Objective To investigate the effect of exercise on the cardiovascular autonomic neuropathy (CAN) in type 2 diabetes mellitus(T2DM) and related risk factors of heart rate recover (HRR).Methods One hundred and five patients with definitely diagnosed T2DM were selected as the research subjects.All patients underwent the oral glucose tolerance test and treadmill exercise test before and after treatment.The related risk factors leading to abnormal HRR were analyzed.Abnormal HRR was divided into the general therapy group (GT) and the intensive therapy group (IT) according to different treatment schemes.The GT group used metformin and diet control,whereas on this basis the IT group accepted the mild enhancement exercise training.The clinical biochemical indicators and HRR change before and after treatment were compared between the two groups.Results Abnormal HRR had significant correlation with FBG,HbA1c,resting heart rate,maximal heart rate and systolic blood pressure(SBP)(P＜0.05).After two-month mild enhancement exercise training,FBG,HbA1c and resting heart rate in the GT group and IT group were significantly decreased compared with those before treatment(P＜0.05),while HRR was significantly increased;compared with those after treatment in the GT group,the FBG,HbA1c levels and resting heart rate in the IT group were significantly decreased,while HRR was significantly increased (P＜0.05).Conclusion FBG,HbA1c and resting heart rate are the important risk factors for abnormal HRR in T2DM patients,mild enhancement exercise training could reduce blood glucose level and increases HRR,thus effectively improve cardiac autonomic neuropathy.

OBJECTIVE To investigate the effect of erianin on the angiogenesis of glomerular endothelial cells in diabetic nephropathy(DN)rats and the role of slit homolog 2 protein(Slit2)/roundabout homolog 1(Robo1)consecutive signaling pathway.METHODS Rats were fed with high sugar and high fat feed for 8 weeks,before being intraperitoneally injected with streptozotocin solution(35 mg·kg-1)to prepare a DN rat model.DN rats were divided into the model group and model+erianin 10,20 and 40 mg·kg-1 groups,with 10 rats in each,while another 10 rats served as normal control group.The urine protein quantification kit was used to measure the 24 h urine protein level of rats in each group while the automatic biochemical analyzer was used to detect the fasting plasma glucose(FPG)and serum creatinine(Scr)levels of rats in each group.PAS staining was applied to observe the pathological changes in the renal tissue of rats in each group.Immunofluorescence was used to detect the expressions of platelet endo-thelial cell adhesion molecule-31(CD31)and podocalyxin(PCX)in kidney tissue of rats in each group.Western blot was adopted to detect the expressions of Slit2 and Robo1 proteins in the renal tissues of rats in each group.RESULTS Compared with normal control group,the CD31 protein expressions,FPG,Scr,24 h urine protein levels,and renal tissue Slit2 and Robo1 protein expressions were significantly increased in the model group(P<0.05).Pathological and immunofluorescence results suggested that rats in the model group developed many neoplastic glomerular capillaries,glomerular hypertrophy,and dilated mesangial areas,with non-tubular CD31 staining lacking adjacent PCX staining,and partial staining of tubular areas of CD31 lacking adjacent PCX staining.Compared with the model group,the CD31 glomerular endothelial area,FPG,Scr,24 h urine protein levels,and protein expressions of Slit2 and Robo1 in renal tissues were significantly reduced in the model+erianin 10,20 and 40 mg·kg-1 groups(P<0.05).Pathological and immunofluorescence results showed new glomerular capillaries,glomerular hypertrophy and dilatation of the thylakoid area were attenuated in rats,and CD31 tubular region staining was essentially adjacent to the PCX foot cell region staining in the model+erianin 10,20 and 40 mg·kg-1 groups.CONCLUSION Erianin may inhibit angiogenesis in glomerular endothelial cells of DN model rats by inhibiting the Slit2/Robo1 signaling pathway.