Peak bone mass is a major determinant of osteoporosis pathogenesis during aging. Respective influences of energy and protein supplies on skeletal growth remains unclear. We investigated the effect of a 5-mo dietary restriction on bone status in young rats randomized into six groups (n ϭ 10 per group). Control animals were fed a diet containing a normal (13%) (C-NP) or a high-protein content (26%) (C-HP). The other groups received a 40% protein energy-restricted diet (PER-NP and PER-HP) or a 40% energyrestricted diet (ER-NP and ER-HP). High-protein intake did not modulate bone acquisition, although a metabolic acidosis was induced and calcium retention impaired. PER and ER diets were associated with a decrease in femoral bone mineral density. The compensation for protein intake in energy-restricted conditions induced a bone sparing effect. Plasma osteocalcin (OC) and urinary deoxypyridinoline (DPD) assays revealed a decreased OC/DPD ratio in restricted rats compared with C animals, which was far more reduced in PER than in ER groups. Circulating IGF-1 levels were lowered by dietary restrictions. In conclusion, both energy and protein deficiencies may contribute to impairment in peak bone mass acquisition, which may affect skeleton strength and potentially render individuals more susceptible to osteoporosis. In particular, alterations in energy intake have been demonstrated to impair bone quality and strength in rodent models (1-5). Lamothe et al. (1) and Mardon et al. (2) reported that energy restriction adversely affected bone mineral content (BMC), bone mineral density (BMD), and mechanical properties in old rats, despite a micronutrient compensation. Nevertheless, the impact of energy restriction on bone was suggested to be modulated by the age at onset of restriction (5,6). To date, no clear consensus regarding the effects of energy restriction on peak bone mass acquisition has been established.Protein intake is widely linked to bone growth, hence to bone strength (7). Indeed, collagen is the major constituent of bone organic matrix, and noncollagenic proteins are involved in the regulation of the mineralization process. Dietary proteins provide the essential amino acids necessary for new matrix synthesis and may modulate circulating IGF-1 levels as well, an osteotrophic growth factor (8). In growing animals, protein deficiency was demonstrated to lead to decreased bone status (9). Ammann et al. (10) also reported that a 2.5% casein diet during 16 wk in 5-mo-old rats was associated with bone loss.Consequently, one would expect high-protein intake to promote bone health. However, other reports suggest that such a diet may alter calcium homeostasis in ways that could lead to bone loss (11,12). The metabolic acidosis, derived from sulfur amino acids catabolism, would also exert a direct stimulatory effect on bone resorption and an inhibitory action on matrix mineralization (13,14). Actually, the role of dietary protein on bone remains controversial.In the current context of rising incidence of obesity...