Carry over effects of dietary crude protein and methimazole in broiler chickens.

Growth Development and Aging Pub Date : 2002-01-01
R W Rosebrough
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Abstract

Seven day old male broiler chickens were fed diets containing 12, 18 or 24% crude protein + 0 or 1 g methimazole/kg diet for 21 days to examine the interaction of the birds' thyroid status and crude protein levels on metabolism. Methimazole (1-methyl-2-mercaptimidazole) inhibits thyroidal production of thyroid hormones and results in hypothyroidism. Birds were fed a diet containing 18% crude protein for an additional 21 days to determine the carry over effects of treatments. Birds were killed at 28 and 49 d. In vitro lipogenesis was inversely related (P < 0.05) to dietary protein levels in control birds at 28 d. Dietary methimazole attenuated (P < 0.05) this effect, resulting in a common rate similar to that attained in the birds fed the highest level of protein without methimazole. Birds fed methimazole for an initial 21-day period (7 to 28 d of age) had greater lipogenic rates (P < 0.05) at 49 d than did their control counterparts. In contrast, methimazole increased (P < 0.05) abdominal fat pad (AFP) lipoprotein lipase (LPL) at both age periods, indicating increased ability by the AFP to remove triglycerides from systemic circulation. Observations at 49 d suggest that perturbations in the thyroid of the young bird may substantially change metabolism in later life. Results also show that obesity in hypothyroid birds cannot be explained by increases in de novo lipogenesis, but probably relates to changes in LPL activity.

饲粮粗蛋白质和甲巯咪唑对肉鸡的传递效应。
研究7日龄肉鸡饲粮中粗蛋白质含量分别为12、18或24% + 0或1 g /kg的甲巯咪唑,连续21 d,观察甲状腺状态和粗蛋白质水平对代谢的影响。甲巯咪唑(1-甲基-2-巯基咪唑)抑制甲状腺激素的产生,导致甲状腺功能减退。再饲喂含18%粗蛋白质的饲粮21天,以确定处理的结转效应。在28和49 d时,禽类被杀死。28 d时,对照禽类的体外脂肪生成与饲粮蛋白质水平呈负相关(P < 0.05)。饲粮中添加甲巯咪唑减弱了这种影响(P < 0.05),其总体脂肪生成率与饲喂最高蛋白质水平但不添加甲巯咪唑的禽类相似。第21天(7 ~ 28日龄)饲喂甲巯咪唑的雏鸟在第49天的脂肪生成率高于对照组(P < 0.05)。相比之下,甲巯咪唑在两个年龄阶段均增加了腹部脂肪垫(AFP)脂蛋白脂肪酶(LPL) (P < 0.05),表明AFP清除体循环甘油三酯的能力增强。49 d时的观察表明,幼鸟甲状腺的扰动可能会在以后的生活中实质性地改变代谢。结果还表明,甲状腺功能减退鸟类的肥胖不能用新生脂肪生成的增加来解释,而可能与LPL活性的变化有关。
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