Mohammad Afzal Khan, Faris Mohammed Nour Altaf, Muhammad Naeem Chaudhry.
CHRONIC EXPERIMENTAL DIABETES MELLITUS; Quantitative changes in dorsal root ganglion cells.
Professional Med J Jan ;22(12):1560-4.

Multiple factors operate in the development of diabetic neuropathy. Sensory neurons are not protected by blood-brain or blood-nerve barrier; also the dorsal root ganglion cells (DRG) have a higher metabolic requirement than the nerve trunks. Oxygen level at the dorsal root ganglions also appears to be lower. All these physiological characteristics suggest that DRG may be particularly susceptible to damage in prolonged diabetic conditions. Objectives: To observe the quantitative cellular changes in dorsal root ganglion cells in rats with prolonged experimental diabetes. Study Design: An experimental study. Setting: Department of Human Anatomy, Faculty of Medicine, Umm al Qura University, Makkah, Saudi Arabia. Period: Fifteen months to complete. Material and methods: Observations were made on six control and six streptozotocin-treated male Sprague-Dawley rats after 12 months of diabetes. Cell count was done on silver-stained paraffin sections. DRG cells were arbitrarily grouped as large A-type and small B-type. Statistical examination of the cell count was done using a two-tailed t-test. Values were considered significant at P ≤ 0.05. Results: In the control group of animals the mean total number was 15856.33 ± 552.538 while in the diabetic animals it was 11836.666 ±583.177; the reduction in the number of cells was significant. The number of A-type and B-type cells and their percentages in the control group and the diabetic group of animals were 2753.833±257.683 (17.36%), 13102.5±443.092 (82.63%) and 1202.833±87.082 (10.16%), 10633.833±517.900 (89.83%) respectively. The differences in the number of A-type and B-type of cells when compared between control and diabetic groups of animals were statistically highly significant. Conclusion: Selective cells damage to DRG cells may be the harbinger of diabetic neuropathy in experimentally induced diabetic rats.

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