Université Clermont Auvergne, INRA, UNH, Unité de Nutrition Humaine, Clermont-Ferrand, France.
UMR 5200, CNRS, Université de Bordeaux, Villenave d'Ornon, France.
Mol Nutr Food Res. 2017 Nov;61(11). doi: 10.1002/mnfr.201700287. Epub 2017 Sep 12.
One strategy to manage malnutrition in older patients is to increase protein and energy intake. Here, we evaluate the influence of protein quality during refeeding on improvement in muscle protein and energy metabolism.
Twenty-month-old male rats (n = 40) were fed 50% of their spontaneous intake for 12 weeks to induce malnutrition, then refed ad libitum with a standard diet enriched with casein or soluble milk proteins (22%) for 4 weeks. A 13C-valine was infused to measure muscle protein synthesis and expression of MuRF1, and MAFbx was measured to evaluate muscle proteolysis. mTOR pathway activation and mitochondrial function were assessed in muscle. Malnutrition was associated with a decrease in body weight, fat mass, and lean mass, particularly muscle mass. Malnutrition decreased muscle mTOR pathway activation and protein FSR associated with increased MuRF1 mRNA levels, and decreased mitochondrial function. The refeeding period partially restored fat mass and lean mass. Unlike the casein diet, the soluble milk protein diet improved muscle protein metabolism and mitochondrial function in old malnourished rats.
These results suggest that providing better-quality proteins during refeeding may improve efficacy of renutrition in malnourished older patients.
管理老年患者营养不良的一种策略是增加蛋白质和能量摄入。在这里，我们评估再喂养期间蛋白质质量对改善肌肉蛋白质和能量代谢的影响。
20 月龄雄性大鼠（n = 40）喂养 50%的自发摄入量 12 周以诱导营养不良，然后用富含酪蛋白或可溶性牛奶蛋白（22%）的标准饮食自由进食 4 周。通过 13C-缬氨酸输注来测量肌肉蛋白质合成和 MuRF1 的表达，并测量 MAFbx 来评估肌肉蛋白分解。在肌肉中评估 mTOR 通路激活和线粒体功能。营养不良与体重、脂肪量和瘦体重（特别是肌肉量）减少有关。营养不良降低了肌肉 mTOR 通路的激活和与 MuRF1 mRNA 水平升高相关的蛋白质 FSR，并降低了线粒体功能。再喂养期部分恢复了脂肪量和瘦体重。与酪蛋白饮食不同，可溶性牛奶蛋白饮食改善了老年营养不良大鼠的肌肉蛋白质代谢和线粒体功能。
这些结果表明，在再喂养期间提供更好质量的蛋白质可能会提高营养不良老年患者营养恢复的效果。
