Department of Kinesiology and Health, Miami University, Oxford, Ohio.
Departments of Physical Therapy and Athletic Training, University of Utah, Salt Lake City, Utah.
J Appl Physiol (1985). 2021 Mar 1;130(3):537-544. doi: 10.1152/japplphysiol.00954.2020. Epub 2020 Dec 24.
Physical inactivity influences the development of muscle insulin resistance yet is far less understood than diet-induced muscle insulin resistance. Progress in understanding the mechanisms of physical inactivity-induced insulin resistance is limited by a lack of an appropriate preclinical model of muscle insulin resistance. Here, we discuss differences between diet and physical inactivity-induced insulin resistance, the advantages and disadvantages of the available rodent inactivity models to study insulin resistance, and our current understanding of the mechanisms of muscle insulin resistance derived from such preclinical inactivity designs. The burgeoning rise of health complications emanating from metabolic disease presents an alarming issue with mounting costs for health care and a reduced quality of life. There exists a pressing need for more complete understanding of mechanisms behind the development and progression of metabolic dysfunction. Since lifestyle modifications such as poor diet and lack of physical activity are primary catalysts of metabolic dysfunction, rodent models have been formed to explore mechanisms behind these issues. Particularly, the use of a high-fat diet has been pervasive and has been an instrumental model to gain insight into mechanisms underlying diet-induced insulin resistance (IR). However, physical inactivity (and to some extent muscle disuse) is an often overlooked and much less frequently studied lifestyle modification, which some have contended is the primary contributor in the initial development of muscle IR. In this mini-review we highlight some of the key differences between diet- and physical inactivity-induced development of muscle IR and propose reasons for the sparse volume of academic research into physical inactivity-induced IR including infrequent use of clearly translatable rodent physical inactivity models.
身体活动不足会影响肌肉胰岛素抵抗的发展，但人们对其的了解远不及饮食引起的肌肉胰岛素抵抗。由于缺乏适当的肌肉胰岛素抵抗临床前模型，人们对身体活动引起的胰岛素抵抗机制的理解进展有限。在这里，我们讨论了饮食和身体活动引起的胰岛素抵抗之间的差异，讨论了现有用于研究胰岛素抵抗的啮齿动物不活动模型的优缺点，以及我们目前对这些临床前不活动设计中肌肉胰岛素抵抗机制的理解。代谢疾病引起的健康并发症不断增加，给医疗保健带来了惊人的成本上升和生活质量下降的问题。人们迫切需要更全面地了解代谢功能障碍发展和进展的机制。由于生活方式的改变，如不良饮食和缺乏身体活动，是代谢功能障碍的主要诱因，因此已经建立了啮齿动物模型来探索这些问题背后的机制。特别是，高脂肪饮食的使用已经很普遍，并且是深入了解饮食引起的胰岛素抵抗（IR）机制的重要模型。然而，身体活动不足（在某种程度上还有肌肉失用）是一种经常被忽视且研究得较少的生活方式改变，一些人认为它是肌肉 IR 最初发展的主要原因。在这个小型综述中，我们强调了饮食和身体活动引起的肌肉 IR 发展之间的一些关键差异，并提出了身体活动引起的 IR 研究相对较少的原因，包括不常使用可明显转化的啮齿动物身体活动不足模型。
