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Brief Communication: Sexual dimorphic expression of myostatin and follistatin like-3 in a rat trans-generational under-nutrition model

机译:简述:大鼠跨代营养不良模型中肌肉生长抑制素和卵泡抑素样3的性二态表达

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摘要

The detrimental effects of maternal under-nutrition during gestation on fetal development are well known with an increased propensity of metabolic disorders identified in the adult offspring. Understanding exactly how and by which molecular pathways inadequate nutrition can impact upon offspring phenotype is critical and necessary for the development of treatment methods and ultimately prevention of any negative health effects. Myostatin, a negative regulator of muscle development, has recently been shown to effect glucose homeostasis and fat deposition. The involvement of myostatin in glucose metabolism and adipogenesis thus supports its ability to act in the continued alterations to the postnatal phenotype of the offspring. This hypothesis was examined in the current study using a trans-generational gestationally under-nourished rat model exposed to a high-fat (HF) diet post-weaning. The body weight, body fat, plasma glucose and insulin concentrations of the offspring, both male and female, were investigated in relation to the protein expression of myostatin and its main inhibitor; follistatin like-3 (FSTL-3), in skeletal muscle of mature offspring. Sexual dimorphism was clearly evident in the majority of these measures, including myostatin and FSTL-3 expression. Generally males displayed higher (P < 0.05) myostatin precursor and dimer expression than females, which was especially apparent (P < 0.01) in both chow and HF trans-generationally undernourished (UNAD) groups. In females only, myostatin precursor and dimer expression was altered by both trans-generational under-nutrition and postnatal diet. Overall FSTL-3 expression did not differ between sexes, although difference between sexes within certain treatments and diets were evident. Most notably, HF fed UNAD females had higher (P < 0.05) FSTL-3 expression than HF fed UNAD males. The former group also displayed higher (P < 0.01) FSTL-3 expression compared to all other female groups. In summary, myostatin may prove to be a key mediator of the effects of inadequate prenatal nutrition, independently or in combination with a high-fat postnatal diet on offspring phenotype. Consequently, further study of myostatin may provide a novel therapeutic pathway for the treatment of metabolic disorders; however, it is vital that the influence of nutrition and gender should be taken into consideration.
机译:众所周知,孕期母亲营养不良对胎儿发育的不利影响是在成年后代中发现的代谢紊乱倾向增加。准确了解营养不足的分子途径如何以及通过何种途径影响后代表型,对于发展治疗方法并最终预防任何不良健康影响至关重要,也是必不可少的。肌生长抑制素是肌肉发育的负调节剂,最近已显示出可实现葡萄糖稳态和脂肪沉积。肌生长抑制素参与葡萄糖代谢和脂肪生成,从而支持其在后代出生后表型的持续改变中起作用的能力。在当前的研究中,使用断奶后暴露于高脂(HF)饮食的跨代妊娠营养不良的大鼠模型检验了这一假设。研究了男性和女性后代的体重,体脂,血浆葡萄糖和胰岛素浓度,与肌肉生长抑制素及其主要抑制剂的蛋白质表达有关;成熟后代骨骼肌中的卵泡抑素类似物3(FSTL-3)。在大多数这些措施中,包括肌生长抑制素和FSTL-3表达,明显存在性二态性。通常,男性比女性表现出更高的(P <0.05)肌生长抑制素前体和二聚体表达,在成年和HF世代营养不良(UNAD)组中尤为明显(P <0.01)。仅在女性中,跨代营养不良和产后饮食都改变了肌生成抑制素前体和二聚体的表达。性别之间的总体FSTL-3表达没有差异,尽管在某些治疗和饮食中性别之间的差异是明显的。最值得注意的是,HF喂养的UNAD雌性比HF喂养的UNAD雄性具有更高的(P <0.05)FSTL-3表达。与所有其他女性组相比,前一组还显示出更高的(P <0.01)FSTL-3表达。总之,肌生长抑制素可能被证明是单独或与高脂的产后饮食组合对后代表型影响不足的产前营养影响的关键介质。因此,对肌生长抑制素的进一步研究可能为代谢性疾病的治疗提供新的治疗途径。但是,至关重要的是应考虑营养和性别的影响。

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