Exercise Induces an Augmented Skeletal Muscle Mitochondrial Unfolded Protein Response in a Mouse Model of Obesity Produced by a High-Fat Diet

被引：6

作者：

Apablaza, Pia ^{[1
,2
]}

Borquez, Juan Carlos ^{[3
]}

Mendoza, Rodrigo ^{[2
]}

Silva, Monica ^{[4
]}

Tapia, Gladys ^{[5
]}

Espinosa, Alejandra ^{[6
]}

Troncoso, Rodrigo ^{[3
]}

Videla, Luis A. ^{[5
]}

Juretic, Nevenka ^{[1
]}

del Campo, Andrea ^{[2
]}

机构：

[1] Univ Chile, Fac Med, Programa Biol Celular & Mol, Inst Ciencias Biomed, Santiago 8380000, Chile

[2] Pontificia Univ Catolica Chile, Escuela Quim & Farm, Fac Quim & Farm, Lab Fisiol & Bioenerget Celular, Santiago 7820436, Chile

[3] Univ Chile, Lab Invest Nutr & Actividad Fis LABINAF, INTA, Santiago 7830490, Chile

[4] Univ Chile, Fac Med, Ctr Estudios Ejercicio Metab & Canc, Programa Fisiol & Biofis,Inst Ciencias Biomed, Santiago 8380000, Chile

[5] Univ Chile, Fac Med, Programa Farmacol Mol & Clin, Inst Ciencias Biomed, Santiago 8380000, Chile

[6] Univ Valparaiso, Escuela Med, Valparaiso 2340000, Chile

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2023年 / 24卷 / 06期

关键词：

obesity; UPRmt; skeletal muscle; exercise; INSULIN-RESISTANCE; OXIDATIVE STRESS; LON PROTEASE; ACTIVATION; ATF4;

D O I：

10.3390/ijms24065654

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Increase in body fat contributes to loss of function and changes in skeletal muscle, accelerating sarcopenia, a phenomenon known as sarco-obesity or sarcopenic obesity. Studies suggest that obesity decreases the skeletal muscle (SM)'s ability to oxidize glucose, increases fatty acid oxidation and reactive oxygen species production, due to mitochondrial dysfunction. Exercise improves mitochondrial dysfunction in obesity; however, it is not known if exercise regulates the mitochondrial unfolded protein response (UPRmt) in the SM. Our study aimed to determine the mito-nuclear UPRmt in response to exercise in a model of obesity, and how this response is associated with the improvement in SM functioning after exercise training. C57BL/6 mice were fed a normal diet and high-fat diet (HFD) for 12 weeks. After 8 weeks, animals were subdivided into sedentary and exercised for the remaining 4 weeks. Grip strength and maximal velocity of mice submitted to HFD improved after training. Our results show an increase in the activation of UPRmt after exercise while in obese mice, proteostasis is basally decreased but shows a more pronounced increase with exercise. These results correlate with improvement in the circulating triglycerides, suggesting mitochondrial proteostasis could be protective and could be related to mitochondrial fuel utilization in SM.

引用

页数：10