| 胎儿应对宫内生长迟缓造成的肌细胞功能和骨骼肌代谢损伤的发育编程 |
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| 作者： 储明星 2013-12-02 | |
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[中文题目] 胎儿应对宫内生长迟缓造成的肌细胞功能和骨骼肌代谢损伤的发育编程。 [全部的英文单位] Department of Animal Sciences, University of Arizona, Tucson, AZ 85721-0038, USA. [出处] Yates DT, Macko AR, Nearing M, Chen X, Rhoads RP, Limesand SW. Developmental programming in response to intrauterine growth restriction impairs myoblast function and skeletal muscle metabolism. [ABSTRACT] Fetal adaptations to placental insufficiency alter postnatal metabolic homeostasis in skeletal muscle by reducing glucose oxidation rates, impairing insulin action, and lowering the proportion of oxidative fibers. In animal models of intrauterine growth restriction (IUGR), skeletal muscle fibers have less myonuclei at birth. This means that myoblasts, the sole source for myonuclei accumulation in fibers, are compromised. Fetal hypoglycemia and hypoxemia are complications that result from placental insufficiency. Hypoxemia elevates circulating catecholamines, and chronic hypercatecholaminemia has been shown to reduce fetal muscle development and growth. We have found evidence for adaptations in adrenergic receptor expression profiles in myoblasts and skeletal muscle of IUGR sheep fetuses with placental insufficiency. The relationship of β-adrenergic receptors shifts in IUGR fetuses because Adrβ2 expression levels decline and Adrβ1 expression levels are unaffected in myofibers and increased in myoblasts. This adaptive response would suppress insulin signaling, myoblast incorporation, fiber hypertrophy, and glucose oxidation. Furthermore, this β-adrenergic receptor expression profile persists for at least the first month in IUGR lambs and lowers their fatty acid mobilization. Developmental programming of skeletal muscle adrenergic receptors partially explains metabolic and endocrine differences in IUGR offspring, and the impact on metabolism may result in differential nutrient utilization. [中文摘要] 为了增强对胎盘功能不全的适应性，胎儿通过降低葡萄糖氧化率、降低胰岛素活性，降低氧化纤维的含量改变了出生后骨骼肌中的新陈代谢。在宫内生长受限的动物模型中，骨骼肌肌纤维中myonuclei的含量下降。这意味着myonuclei的唯一来源成肌细胞的生长收到了抑制。胎儿低血糖和血氧不足并发症是由于胎盘功能不全引起的。血氧不足提高了儿茶酚胺的循环，慢性儿茶酚胺增多症可使胎儿肌肉生长发育迟缓。研究发现由于胎盘功能造成的宫内生长受限的胎羊的成肌细胞和骨骼肌的肾上腺素受体的表达谱显示其发生了适应性的改变。β-肾上腺素受体的改变是由于胎儿在胎内生长受限引起了肾上腺素β2 下降和肾上腺素β1 在肌纤维中的表达量不变，而在成肌细胞中的表达上调。这种适应性的改变可能会抑制胰岛素的信号、成肌细胞合并、肌纤维的生长、葡萄糖的氧化。此外，β-肾上腺素受体表达的改变在宫内生长迟缓的胎儿出生后的至少一个月都会存在，并且会影响它们对脂肪的动员。肾上腺受体在骨骼肌内的发育编程解释了宫内生长迟缓的胎儿在新陈代谢和激素水平上与正常胎儿的不同，并且揭示这种新陈代谢上的差异可能是由于营养物质的差异造成的。 相关信息: |
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