骨骼肌在代谢综合征中的生理作用的遗传学解剖

N. Hagiwara
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引用次数: 6

摘要

代谢综合征的主要缺陷是胰岛素抵抗,其中胰岛素反应的外周组织不能维持葡萄糖稳态。由于骨骼肌是胰岛素诱导的葡萄糖摄取的主要部位,骨骼肌胰岛素反应性损伤在胰岛素抵抗和2型糖尿病的发展中起着重要作用。例如,2型糖尿病患者及其后代的骨骼肌表现出缓慢氧化肌的比例降低。这些观察结果提示应用肌肉重塑来恢复代谢综合征胰岛素敏感性的可能性。骨骼肌对运动等外部刺激具有高度适应性;然而,在实践中,通常不实际或不可能强制实施必要的强度以获得代谢综合征患者群体可测量的益处。因此,确定诱导肌肉重塑的分子靶点将为代谢综合征的治疗提供新的途径。本文将对骨骼肌的生理特性、代谢综合征在人群和模式生物中的遗传分析以及基因工程小鼠模型进行讨论,以期将骨骼肌重塑作为代谢综合征可能的治疗方法。
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Genetic Dissection of the Physiological Role of Skeletal Muscle in Metabolic Syndrome
The primary deficiency underlying metabolic syndrome is insulin resistance, in which insulin-responsive peripheral tissues fail to maintain glucose homeostasis. Because skeletal muscle is the major site for insulin-induced glucose uptake, impairments in skeletal muscle’s insulin responsiveness play a major role in the development of insulin resistance and type 2 diabetes. For example, skeletal muscle of type 2 diabetes patients and their offspring exhibit reduced ratios of slow oxidative muscle. These observations suggest the possibility of applying muscle remodeling to recover insulin sensitivity in metabolic syndrome. Skeletal muscle is highly adaptive to external stimulations such as exercise; however, in practice it is often not practical or possible to enforce the necessary intensity to obtain measurable benefits to the metabolic syndrome patient population. Therefore, identifying molecular targets for inducing muscle remodeling would provide new approaches to treat metabolic syndrome. In this review, the physiological properties of skeletal muscle, genetic analysis of metabolic syndrome in human populations and model organisms, and genetically engineered mouse models will be discussed in regard to the prospect of applying skeletal muscle remodeling as possible therapy for metabolic syndrome.
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