Department of Nutrition, Food and Exercise Sciences, Florida State University, 120 Convocation Way, Tallahassee, FL 32306; The Center for Advancing Exercise and Nutrition Research on Aging, Florida State University, Tallahassee, 120 Convocation Way, Tallahassee, FL 32306.
Department of Nutrition, Food and Exercise Sciences, Florida State University, 120 Convocation Way, Tallahassee, FL 32306.
Nutr Res. 2020 Dec;84:14-24. doi: 10.1016/j.nutres.2020.10.002. Epub 2020 Oct 13.
Vitamin D (VitD) possesses antiadipogenic and ergogenic properties that could be effective to counteract obesity-related adverse health consequences. Therefore, our overall hypothesis was that VitD could ameliorate obesity-induced insulin resistance, systemic inflammation, and loss of skeletal muscle mass and function in an obesity animal model, p62-deficient mice. Furthermore, it was hypothesized that resistance exercise training (RT) could enhance the benefits of VitD by upregulating protein expression of vitamin D receptor in skeletal muscle. Forty 24-week-old male p62-deficient mice were assigned to the following 4 groups (10/group) for a 10-week intervention: control (p62C, no treatment), VitD (VD, 1000 IU vitamin D/kg/d), RT (ladder climbing, 3 times per week), or combined treatment (VRT, VD + RT). Serum VitD levels increased in VD and VRT (P < .05). Total body mass increased in p62C, VD, and VRT, but fat mass increased only in p62C (P < .05). Loss of skeletal muscle function was reported only in p62C (P < .05). Improved blood glucose levels and lower spleen mass were reported in RT and VRT compared to p62C (P < .05). However, the hindlimb muscle wet weights; myofiber cross-sectional area; and expression levels of the regulatory proteins for insulin signaling, inflammation, and muscle growth were not changed by any intervention. In conclusion, VitD administration attenuated the progression of obesity and preserved skeletal muscle function in p62-deficient mice. However, the obese mice improved systemic insulin sensitivity and inflammation only when the intervention involved RT.
维生素 D（VitD）具有抗脂肪生成和增强体力的特性，可有效对抗肥胖相关的健康不良后果。因此，我们的总体假设是，VitD 可以改善肥胖诱导的胰岛素抵抗、全身炎症和骨骼肌质量和功能的丧失在肥胖动物模型中，p62 缺陷小鼠。此外，还假设阻力运动训练（RT）可以通过上调骨骼肌中维生素 D 受体的蛋白表达来增强 VitD 的益处。40 只 24 周龄雄性 p62 缺陷小鼠被分为以下 4 组（每组 10 只）进行 10 周干预：对照组（p62C，未治疗）、VitD（VD，1000 IU 维生素 D/kg/d）、RT（爬梯，每周 3 次）或联合治疗（VRT，VD+RT）。VD 和 VRT 组血清 VitD 水平升高（P<.05）。全身总质量在 p62C、VD 和 VRT 中增加，但脂肪质量仅在 p62C 中增加（P<.05）。仅在 p62C 中报告了骨骼肌功能丧失（P<.05）。与 p62C 相比，RT 和 VRT 报告了血糖水平的改善和脾脏质量的降低（P<.05）。然而，后肢肌肉湿重；肌纤维横截面积；以及胰岛素信号、炎症和肌肉生长的调节蛋白的表达水平不受任何干预的影响。总之，VitD 给药可减轻 p62 缺陷小鼠肥胖的进展并维持骨骼肌功能。然而，只有当干预涉及 RT 时，肥胖小鼠才能改善全身胰岛素敏感性和炎症。
