| Autor: |
Huang CJ; Exercise Biochemistry Laboratory, Department of Exercise Science and Health Promotion, Florida Atlantic University, Boca Raton, FL, USA., Rodriguez AL; Exercise Biochemistry Laboratory, Department of Exercise Science and Health Promotion, Florida Atlantic University, Boca Raton, FL, USA., Visavadiya NP; Exercise Biochemistry Laboratory, Department of Exercise Science and Health Promotion, Florida Atlantic University, Boca Raton, FL, USA., Fico BG; Department of Kinesiology and Health Education, University of Texas, Austin, TX, USA., Slusher AL; School of Kinesiology, University of Michigan, Ann Arbor, MI, USA., Ferrandi PJ; Department of Health and Kinesiology, Purdue University, West Lafayette, IN, USA., Whitehurst M; Exercise Biochemistry Laboratory, Department of Exercise Science and Health Promotion, Florida Atlantic University, Boca Raton, FL, USA. |
| Abstrakt: |
Autophagy is a critical molecular process in promoting cell survival against apoptosis. This study examined whether maximal aerobic exercise-mediated apoptosis in obesity might be underlying the involvement of autophagy in the peripheral blood mononuclear cells (PBMCs). Twelve healthy male subjects (6 obese and 6 normal-weight) were recruited to participate in a maximal graded exercise test on a treadmill. Obese subjects exhibited a significantly lower Bax, but a higher Bcl-2 protein level in conjunction with a reduced Bax/Bcl-2 AUCi compared to normal-weight subjects following exercise. Furthermore, a greater LC3-II/LC3-I ratio and LC3-II/LC3-I AUCi was observed in obese subjects compared to normal-weight subjects. LC3-II/LC3-I AUCi was also positively associated with obesity-associated parameters (BMI, waist/hip circumference, and fasting insulin level), but was negatively correlated with Bax/Bcl-2 AUCi. These findings demonstrate that maximal aerobic exercise differentially mediates the intrinsic apoptotic pathway and autophagic activity in human PBMCs isolated from obese compared to normal-weight individuals. |
