The impact of supplemental zinc concentrations and either ractopamine hydrochloride or dietary energy content on blood metabolite measures
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The impact of supplemental zinc concentrations and either ractopamine hydrochloride or dietary energy content on blood metabolite measures P. E. Wise, R. N. Carmichael and S. L. Hansen This study researched whether increased dietary zinc supports growth within the beta-agonist cascade (Exp. 2) or by ulterior mechanisms (Exp. 1—dietary energy content). Angus-type steers received one of three Zn supplementations (ZNTRT). ZNTRT included CON (0 mg Zn/kg DM supplemental zinc), ZS (120 mg Zn/kg DM as ZnSO4), and ZA (60 mg Zn/kg DM as ZnSO4 + 60 mg Zn/kg DM as Zn-AA complex). In Exp. 1, half received LOW diets (~1.6 kg/d ADG fed for initial 60 d to all steers) and half HI diets (~2 kg/d ADG). In Exp. 2, half received a beta-agonist—RAC (300 mg ractopamine HCl·steer ·-1d ·-1) and half did not—NON (0 mg ractopamine HCl·steer ·-1d ·-1 ). Blood was sampled throughout the trial periods (four days for Exp. 1 and five days for Exp. 2) and analyzed for blood urea nitrogen (BUN) and non-esterified fatty acid (NEFA) concentrations. Overall, NEFA concentration was unaffected by ZNTRT but was affected by energy in Exp. 1 (P = 0.02). BUN concentration increased in Exp. 2 during pre-RH and RH periods when fed ZA diets (P < 0.01, P = 0.09, respectively). BUN concentration in Exp. 2 decreased with supplementation of RAC (P = 0.01).