In this experiment, we assessed the effect of amino acid (AA) intake restriction in entire male Yorkshire pigs between 15 and 38 kg BW (restriction phase) on BW gain, body composition and plasma levels of blood urea nitrogen (BUN), cortisol, insulin-like growth factor I (IGF-I), growth hormone (GH) and leptin during the subsequent re-alimentation phase. During the restriction phase, 36 pigs were allotted to one of two dietary treatments: adequate AA intake (control) or AA-limiting diets (AA-30%). Thereafter, pigs were fed common non-limiting diets up to 110 kg BW. Throughout the experiment, pigs were scale-fed at 90% of the estimated voluntary daily digestible energy intake. At the end of the restriction phase, pigs on AA-30% had lesser BW gain (650 v. 784 g/day; P < 0.001), loin area (LA; 12.2 v. 14.2 cm2; P < 0.001), BUN (4.6 v. 6.3 mg/dl; P < 0.02), lesser plasma levels of IGF-I (440 v. 640 ng/m; P < 0.001) and cortisol (8.2 v. 19.2 μg/dl; P < 0.001), greater backfat thickness (BF; 7.56 v. 6.56 mm; P < 0.02), and greater plasma levels of leptin (2.7 v. 1.8 ng/ml; P = 0.027) and GH (3.3 v. 2.0 ng/ml; P = 0.05) than pigs on control. During the re-alimentation phase, previously restricted pigs showed full compensatory growth (CG) in terms of BW gain (1170 v. 1077 g/day; P < 0.002), whole-body protein deposition (Pd) (179 v. 163 g/day; P < 0.001) as well as physical and chemical body composition (whole-body lipid to body protein mass ratio, LB/PB; 1.14 v. 1.15; P > 0.10). Besides GH at 45 kg BW (4.2 v. 2.4 ng/ml; P = 0.066), there were no effects of previous AA intake restriction on leptin, IGF-I and BUN during the re-alimentation phase (P > 0.10). Plasma cortisol and IGF-I levels may act as an indicator of AA-induced restriction in Pd in growing pigs. Plasma BUN level does not appear as a sensitive indicator for compensatory Pd. Plasma leptin and GH levels allow for the involvement of the brain in controlling chemical body composition. Full CG was observed during the energy-dependent phase of Pd in growing pigs and might be driven by a target LB/PB, possibly mediated via plasma leptin, IGF-I and GH levels.