The amount of fat in the carcass has been proposed as a regulator of initiation of puberty in cattle. To test if changes in energy intake and in circulating leptin concentration are each capable of altering age, BW, and body composition at puberty, 36 prepubertal Nellore heifers, 18 to 20 mo old, 275.8 ± 17.2kg BW, and BCS of 5 ± 0.5 (1 to 9 scale), were randomly assigned to each of 3 treatments (n = 12): High (high energy diet), Low (low energy diet), and LL [low energy diet + ovine leptin (oLeptin)]. Diets were formulated to promote BW gain of 0.4 kg/d (groups Low and LL) or 1.2 kg/d (High group). After 14 d of adjustment to diet, heifers in LL group received subcutaneous injections of oLeptin at 4.8 μg/kg BW twice a day for 56 d. Groups High and Low received similar injections of 2 mL saline solution. Age at puberty was considered to be the age on first detection of a corpus luteum, confirmed by plasma concentrations of progesterone of >1 ng/mL. Heifers were slaughtered on the second day after first corpus luteum detection. Expression of leptin gene was quantified by real-time PCR using ribosomal protein-L19 (RPL19) as a control gene. Leptin administration increased (P = 0.04) leptin serum concentration but had no effect (P > 0.05) on age, BW, or BCS at puberty. High energy intake increased (P < 0.01) leptin concentration, accelerated (P = 0.02) puberty, and increased (P < 0.01) BCS at puberty, without altering (P = 0.17) BW at puberty. High energy intake also accelerated (P = 0.04) follicular development. Leptin administration caused a significant (P < 0.05) but transient increase in follicular development, which was similar to the transient increase in leptin serum concentration. Results from leptin gene expression demonstrated that high energy intake increased (P < 0.01) and leptin administration decreased (P < 0.01) leptin expression in 3 adipose tissues. The observed decrease in leptin gene expression after administration of leptin could explain the reduction in leptin serum concentration after 30 d of treatment and consequently the failure of leptin to accelerate puberty. Our findings did not support the hypothesis that reduced serum concentration of leptin is an important hindrance for puberty onset in malnourished zebu heifers. Although exogenous administration of leptin temporarily enhanced rate of follicular growth, it did not accelerate puberty
