Objective:To study the correlation between the time within the target range of blood glucose and the reduction of muscle mass in middle-aged and elderly patients with type 2 diabetes (T2DM).Methods:A total of 245 middle-aged and elderly T2DM patients admitted to the Second People′s Hospital of Hefei from December 2020 to December 2021 were selected. All enrolled patients wore MeiQi blood glucose monitor to obtain time in range (TIR), time above range (TAR), time below range (TBR), mean amplitude of glycemic excursions (MAGE), coefficient of variation (CV), blood glucose standard deviation (SD), largest amplitude of glycemic excursions (LAGE), which was for assessing blood sugar fluctuation. The incidence of muscle mass reduction and sarcopenia was statistically analyzed, and the differences invarious observation indicators between the muscle mass reduction group and the non muscle mass reduction group were compared. Spearman correlation analysis was used to investigate the correlation between clinical indicators and limb skeletal muscle mass index (ASMI), and logistic regression was used to analyze the influencing factors of muscle mass reduction in middle-aged and elderly T2DM patients.Results:The prevalence of muscle mass loss in 245 T2DM patients was 25.71%(63/245), and the prevalence of sarcopenia was 13.06%(32/245). There were statistically significant differences in age, gender, body mass index (BMI), blood phosphorus, homeostatic model assessment of insulin resistance (HOMA-IR), urine albumin creatine ratio (ACR), 25 hydroxyvitamin D, diabetes nephropathy (DN) patient proportion, ASMI, grip strength, and 5 sit up test times between the muscle mass reduction group and the non muscle mass reduction group (all P<0.05). The TIR of the muscle mass reduction group was lower than that of the non muscle mass reduction group, while the TAR and mean blood glucose (MG) were higher than those of the non muscle mass reduction group, with statistically significant differences (all P<0.05). ASMI was negatively correlated with age, males, and HOMA-IR (all P<0.05), but positively correlated with BMI and 25 hydroxyvitamin D (all P<0.05). ASMI was positively correlated with SD and TIR (mean P<0.05), and negatively correlated with CV, LAGE, TAR, and MG (all P<0.05). The results of univariate regression analysis showed that age, male gender, DN, and TAR were risk factors for muscle mass reduction, while BMI, 25 hydroxyvitamin D, and TIR were protective factors for muscle mass reduction (all P<0.05). After adjusting for other related factors, TIR remained a protective factor for decreased muscle mass (all P<0.05). Conclusions:TIR is an independent protective factor for muscle mass loss in middle-aged and elderly T2DM patients, and the incidence of muscle mass loss can be reduced by increasing TIR levels in clinical practice.

Objective: To investigate the effect of TNF-α on the expressions of tight junction protein ZO-1 and Claudin-4 in rat alveolar epithelial typeⅡ cells (AEC-Ⅱ). Methods: Rat AEC-Ⅱ cells were cultured in vitro and divided into the control group, and TNF-α 24 h, 48 h, 72 h groups. The control group was cultured with DME F12 medium containing fetal bovine serum, and the TNF-α groups were intervened by TNF-α with a concentration of 10 ng/mL for 24 h, 48 h, and 72 h, respectively. After co-culture, the transmission electron microscopy was used to identify and observe the ultrastructural changes of rat AEC-Ⅱ cells. The cell inhibition rate was determined by MTT assay, and the cell apoptosis rate was measured by flow cytometry. The expression and distribution of tight junction protein ZO-1 and Claudin-4 in each group were observed by immunofluorescence method. The transcriptional levels of ZO-1 and Claudin-4 were detected by real-time fluorescent quantitative PCR. The expressions of ZO-1 and Claudin-4 were detected by Western blot. One-way analysis of variance (ANOVA) was used for comparisons among groups and SNK-q test was used for pairwise comparisons between groups. The non-parametric test of rank transformation was used when homogeneity of variance were not met. The value of P<0.05 was considered significantly different. Results: Transmission electron microscopy showed that the AEC-Ⅱ cells in the control group obtained characteristic lamellar bodies of different sizes. The lamellar bodies in each TNF-α group were gradually emptied and apoptotic cells were observed under the visual field. The cell inhibition rate and early apoptosis rate of each TNF-α group were significantly higher than those of the control group (all P<0.05). Confocal microscopy showed that ZO-1 was linearly distributed along the cell membrane, and Claudin-4 was scattered along the cell membrane. In the TNF-α groups, the fluorescence intensity of ZO-1 was weakened and the continuity was broken as well as the linear structure. The fluorescence intensity and density of Claudin-4 were decreased in the TNF-α groups. Besides, the transcription and expression of ZO-1 in the TNF-α 24 h group were lower than those in the control group, but there was no significant difference (P>0.05). However, the mRNA level of ZO-1 in the TNF-α 48 h group (0.28±0.06) and 72 h group (0.13±0.07) were significantly lower than those in the control group. And their protein levels of TNF-α 48 h group (0.44±0.09) and of TNF-α 72 h group (0.2±0.01) were lower than that of the control group (0.69±0.12). Compared with the control group, the transcription level (24 h: 0.16±0.03; 48 h: 0.04±0.01; 72 h: 0.01±0.00 vs 1.00±0.00) and expression (24 h: 0.49±0.08; 48 h: 0.34±0.05; 72 h: 0.04±0.01 vs 0.96±0.13) of Claudin-4 in each TNF-α group were significantly decreased, and showed a decreasing trend with time (all P<0.05). Conclusions TNF-α can damage the pulmonary epithelial barrier by damaging alveolar epithelial typeⅡ cells and down-regulating the expression and distribution of ZO-1 and Claudin-4.