Objective To investigate motor nerve function status in rats with diabetes mellitus by motor unit number estimation (MUNE), and discuss it′s early diagnostic value in diabetic peripheral neuropathy (DPN). Methods Diabetic rat model (DM group) was induced by streptozotocin. The MUNE of gastrocnemius muscle and motor nerve conduction (MCV, CMAP) of the sciatic nerve were measured at the 4th, 8th and 12th week after onset of hyperglycemia in the DM group and the control group (normal SD rats). The ultrastructure of sciatic nerve was observed by electron microscope. Results At the 4th week, MUNE of gastrocnemius muscle was significantly decreased in DM group compared to that of the control group (275.88 ± 87.87 vs 369.71 ± 75.64,P<0.05). There were no significant differences in MCV and CMAP of sciatic nerve be?tween two groups. The electron microscopy observation showed that most nerve fibers were normal;a small amount of axonal atrophy, and myelin lamellar structure was separated in DM group. At the 8th week, compared with the control group, MUNE were reduced in gastrocnemius muscle in DM group (357.49±72.68 vs 221.26±92.41, P<0.01). There were no significant dif?ferences in MCV and CMAP of the sciatic nerve between DM group and control group. The electron microscope observation showed that part of nerve fibers were normal, the myelin focal plate layer was loose and separated, axonal atrophy, the axonal membrane and myelin sheath inner layer was separated with big gap. At the 12th week, MUNE of gastrocnemius muscle (127.87±19.80 vs 366.85±51.25), sciatic nerve MCV [(35.06±4.43) m/s vs (50.47±6.07) m/s] and CMAP [(2.91±1.37) mV vs (5.98±2.14) mV] were significantly decreased in DM group than those of control group (P<0.01). The electron microscopy observation showed severely damaged myelin flex and axonal squeeze. Conclusion MUNE is much earlier in detecting ear?ly motor nerve dysfunction in DM than conventional motor nerve conduction test.

Objective To assess the function of motor nerve fiber in patients with diabetic peripheral neuropathy (DPN) by single-fiber conduction studies.Methods According to the diagnostic standard of DPN issued in Toronto meeting in 2009,on the basis of the result of peroneal nerve conventional conduction study,a total of 65 patients with DPN in the Department of Endocrinology and the Department of Neurology of Tianjin Third Central Hospital from October 2012 to October 2013 were enrolled into the study,from whom 33 had abnormal sensory conduction (sensory-diabetic peripheral neuropathy group,S-DPN group),32 had abnormal sensory motor conduction (sensory motor-diabetic peripheral neuropathy group,SM-DPN group).Single-fiber conduction velocity (SF-CV) and single-fiber distal motor latency (SF-DML)were detected in all subjects.The obtained results were compared with the data from 34 healthy volunteers (control group).The relationship of SF-CV,SF-DML and the duration of diabetes mellitus,fasting glucose,HbA1 c was also studied in DPN patients.Results The SF-CV ((43.1 ± 3.6) m/s) was decreased in S-DPN group compared with control group ((47.5 ± 3.3) m/s,t =5.077,P ＜ 0.01).There were no significant differences in SF-DML ((3.6 ± 0.7) ms),motor nerve conduction velocity (MCV (49.5 ± 2.6)m/s) and DML ((3.4 ± 0.6) ms) in S-DPN group compared with that of control group ((3.4 ± 0.5) ms,(50.9 ± 3.5) m/s,(3.2 ± 0.5) ms,respectively).SM-DPN group had lower SF-CV ((35.2 ± 3.6)m/s,t =9.119,14.219),MCV ((40.9 ± 3.2) m/s,t =11.131,13.025) and increased SF-DML ((4.5±0.7) ms,t=5.692,7.231),DML ((4.2 ±0.7) ms,t=5.561,6.975) compared with the other two groups (P ＜0.01).SF-CV in DPN patients was negatively related to the diabetic duration (r =-0.340,P =0.006),while SF-DML had no correlation with duration of DM,fasting blood glucose and HbAlc.Conclusions Detection of SF-CV is easy to find early motor nerve dysfunction in DPN patients.SF-CV is decreased with the increasing duration of diabetes.

Humans ; Proto-Oncogene Proteins p21(ras)/genetics* ; Prognosis ; Biomarkers, Tumor/genetics* ; Mutation/genetics* ; Colorectal Neoplasms/genetics* ; Proto-Oncogene Proteins B-raf/metabolism*