Submitted to: Journal of Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 11, 2000
Publication Date: N/A
Interpretive Summary: Excess fat production by the modern broiler chicken presents a two-fold problem. The consumer has health concerns about the link between cardiovascular disease and dietary fat. The producer would like to produce more lean meat rather than fat that is condemned at the processing plant. Adding dietary thyroid active substances to the broiler diet will depress the ability of the chicken to synthesize fat from dietary carbohydrate and protein sources. Historically this shift in metabolism has resulted in dietary fat being merely shunted to replace that synthesized from other feed ingredients. We have found that altering the thyroid axis in the broiler will cause permanent changes in fat synthesis and storage, such that dietary fat will not be shunted to body fat stores. The present study demonstrates that graded levels of chicken growth hormone will depress fat synthesis in the broiler. This study further indicates that both dietary fat and thyroid hormones change avian lipid metabolism. This finding is opposite to that noted in mammals. Cost-benefit data must be derived for each producer before a blanket recommendation can be made for using growth hormone in growing broilers.
In contrast to most vertebrates, growth hormone (GH) reportedly has no effect upon somatic growth of the chicken (c). However, previous studies employed only 1-2 dosages of the hormone, and limited evidence exists of a hyperthyroid response that may confound its anabolic potential. This study evaluated effects of 0, 10, 50, 100 and 200 mg/kg BW/d cGH (0-200GH) infused i.v. for 7 days in a pulsatile pattern to immature, growing broile chickens (9-10 birds/dosage). Comprehensive profiles of thyroid hormone metabolism and measures of somatic growth were obtained. Overall body weight gain was reduced 25% by GH, with a curvilinear, dose-dependent decrease in skeletal (breast) muscle mass that was maximal (12%) at 100GH. This profile mirrored GH dose-dependent decreases in hepatic type III deiodinase (5DIII) activity and increases in plasma T3, with both also maximal (74 and 108%, respectively) at 100GH. The results of this study support a pathway by which GH impacts on thyroid hormone metabolism, beginning at the transcriptional level of control with reduced hepatic 5DIII gene expression, translating to reduced protein (enzyme) expression, and reflected in a reduced level of peripheral T3-degrading activity. This contributes to decreased conversion of T3 to its inactive form, thereby elevating circulating T3 levels. The hyper-T3 state leads to reduced net skeletal muscle deposition, and may impair release of GH-enhanced, hepatic IGF-1. In conclusion, GH has significant biological effects in the chicken, but profound metabolic actions predominate that may confound positive, IGF- 1-mediated skeletal muscle growth.