Yan Xia, Niu Qiaohua, Gao Xuli, Shen Shenyang, He Nan, Wang Huiping, Fang Rongrong, Gao Yunfang, Chang Hui
Shaanxi Key Laboratory for Animal Conservation, Northwest University, Xi'an, 710069, P.R. China. E-mail:
Key Laboratory of Resource Biology and Biotechnology in Western China (College of Life Sciences, Northwest University), Ministry of Education, Xi'an, 710069, P.R. China. E-mail:
Zool Stud. 2021 Mar 8;60:e6. doi: 10.6620/ZS.2021.60-06. eCollection 2021.
We focused on pathological obesity induced by excessive fat intake (nutritional obesity) in non-hibernator and healthy obesity due to pre-hibernation (PRE) fat storage in hibernator to study the effects of different types of obesity on skeletal muscle protein metabolism and cell regeneration. Kunming mice were fed with high-fat diet for 3 months to construct a pathological obesity model. Daurian ground squirrels fattened naturally before hibernation were used as a healthy obesity model. Body weight, adipose tissue wet weight, gastrocnemius muscle wet weight, muscle fiber cross-sectional area (CSA) and fiber type distribution were measured. The protein expression levels related to protein degradation (MuRF-1, atrogin-1, calpain1, calpain2, calpastatin, desmin, troponin T, Beclin-1, LC3-II), protein synthesis (P-Akt, P-mTORC1, P-S6K1, P-4E-BP1) and cell regeneration (MyoD, myogenin, myostatin) were detected by Western blot. As a result, the body weight and adipose tissue wet weight were both significantly increased in high fat obese (OB) mice and pre-hibernation fat (PRE) ground squirrels. The muscle wet weight, ratio of muscle wet weight to body weight, and muscle fiber CSA were significantly decreased, while the percentage of MHC I fiber isoform was significantly increased in gastrocnemius muscle of OB mice compared with the control (CON) group. The protein expression levels of P-Akt, P-mTORC1, P-4E-BP1 and myogenin were significantly decreased, while those of calpain1, calpain2, MuRF-1 and myostatin were significantly increased in the OB mice. In the ground squirrels, the muscle wet weight, muscle fiber CSA and percentage of MHC I fiber isoform all showed no change in the gastrocnemius muscle in the PRE group compared with the summer active (SA) group. The protein expression levels of P-Akt, P-mTORC1, P-S6K1 and MyoD were significantly increased, while those of Beclin-1 and LC3-II were significantly decreased in the PRE ground squirrels. This study demonstrated that the decrease in protein expression levels in the Akt/mTOR pathway (P-Akt, P-mTORC1 and P-4E-BP1) and cell regeneration (myogenin) and the increase in protein expression levels of the calpain pathway (calpain1 and calpain2) and ubiquitin-proteasome pathway (MuRF-1) were involved in the mechanism of muscle atrophy in gastrocnemius muscle of the pathologically obese Kunming mice induced by high-fat diet. In contrast, the increased protein expression levels of the Akt/mTOR pathway (P-Akt, P-mTORC1 and P-S6K1) and cell regeneration (MyoD), and the decreased protein expression levels of the autophagy lysosomal pathway (Beclin-1 and LC3-II) were involved in the mechanism of anti-atrophy in gastrocnemius muscle of the healthy obese ground squirrels fattened before hibernation.
我们聚焦于非冬眠动物因脂肪摄入过多导致的病理性肥胖(营养性肥胖)以及冬眠动物因冬眠前(PRE)脂肪储存引起的健康肥胖,以研究不同类型肥胖对骨骼肌蛋白质代谢和细胞再生的影响。给昆明小鼠喂食高脂饮食3个月以构建病理性肥胖模型。将冬眠前自然育肥的达乌尔黄鼠用作健康肥胖模型。测量体重、脂肪组织湿重、腓肠肌湿重、肌纤维横截面积(CSA)和纤维类型分布。通过蛋白质免疫印迹法检测与蛋白质降解(MuRF-1、atrogin-1、calpain1、calpain2、钙蛋白酶抑制蛋白、结蛋白、肌钙蛋白T、Beclin-1、LC3-II)、蛋白质合成(P-Akt、P-mTORC1、P-S6K1、P-4E-BP1)和细胞再生(MyoD、肌细胞生成素、肌肉生长抑制素)相关的蛋白质表达水平。结果显示,高脂肥胖(OB)小鼠和冬眠前脂肪(PRE)黄鼠的体重和脂肪组织湿重均显著增加。与对照组(CON)相比,OB小鼠的肌肉湿重、肌肉湿重与体重之比以及肌纤维CSA显著降低,而腓肠肌中MHC I纤维亚型的百分比显著增加。OB小鼠中P-Akt、P-mTORC1、P-4E-BP1和肌细胞生成素的蛋白质表达水平显著降低,而calpain1、calpain2、MuRF-1和肌肉生长抑制素的蛋白质表达水平显著增加。在黄鼠中,与夏季活跃(SA)组相比,PRE组腓肠肌的肌肉湿重、肌纤维CSA和MHC I纤维亚型的百分比均无变化。PRE黄鼠中P-Akt、P-mTORC1、P-S6K1和MyoD的蛋白质表达水平显著增加,而Beclin-1和LC3-II的蛋白质表达水平显著降低。本研究表明,高脂饮食诱导的病理性肥胖昆明小鼠腓肠肌肌肉萎缩机制涉及Akt/mTOR通路(P-Akt、P-mTORC1和P-4E-BP1)中蛋白质表达水平降低以及细胞再生(肌细胞生成素)减少,同时钙蛋白酶通路(calpain1和calpain2)和泛素-蛋白酶体通路(MuRF-1)中蛋白质表达水平增加。相反,冬眠前育肥的健康肥胖黄鼠腓肠肌抗萎缩机制涉及Akt/mTOR通路(P-Akt、P-mTORC1和P-S6K1)中蛋白质表达水平增加以及细胞再生(MyoD)增加,同时自噬溶酶体通路(Beclin-1和LC3-II)中蛋白质表达水平降低。