RESUMO
BACKGROUND: Body composition alterations may participate in the pathophysiological processes of type 2 diabetes (T2D). A sedentary lifestyle may be responsible for alterations of body composition and adverse consequences, but on which body composition of patients with T2D and to what extent the sedentary lifestyle has an effect have been poorly investigated. METHODS: We recruited 402 patients with T2D for this cross-sectional study. All patients received questionnaires to evaluate sedentary time and were further divided into three subgroups: low sedentary time (LST, < 4 h, n = 109), middle sedentary time (MST, 4-8 h, n = 129) and high sedentary time (HST, > 8 h, n = 164). Each patient underwent a dual energy X-ray absorptiometry (DXA) scan to detect body composition, which included body fat percentage (B-FAT), trunk fat percentage (T-FAT), appendicular skeletal muscle index (ASMI), lumbar spine bone mineral density (BMD) (LS-BMD), femoral neck BMD (FN-BMD), hip BMD (H-BMD) and total BMD (T-BMD). Other relevant clinical data were also collected. RESULTS: With increasing sedentary time (from the LST to HST group), B-FAT and T-FAT were notably increased, while ASMI, LS-BMD, FN-BMD, H-BMD and T-BMD were decreased (p for trend < 0.01). After adjustment for other relevant clinical factors and with the LST group as the reference, the adjusted mean changes [B (95% CI)] in B-FAT, T-FAT, ASMI, LS-BMD, FN-BMD, H-BMD and T-BMD in the HST group were 2.011(1.014 to 3.008)%, 1.951(0.705 to 3.197)%, - 0.377(- 0.531 to - 0.223) kg/m2, - 0.083(- 0.124 to - 0.042) g/cm2, - 0.051(- 0.079 to - 0.024) g/cm2, - 0.059(- 0.087 to - 0.031) g/cm2 and - 0.060(- 0.088 to - 0.033) g/cm2, p < 0.01, respectively. CONCLUSIONS: A sedentary lifestyle may independently account for increases in trunk and body fat percentage and decreases in appendicular skeletal muscle mass and BMD of the lumbar spine, femoral neck, hip and total body in patients with T2D.
RESUMO
Cellular senescence has been considered an important driver of many chronic lung diseases. However, the specific mechanism of cellular senescence in silicosis is still unknown. In the present study, silicotic rats and osteoclast stimulatory transmembrane protein (Ocstamp) overexpression of MLE-12 cells were used to explore the mechanism of OC-STAMP in cellular senescence in alveolar epithelial cell type II (AEC2). We found an increasing level of OC-STAMP in AEC2 of silicotic rats. Overexpression of Ocstamp in MLE-12 cells promoted epithelial-mesenchymal transition (EMT), endoplasmic reticulum (ER) stress, and cellular senescence. Myosin heavy chain 9 (MYH9) was a potential interacting protein of OC-STAMP. Knockdown of Ocstamp or Myh9 inhibited cellular senescence in MLE-12 cells transfected with pcmv6-Ocstamp. Treatment with 4-phenylbutyrate (4-PBA) to inhibit ER stress also attenuated cellular senescence in vitro or in vivo. In conclusion, OC-STAMP promotes cellular senescence in AEC2 in silicosis.
