Li Jing, Yi Xuejie, Li Tao, Yao Tingting, Li Dongyang, Hu Guangxuan, Ma Yongqi, Chang Bo, Cao Shicheng
School of Physical Education, Liaoning Normal University, Dalian, Liaoning, China.
Exercise and Health Research Center, Department of Kinesiology, Laboratory Management Center, Shenyang Sport University, Shenyang, Liaoning, China.
Endocr Connect. 2022 Mar 14;11(3):e210625. doi: 10.1530/EC-21-0625.
Obesity is a growing problem worldwide, and newer therapeutic strategies to combat it are urgently required. This study aimed to analyze the effect of diet and exercise interventions on energy balance in mice and elucidate the mechanism of the peroxisome proliferator-activated receptor-gamma co-activator-1-alpha-IRISIN-uncoupling protein-1 (PGC-1α-IRISIN-UCP-1) pathway in the beigeization of white adipose tissue.
Four-week-old male C57BL/6 mice were randomly divided into normal (NC) and high-fat diet (HFD) groups. After 10 weeks of HFD feeding, obese mice were randomly divided into obesity control (OC), obesity diet control (OD), obesity exercise (OE), and obesity diet control exercise (ODE) groups. Mice in OE and ODE performed moderate-load treadmill exercises: for OD and ODE, the diet constituted 70% of the food intake of the OC group for 8 weeks.
Long-term HFD inhibits white adipose tissue beigeization by downregulating PGC-1α-IRISIN-UCP-1 in the adipose tissue and skeletal muscles. Eight weeks of exercise and dietary interventions alleviated obesity-induced skeletal muscle, and adipose tissue PGC-1α-IRISIN-UCP-1 pathway downregulation promoted white adipose tissue beigeization and reduced body adipose tissue. The effects of the combined intervention were better than those of single interventions.
Diet and exercise intervention after obesity and obesity itself may affect the beigeization of WAT by downregulating/upregulating the expression/secretion of skeletal muscle and adipose PGC-1α-IRISIN, thereby influencing the regulation of bodyweight. The effects of the combined intervention were better than those of single interventions.
肥胖是一个在全球范围内日益严重的问题，迫切需要新的治疗策略来应对。本研究旨在分析饮食和运动干预对小鼠能量平衡的影响，并阐明过氧化物酶体增殖物激活受体γ共激活因子-1α-鸢尾素-解偶联蛋白-1（PGC-1α-鸢尾素-UCP-1）通路在白色脂肪组织米色化过程中的作用机制。
将4周龄雄性C57BL/6小鼠随机分为正常（NC）组和高脂饮食（HFD）组。高脂饮食喂养10周后，将肥胖小鼠随机分为肥胖对照组（OC）、肥胖饮食控制组（OD）、肥胖运动组（OE）和肥胖饮食控制运动组（ODE）。OE组和ODE组的小鼠进行中等负荷的跑步机运动；对于OD组和ODE组，饮食量为OC组食物摄入量的70%，持续8周。
长期高脂饮食通过下调脂肪组织和骨骼肌中的PGC-1α-鸢尾素-UCP-1来抑制白色脂肪组织的米色化。8周的运动和饮食干预减轻了肥胖诱导的骨骼肌和脂肪组织中PGC-1α-鸢尾素-UCP-1通路的下调，促进了白色脂肪组织的米色化并减少了身体脂肪组织。联合干预的效果优于单一干预。
肥胖后进行饮食和运动干预以及肥胖本身可能通过下调/上调骨骼肌和脂肪组织中PGC-1α-鸢尾素的表达/分泌来影响白色脂肪组织的米色化，从而影响体重调节。联合干预的效果优于单一干预。
