The Impact of Diabetes Mellitus on Nerve Regeneration at a Critical Level

Abstract

Randomly assigning sixteen healthy mongrel dogs (4-6 months old) to one of four groups—"control," "diabetic one," "diabetic two," or "diabetic three" they were all given intramuscular injections of ketamine and xylazine to put them to sleep. Injecting 120 mg/kg of alloxan monohydrate intraperitoneally (quarter, half, and full doses, respectively) caused diabetes mellitus in the diabetic group. Each animal had left-sided sciatic nerve induction damage prior to the experiment. For eleventh-two days, the canines were monitored using clinical reflexes of the sciatic nerve, including motor and sensory. Displayed an impressive degree of converging between the control and D1 groups as well as D2 and D3 parties. Along with the aforementioned clinical symptoms, diabetic groups also exhibit elevated blood glucose levels, depressive symptoms, polyuria, and increased water intake. The control and D1 groups had the largest ratio of relative gastrocnemius muscle means weight (0.75), and the least amount of muscle atrophy (0.70), on day 112 postoperatively (PO), compared to the D2 and D3 groups, which had the lowest ratios (0.55) (Table 4.3).  The relative mean weight of the gastrocnemius muscle began to atrophy following sciatic nerve damage, according to a comparison. Based on the data shown significant differences between the left sciatic nerve (OP) and right sciatic nerve in the same group, but no significant differences between the control and D1 groups. Histopathological analyses revealed that all groups converged on a few key metrics, including the proliferation of schwann cells and the orientation of regenerative nerve fibres; however, at 16 weeks post-operatively, both the control and D1 groups showed a comparative advantage in the quantity and quality of nerve fibrous formatting. The conclusion was determined that the danger level for diabetes, which impedes and delays nerve regeneration, is 300-400 mg/dl.