Submitted to: Comparative Biochemistry and Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/25/2008
Publication Date: 2/6/2009
Citation: Rosebrough, R.W., Russell, B.A., Richards, M.P. 2009. Effects of Short Term Triiodothyronine administration to broiler chickens fed methimazole. Comparative Biochemistry and Physiology. 150:72-78.
Interpretive Summary: ACTION: A strain of male chicks noted for its rapid growth was used to study the effects of dietary protein, triiodothyronine and feeding regimens in controlling fat synthesis. Scientists in the Animal Biosciences and Biotechnology Laboratory investigated the role of triiodothyronine in regulating lipid synthesis in broilers. Birds were first made hypothyroid by feeding methimazole in their diets. Thyroid function was then restored by feeding the thyroid hormone, triiodothyronine. RESULTS: Hypothyroidism depressed the ability of broilers to synthesize fat by changing the activity of rate-limiting metabolic steps. These steps are regulated by certain genes that are dynamically controlled by the thyroid status of the bird. IMPACT: Triiodothyronine attenuated some of the deleterious effects noted when chickens were switched from a starter to a low protein grower diet. Regimens described in this study may be of value if the slight growth-depressing effect of triiodothyronine can be overcome.
Technical Abstract: The purpose of these experiments were to determine possible relationships among certain indices of lipid metabolism and specific gene expression in chickens fed methimazole to induce a kind of artificial hypothyroidism. In both experiments, male, broiler chickens growing from 14 to 28 days of age were fed diets containing 18% crude protein and either 0 or 1 g methimazole per kg of diet. At 28 days, these two groups were further subdivided into groups receiving 18% crude protein diets containing either 0 or 1 mg triiodothyronine (T3) per kg. In the first experiment, birds were sampled at 0, 1, 2 & 4 days post relief from diet containing methimazole. In the second experiment, birds were sampled at 0, 3, 6, 9, 24 & 48 hr post relief from the methimazole diet. Measurements taken in the first experiment included in vitro lipogenesis (IVL), malic enzyme (ME), isocitrate dehydrogenase (ICD-NADP), aspartate aminotransferase (AST) enzyme activities and the expression of the genes for ME, fatty acid synthase (FAS) and acetyl coenzyme carboxylase (ACC), ICD-NADP and AST. The same enzyme activities and gene expressions were assayed over the intervals mentioned above. In vitro lipogenesis was eliminated due to constraints imposed by sampling times. Gene expression was estimated with real time RT-PCR assays. Gene specific primers were designed with Primer 3. Expression rates were noted as Ct’s or cycles to significant deviation from baselines. Hypothyroidism (dietary methimazole) decreased IVL and ME at 28 d of age. T3 supplementation for 1 d restored both IVL and ME. Continuing T3 replenishment decreased IVL without affecting ME activity. Although methimazole decreased ME gene expression, there was only a transitory relationship between enzyme activity and gene expression when plasma T3 was replenished with exogenous T3.