Gatineau Eva, Savary-Auzeloux Isabelle, Migné Carole, Polakof Sergio, Dardevet Dominique, Mosoni Laurent
National Institute of Agronomic Research, Joint Research Unit 1019 for Human Nutrition, Saint Genès Champanelle, France; and Clermont 1 University, Research and Training Unit Medicine, Joint Research Unit 1019 for Human Nutrition, Clermont-Ferrand, France.
National Institute of Agronomic Research, Joint Research Unit 1019 for Human Nutrition, Saint Genès Champanelle, France; and Clermont 1 University, Research and Training Unit Medicine, Joint Research Unit 1019 for Human Nutrition, Clermont-Ferrand, France
J Nutr. 2015 May;145(5):923-30. doi: 10.3945/jn.114.205583. Epub 2015 Mar 25.
Today, high chronic intake of added sugars is frequent, which leads to inflammation, oxidative stress, and insulin resistance. These 3 factors could reduce meal-induced stimulation of muscle protein synthesis and thus aggravate the age-related loss of muscle mass (sarcopenia).
Our aims were to determine if added sugars could accelerate sarcopenia and to assess the capacity of antioxidants and anti-inflammatory agents to prevent this.
For 5 mo, 16-mo-old male rats were starch fed (13% sucrose and 49% wheat starch diet) or sucrose fed (62% sucrose and 0% wheat starch diet) with or without rutin (5 g/kg diet), vitamin E (4 times), vitamin A (2 times), vitamin D (5 times), selenium (10 times), and zinc (+44%) (R) supplementation. We measured the evolution of body composition and inflammation, plasma insulin-like growth factor 1 (IGF-I) concentration and total antioxidant status, insulin sensitivity (oral-glucose-tolerance test), muscle weight, superoxide dismutase activity, glutathione concentration, and in vivo protein synthesis rates.
Sucrose-fed rats lost significantly more lean body mass (-8.1% vs. -5.4%, respectively) and retained more fat mass (+0.2% vs. -33%, respectively) than starch-fed rats. Final muscle mass was 11% higher in starch-fed rats than in sucrose-fed rats. Sucrose had little effect on inflammation, oxidative stress, and plasma IGF-I concentration but reduced the insulin sensitivity index (divided by 2). Meal-induced stimulation of muscle protein synthesis was significantly lower in sucrose-fed rats (+7.3%) than in starch-fed rats (+22%). R supplementation slightly but significantly reduced oxidative stress and increased muscle protein concentration (+4%) but did not restore postprandial stimulation of muscle protein synthesis.
High chronic sucrose intake accelerates sarcopenia in older male rats through an alteration of postprandial stimulation of muscle protein synthesis. This effect could be explained by a decrease of insulin sensitivity rather than by changes in plasma IGF-I, inflammation, and/or oxidative stress.
如今，高糖慢性摄入的情况很常见，这会导致炎症、氧化应激和胰岛素抵抗。这三个因素会降低进餐诱导的肌肉蛋白质合成刺激，从而加剧与年龄相关的肌肉量减少（肌肉减少症）。
我们的目的是确定添加糖是否会加速肌肉减少症，并评估抗氧化剂和抗炎剂预防这种情况的能力。
16月龄雄性大鼠喂食淀粉（13%蔗糖和49%小麦淀粉饮食）或蔗糖（62%蔗糖和0%小麦淀粉饮食）5个月，同时补充或不补充芦丁（5克/千克饮食）、维生素E（4次）、维生素A（2次）、维生素D（5次）、硒（10次）和锌（增加44%）（R）。我们测量了身体成分和炎症的变化、血浆胰岛素样生长因子1（IGF-I）浓度和总抗氧化状态、胰岛素敏感性（口服葡萄糖耐量试验）、肌肉重量、超氧化物歧化酶活性、谷胱甘肽浓度和体内蛋白质合成率。
与喂食淀粉的大鼠相比，喂食蔗糖的大鼠显著损失更多瘦体重（分别为-8.1%和-5.4%），并保留更多脂肪量（分别为+0.2%和-33%）。喂食淀粉的大鼠最终肌肉量比喂食蔗糖的大鼠高11%。蔗糖对炎症、氧化应激和血浆IGF-I浓度影响不大，但降低了胰岛素敏感性指数（减半）。与喂食淀粉的大鼠（+22%）相比，喂食蔗糖的大鼠进餐诱导的肌肉蛋白质合成刺激显著降低（+7.3%）。补充R略微但显著降低了氧化应激并增加了肌肉蛋白质浓度（+4%），但未恢复餐后肌肉蛋白质合成刺激。
长期高蔗糖摄入通过改变餐后肌肉蛋白质合成刺激加速老年雄性大鼠的肌肉减少症。这种作用可能是由胰岛素敏感性降低而非血浆IGF-I、炎症和/或氧化应激的变化来解释。
