Developing Nutritional-Management Protocols which Prevent Tibial Dyschondroplasia

The objectives of this proposal were (1) to develop early age short-term restrict feeding protocols which eliminate the incidence of TD without compromising market weight performance and (2) monitor the components of the PTH/PTHrP cascade in conjunction with the development of the protocols in Objective 1. In this investigation it was established that changes in gene expression associated with TD occur as early as 13 days of age. This means that management strategies for the control of this disease must be established during the initial two weeks of rearing. In order to determine a focus for these management strategies, attempts were made to identify the metabolic defect responsible for tibial dyschondroplasia. Therefore, the parathyroid hormone/parathyrod related peptide (PTH/PTHrP) cascade of events was investigated. This emphasis was based on the fact that many nutritional factors that influence TD could be operating through this system. Secondly, the receptor for these peptides acts as the gatekeeper of chondrocyte differentiation. Examination of many aspects of this cascade led to the conclusion that TD is not the direct result of perturbation of this PTH/PTHrP receptor but is likely to develop from an interruption of a pathway downstream from this receptor.