Effects of a high fat diet on bone of growing rats. Correlations between visceral fat, adiponectin and bone mass density.

In this study, we investigated some bone parameters (bone mineral content, bone mineral density, skeleton area) in growing rats fed with a high fat diet. Correlations between bone and body composition parameters are reported. Two groups of Wistar male rats (35 days old, body mass 80 +/- 6 g) were used. Water and food were given "ad libitum" during 10 weeks. Sixteen rats (L) were given a lipid enriched diet and were compared to 16 rats (S) fed with a standard diet. Body composition and bone parameters were assessed using DXA. Results indicated that L rats had lower body mass, lean body mass; fat mass was not different between the two groups. Bone mineral content, bone mineral density, skeleton area of L rats were lower compared with S rats. Significant correlations were noted between body composition, adiponectin and bone parameters. High fat diet intake during the growing period has deleterious effects on bone parameters in rats. This study confirms in growing rats that a high fat diet is pathogenic, including bone metabolism.

Effect of a moderate exercise on the regulatory hormones of food intake in rats.

Strategies used to counteract overweight include generally endurance exercise. Force-resistance exercise has not been tested yet with this objective. The aim of this study was to investigate the response of the main regulatory hormones of food intake (insulin, adiponectin, leptin, ghrelin) and corticosterone, to a short force resistance exercise. Two groups of 16 rats, 65 days old, weighing 330g, were constituted. A standard diet (containing glucid: 72.2, lipid: 7.7, protid: 20% calories) was given "ad libitum". One group served as control, the second group was submitted to exercise training during 5 weeks. Training reduced the rats body weight by 6.4% and the total food intake during the 5 weeks by 11%. Training lowered the insulin and ghrelin levels, while corticosterone level was increased. Insulin, ghrelin and corticosterone only reached the significant threshold p<0.05. Thus, it seems that exercise, even of low intensity and duration, induces changes on hormones that regulate food intake and limit overweight.

Molecular impact of clenbuterol and isometric strength training on rat EDL muscles.

Clenbuterol, a beta2-adrenergic-receptor agonist, is known to provoke muscle hypertrophy and a slow-to-fast phenotype change. A more glycolytic phenotype should be paralleled by changes in muscle glycolytic metabolism. Two groups (n=16 for each) of 3-month-old male Wistar rats (UCL: untrained clenbuterol, and ECL: exercised clenbuterol) received a chronic administration of clenbuterol (2 mg/kg body weight/day). Two other groups of animals (U: untrained and E: exercised), were given a 0.9% NaCl solution instead of clenbuterol. E and ECL animals followed an 8-week progressive isometric force strength-training program. Both clenbuterol administration and training resulted in an increase in extensor digitorum longus (EDL) mass despite the fact that this muscle was indirectly mobilised during isometric force strength training. Clenbuterol and training induced a consistent slow-to-fast phenotype change without drastically increasing specific activities of glycolytic enzymes. Except for GAPDH and hexokinase, modifications in glycolytic-enzyme-specific activities were not explained by transcriptional changes. Lactate dehydrogenase activity was not affected by clenbuterol but was strongly augmented by training. In EDL of ECL rats, both treatments presented an opposite effect compensating each other. GLUT1 mRNA expression was augmented in EDL of UCL and ECL animals, whereas monocarboxylate transporter 1 mRNA amounts were decreased in EDL of UCL rats. Citrate synthase activity was reduced by clenbuterol treatment but remained unchanged in EDL of E animals. Creatine kinase activity was enhanced only by clenbuterol alone. These data show that clenbuterol-induced muscle hypertrophy and slow-to-fast phenotype changes are not associated with a glycolytic-enzyme-activity increase. They also suggest that in EDL isometric force strength training can reverse clenbuterol-induced molecular adaptations.