The non-essential amino acid glycine is often considered biologically neutral, and not required for the regulation of protein synthesis under normal healthy conditions
Reduced intracellular levels of glycine have been reported in older individuals [1] and in mouse models of diabetes and muscular dystrophy [2, 3], suggesting that either glycine metabolism is increased during these conditions, or tissue demand exceeds dietary intake
Serum starved glycine-treated myotubes were larger (0.5 mM, 18%; 1 mM, 16%; 2.5 mM, 22%; P < 0.01) compared with serum for h (SF) containing L-alanine-treated myotubes (SF ALA+)
Summary
The non-essential amino acid glycine is often considered biologically neutral, and not required for the regulation of protein synthesis under normal healthy conditions. Our observations in several mouse models of muscle wasting showed that supplementation with glycine preserved muscle mass and metabolic function in a range of conditions where the anabolic response to nutrition was altered [4,5,6]. Dietary glycine supplementation in a mouse model of caloric restriction reduced adiposity (whole-body and epididymal fat mass) and preserved lean mass and muscle mass [5]. Together, these data revealed a positive effect of glycine treatment on skeletal muscle protein metabolism, mass and function during muscle wasting conditions. We tested the hypothesis that glycine would directly attenuate myotube wasting in an mTORC1-dependent manner
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