Ractopamine induces differential gene expression in porcine skeletal muscles
Ractopamine induces differential gene expression in porcine skeletal muscles
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DOI：
10.2527/jas.2006-540
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发表时间：
2007-09-01
影响因子：
3.3
通讯作者：
Gerrard, D. E.
中科院分区：
文献类型：
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作者：
Gunawan, A. M.;Richert, B. T.;Gerrard, D. E.
莱克多巴胺 (RAC) 通过将营养物质从脂肪组织重新分配到骨骼肌来增加瘦肉增加和减少脂肪沉积，从而促进生长。尽管这一过程尚未完全明了，但 RAC 改变了肌纤维类型组成的比例，使其呈现出收缩更快的表型。由于收缩速度的主要决定因素之一是肌球蛋白重链 (MyHC) 同工型的相对丰度，并且编码这些同工型的基因受到转录调控，因此 RAC 可能会改变 MyHC 基因表达。使用实时 PCR，测定了 44 头饲喂 RAC（20 mg/kg）0、1、1 个月的猪的 LM 中个体 I、IIA、IIX 和 IIB 型以及总 MyHC 以及糖原合酶、柠檬酸合酶、乳酸脱氢酶、过氧化物酶体增殖物激活受体 α、β(1)-肾上腺素能受体 (AR) 和 β(2)-AR 转录物的相对丰度。 2 或 4 周。此外，还测定了 48 头饲喂 RAC（20 mg/kg）12、24、48 或 96 小时较短时间的猪的 LM 以及红色半腱肌和白色半腱肌中的 MyHC 亚型表达。 RAC 给药不影响 I 型 MyHC 表达（P > 0.73）。 IIA 型 MyHC 表达在 96 小时时降低（P < 0.0001），在 1 周时降低（P < 0.0001），并在 4 周时恢复正常。 IIX 型 MyHC mRNA 在 2 周时下降（P < 0.001），并在 4 周时继续下降（P < 0.0001）。最有趣的是 IIB 型 MyHC 增加了 12 小时（P < 0.0001），并且在整个 4 周的喂养期间保持在较高水平。糖原合酶转录物丰度在 12 小时内增加（P < 0.05），但在 2 周时与对照没有差异，并且在 4 周时较低（P < 0.01）。 β(1)-AR基因表达不受喂养RAC的影响，而β(2)-AR基因表达在2周时降低(P < 0.05)。这些数据显示 MyHC 基因受到 RAC 的差异调节，并表明 β 肾上腺素能激动剂诱导的重新分配效应部分是通过改变肌纤维类型特异性基因表达（可能是通过 β(2)-AR）介导的。
Ractopamine (RAC) improves growth by increasing lean accretion and decreasing fat deposition through repartitioning nutrients from adipose tissue to skeletal muscle. Although the process is not completely understood, RAC alters the proportion of muscle fiber type composition toward a faster-contracting phenotype. Because one of the primary determinants of contractile speed is the relative abundance of myosin heavy chain (MyHC) isoforms and because the genes encoding these isoforms are transcriptionally regulated, RAC likely alters MyHC gene expression. Using real-time PCR, the relative abundance of transcripts of individual type I, IIA, IIX, and IIB, and total MyHC, as well as glycogen synthase, citrate synthase, lactate dehydrogenase, peroxisome proliferator activated receptor alpha, beta(1)-adrenergic receptor (AR), and beta(2)-AR were determined in the LM of 44 pigs fed RAC (20 mg/kg) for 0, 1, 2, or 4 wk. In addition, MyHC isoform expression was determined in the LM and red semitendinosus and white semitendinosus muscles of 48 pigs fed RAC (20 mg/kg) for shorter periods of 12, 24, 48, or 96 h. Type I MyHC expression was unaffected (P > 0.73) by RAC administration. Type IIA MyHC expression decreased (P < 0.0001) by 96 h, was lower (P < 0.0001) by 1 wk, and returned to normal by 4 wk. Type IIX MyHC mRNA decreased (P < 0.001) by 2 wk and continued to decrease (P < 0.0001) by 4 wk. Most interesting was an increase (P < 0.0001) in type IIB MyHC by 12 h, which was maintained at an elevated level throughout the 4-wk feeding period. Abundance of glycogen synthase transcript was increased (P < 0.05) by 12 h, but was not different from controls at 2 wk, and was lower (P < 0.01) at 4 wk. Gene expression of beta(1)-AR was not affected by feeding RAC, whereas beta(2)-AR gene expression was decreased (P < 0.05) by 2 wk. These data show MyHC genes are differentially regulated by RAC and suggest that the beta adrenergic agonist-induced repartitioning effect is, in part, mediated by changing muscle fiber type-specific gene expression, perhaps through the beta(2)-AR.