Division of Endocrinology and Metabolism, Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa.
Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California.
J Appl Physiol (1985). 2021 Jan 1;130(1):124-138. doi: 10.1152/japplphysiol.00156.2020. Epub 2020 Nov 19.
Diet-induced obesity (DIO) is associated with glucose intolerance, insulin resistance (IR), and an increase in intramyocellular lipids (IMCL), which may lead to disturbances in glucose and protein metabolism. To this matter, it has been speculated that chronic obesity and elevated IMCL may contribute to skeletal muscle loss and deficits in muscle function and growth capacity. Thus, we hypothesized that diets with elevated fat content would induce obesity and insulin resistance, leading to a decrease in muscle mass and an attenuated growth response to increased external loading in adult male mice. Male C57BL/6 mice (8 wk of age) were subjected to five different diets, namely, chow, low-dat-diet (LFD), high-fat-diet (HFD), sucrose, or Western diet, for 28 wk. At 25 wk, HFD and Western diets induced a 60.4% and 35.9% increase in body weight, respectively. Interestingly, HFD, but not Western or sucrose, induced glucose intolerance and insulin resistance. Measurement of isometric torque (ankle plantar flexor and ankle dorsiflexor muscles) revealed no effect of DIO on muscle function. At 28 wk of intervention, muscle area and protein synthesis were similar across all diet groups, despite insulin resistance and increased IMCL being observed in HFD and Western diet groups. In response to 30 days of functional overload, an attenuated growth response was observed in only the HFD group. Nevertheless, our results show that DIO alone is not sufficient to induce muscle atrophy and contractile dysfunction in adult male C57BL/6 mice. However, diet composition does have an impact on muscle growth in response to increased external loading. The effects of diet-induced obesity on skeletal muscle mass are complex and dependent on diet composition and diet duration. The present study results show that chronic exposure to high levels of fatty acids does not affect muscle mass, contractile function, or protein synthesis in obese C57BL/6 mice compared with the consumption of chow. Obesity did result in a delay in load-induced growth; however, only a 45% HFD resulted in attenuated growth following 30 days of functional overload.
饮食诱导的肥胖(DIO)与葡萄糖不耐受、胰岛素抵抗(IR)和肌内脂质(IMCL)增加有关,这可能导致葡萄糖和蛋白质代谢紊乱。对此,有人推测,慢性肥胖和 IMCL 升高可能导致骨骼肌丢失以及肌肉功能和生长能力受损。因此,我们假设高脂肪含量的饮食会导致肥胖和胰岛素抵抗,从而导致成年雄性小鼠的肌肉质量减少和对外界负荷增加的生长反应减弱。雄性 C57BL/6 小鼠(8 周龄)接受了五种不同的饮食,即标准饮食、低脂饮食(LFD)、高脂饮食(HFD)、蔗糖或西方饮食,共 28 周。在 25 周时,HFD 和西方饮食分别使体重增加了 60.4%和 35.9%。有趣的是,HFD 但不是西方或蔗糖饮食导致葡萄糖不耐受和胰岛素抵抗。等长扭矩(踝跖屈肌和踝背屈肌)的测量结果表明,DIO 对肌肉功能没有影响。在干预 28 周时,尽管在 HFD 和西方饮食组中观察到胰岛素抵抗和 IMCL 增加,但所有饮食组的肌肉面积和蛋白质合成均相似。在 30 天的功能超负荷后,仅在 HFD 组观察到生长反应减弱。然而,我们的结果表明,单独的 DIO 不足以导致成年雄性 C57BL/6 小鼠的肌肉萎缩和收缩功能障碍。然而,饮食成分确实会影响肌肉对增加的外部负荷的生长反应。饮食诱导的肥胖对骨骼肌质量的影响是复杂的,取决于饮食成分和饮食时间。本研究结果表明,与食用标准饮食相比,慢性暴露于高水平脂肪酸不会影响肥胖 C57BL/6 小鼠的肌肉质量、收缩功能或蛋白质合成。肥胖确实导致负荷诱导生长延迟;然而,只有 45%的 HFD 在 30 天的功能超负荷后导致生长反应减弱。