Chronic Intake of Sucrose Accelerates Sarcopenia in Older Male Rats through Alterations in Insulin Sensitivity and Muscle Protein Synthesis

J Nutr. 2015 May;145(5):923-30. doi: 10.3945/jn.114.205583. Epub 2015 Mar 25.


Background: 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).

Objectives: 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.

Methods: 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.

Results: 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.

Conclusions: 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.

Keywords: antioxidant; fructose; insulin sensitivity; protein synthesis; rats; sarcopenia.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiposity
  • Aging*
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Antioxidants / therapeutic use
  • Body Composition
  • Dietary Sucrose / adverse effects*
  • Dietary Sucrose / antagonists & inhibitors
  • Dietary Supplements
  • Gene Expression Regulation, Developmental*
  • Glutathione / metabolism
  • Insulin Resistance*
  • Insulin-Like Growth Factor I / analysis
  • Male
  • Muscle Proteins / biosynthesis*
  • Muscle, Skeletal / immunology
  • Muscle, Skeletal / metabolism*
  • Muscle, Skeletal / pathology
  • Oxidative Stress
  • Postprandial Period
  • Random Allocation
  • Rats, Wistar
  • Sarcopenia / etiology*
  • Sarcopenia / immunology
  • Sarcopenia / metabolism
  • Sarcopenia / prevention & control


  • Anti-Inflammatory Agents, Non-Steroidal
  • Antioxidants
  • Dietary Sucrose
  • Muscle Proteins
  • insulin-like growth factor-1, rat
  • Insulin-Like Growth Factor I
  • Glutathione