Abstract

Introduction: Type 2 Diabetes Mellitus (DM2) viewed as a major cause for neurodegenerative and cognitive abnormalities. One of the possible reason for that should be insulin resistance and hyperinsulinemia two main clinical future of DM2. The mechanism relationship between insulin and development of diabetic neuropathy and encephalopathy not clear yet. Material and methods: In 51 DM2 patients in age between 42 and 64 years old, without neurologic complications or with presence of different stages of neuropathy/encephalopathy were observed clinically and diagnosis confirmed by neurologist. Patients divided into two groups according to presence of mild and severe neuropathy or encephalopathy. For lab study cubital venous blood plasma taken for measure of plasma insulin level by ELISA. Results: Neuropathy/encephalopathy were registered in 71% of DM2 patients. HbA1c level were higher than healthy subjects and were comparable in both groups with severe neuropathy/encephalopathy and without. Blood plasma insulin level were between 14 and 21,7 μU/ml, significantly higher than normal ranges (0,7 – 9,07 μU/ml). Plasma insulin level were decreased according to severity of neuropathy/encephalopathy, and suggested about linkage between functional activity of beta-cells and neurodegeneration. Index HOMA-B indicates decreasing of beta-cells functional activity. Index Caro (glucose to insulin ratio) also been decreased and suggested about insulin resistance in these patients. When we analysed blood plasma insulin level according to presence and severity of diabetic neuropathy and encephalopathy there was significant Conclusion: Neurodegeneration is a frequent future of DM2 and were found in 71% cases. Presence and severity of neurodegeneration in DM2 have negative linkage with plasma insulin level and suggest about involvement of insulin resistance into pathogenesis of neurodegeneration. no funding or grants This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

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