340. Monensin Reduces Feed Intake and Alters Glucose, Insulin, and Active Ghrelin Responses in Finishing Beef Steers.

Abstract Monensin is a widely utilized feed additive in feedlot systems, recognized for its ability to improve feed efficiency. The improvement in feed conversion is a product of reduced feed intake accompanied by increased rate of gain. Although the intake-reducing effects of monensin are well-documented, the mechanisms driving this response remain unclear. Therefore, the objective of this experiment was to evaluate the effects of monensin supplementation on glucose, insulin, and active ghrelin dynamics in relation to feed intake regulation in beef steers. Twelve Angus-cross steers (initial body weight [BW] = 373 ± 13.3 kg) were blocked by weight and randomly assigned to 1 of 2 treatments: control or monensin (n = 6 per treatment). Beginning on d 0, steers were offered their respective diets as a total mixed ration ad libitum. Refusals were collected daily to determine dry matter intake (DMI). Body weights and serial blood samples were collected on d 0, 21, 42, and 56. Blood samples were obtained at -1, 0, 2, 4, and 6 h relative to feeding. Blood was processed to obtain plasma which was analyzed for glucose, insulin, and active ghrelin concentrations. Data were analyzed using the MIXED procedure of SAS 9.4 (SAS Inst., Cary, NC). Dry matter intake included fixed effects of treatment, week, and their interaction. Body weight included fixed effects of treatment, day, and their interaction. Plasma variables included fixed effects of treatment, day, time, and their interactions, with time as a repeated measure and steer × day as the subject. Day 0 values for insulin and active ghrelin were included as covariates. A treatment × week interaction was observed for DMI (P < 0.001), where intake decreased in steers receiving monensin as the trial progressed. A treatment effect was observed for BW (P = 0.026), with monensin-fed steers having lower BW; however, no differences in average daily gain were detected (P = 0.18). For plasma glucose, a treatment × day interaction was observed (P = 0.006), with greater concentrations in monensin-fed steers on d 21 and 56. Plasma insulin followed a similar pattern (treatment × day, P = 0.003), with increased concentrations in monensin-fed steers on d 21 and 56. Active ghrelin was decreased in monensin-fed steers (treatment, P = 0.003) and increased over time post-feeding (time, P < 0.001), although concentrations remained lower than control. These data indicate that monensin supplementation alters endocrine signals associated with feed intake regulation, characterized by increased insulin and decreased active ghrelin. These coordinated responses suggest that reductions in DMI may be mediated, in part, by endocrine mechanisms rather than solely by metabolic feedback. Further research is needed to determine how these responses influence feed efficiency and growth performance.