부산대학교 도서관

Purpose: To evaluate chronic stress and voluntary wheel running on murine beta-cell number, insulin-positive area, hind limb skeletal muscle morphology, autophagy protein abundance, and muscle atrophy gene expression. Methods: Forty male Balb/c mice were randomized into four groups: sedentary (N = 10: Sed), sedentary stressed (N = 10: St), exercise (N = 10: Ex), and exercise stressed (N = 10: ExSt). Results: Body weight increased more in ExST than Ex by week four of stress; Ex weighed less than Sed and St mice at study conclusion. Islet area was increased in ExSt (24,223 ± 2670 µm2) vs. Ex mice (16,811 ± 2704 µm2), (P < 0.05) Average β-cell number per islet was higher in ExSt (93.2 ± 5.7) and St (91.0 ± 5.2) mice when compared to Ex (68.6 ± 3.7) or Sed (70.7 ± 4.8), (P < 0.05). Exercise, with or without stress (Ex, ExSt), increased muscle mass vs. Sed and St mice, (P < 0.05). Both the total AKT and the pAKT protein levels were increased in ExSt vs. Sed. TOPORS mRNA expression was reduced in the Ex and ExST compared to both Sed and St; Nedd41 real-time mRNA expression was reduced in Ex vs. Sed, and St. Beclin-1 protein abundance was reduced in Ex and ExSt vs. Sed. Conclusion: Eight weeks of chronic stress increased β-cell proliferation and islet area, but did not increase muscle ubiquitin-associated atrophy gene mRNA levels. Exercise coupled with stress appeared to improve muscle protein accumulation, and therefore could be a potential means to reduce muscle losses under conditions of mild stress or β-cell dysfunction. [ABSTRACT FROM AUTHOR]