ABSTRACT
Background: Diabetes mellitus is a disease caused by an inability of the body to metabolize glucose properly. The prevalence of diabetes is rapidly rising all over the globe at an alarming rate. As Insulin and non-insulin dependent diabetes shows their effect on various physiological systems includes central, peripheral and autonomic nervous systems, musculoskeletal, cardiovascular and other vital systems. A common complications due to the IDDM and NIDDM includes peripheral neuropathy, retinopathy, nephropathy and vascular complication. Insulin and non-insulin dependent diabetes mellitus, both affect the peripheral nervous system significantly. Therefore we would like to find out neurophysiological changes on peripheral nervous systems between insulin and non-insulin dependent diabetes mellitus. Aim: To find out the Neuro-physiological changes between IDDM and NIDDM. Materials and Method: 120 individuals screened with SF36 (general health good and above) were included with age limit between 25 to 60 years. Those individuals having a history of hospitalization in last 1 year, acute fever, present history of radiculopathy and open wound were excluded. They were divided into 2 groups IDDM and NIDDM. For nerve conduction study–distal latency, amplitude and NCV of sensory and motor nerves were performed. Nerve conduction studies of common peroneal, tibial and sural nerves were examined in both groups. Latency, NCV and CMAP/SNAP were taken as outcome measures. Result and Discussion: Bio-statistical analysis has been done using Mann-Whitney test. Result suggest that there is a significant difference in Neurophysiological changes (p<0.05) between IDDM and NIDDM groups. Conclusion: In context to our study and neurophysiological findings, individuals with IDDM must be taken into consideration for promotion, prevention, and care as compared to NIDDM for secondary complications.
ABSTRACT
An A to G mutation at nucleotide 3243 or 8344 of the mitochondrial genome has been associated with insulin dependent diabetes mellitus(IDDM) and noninsulin dependent diabetes mellitus(NIDDM) in some patients whose family members are frequently affected in maternally inherited fashion. The hypothesis is entertained that defective oxidative phosphorylation system(OXPHOS) caused by mitochondrial DNA mutations would hamper the insulin secretion from pancreas beta islet cells, which requires large amount of ATP energy. Recently, a number of study have been reported to examine the frequecy of these mutations in diabetic populations. In this study, efforts have been directed to investigate the frequency of MELAS tRNALeu(3243) and MERRF tRNALys(8344) mutations in 53 Korean IDDM patients. Total genomic DNA extracted from patients' lymphocytes have been amplified using two sets of mitochondrial specific primers to cover the regions of nt 3243 or 8344. PCR-RFLP anlaysis using Apa I for MELAS(3243) or Ban II for MERRF(8344) were utilized to screen the presence of these mutations in 53 IDDM patients. Two positive controls have been directly sequenced to confirm the presence of these mutations. The results showed that none of IDDM patients(0/53) screened carried these mutations. In conclusion, mitochondrial DNA mutations of MELAS(3243) or MERRF(8344) may be very rare causative factor in developing IDDM, though a large number of IDDM patients are needed to be screened.