“…Blood level of lactic acid increased by 45% (p<0.05), antioxidant activity of blood serum was signifi cantly reduced by 52%. Hypoxia during DM reduced aerobic oxidation in tissues, switching from carbohydrate to lipid metabolism and impairing utilization of free fatty acids [1]. Their accumulation produces a detergent effect, induced LPO activation in membranes, and decreases ATP levels in cells.…”
The effect of streptozotocin-induced diabetes mellitus on some parameters of energy metabolism and functional status of cell membranes was studied in experiments on rats. It was found that the development of diabetes mellitus is associated with dramatic changes in the metabolism of blood cells and kidney tissue: inhibition of aerobic ATP synthesis, accumulation of lactate, uncoupling of oxidative phosphorylation, and development of lactic acidosis. Diabetes mellitus leads to restructuring of membrane lipids, changes in microviscosity, and suppression of insulin receptors and membrane-bound Na(+), K(+)-ATPase, and Ca(2+)-ATPase. Sharply increased levels of LPO products and lactic acidosis during DM indicate an imbalance in the LPO-antioxidant system and development of oxidative stress.
“…Blood level of lactic acid increased by 45% (p<0.05), antioxidant activity of blood serum was signifi cantly reduced by 52%. Hypoxia during DM reduced aerobic oxidation in tissues, switching from carbohydrate to lipid metabolism and impairing utilization of free fatty acids [1]. Their accumulation produces a detergent effect, induced LPO activation in membranes, and decreases ATP levels in cells.…”
The effect of streptozotocin-induced diabetes mellitus on some parameters of energy metabolism and functional status of cell membranes was studied in experiments on rats. It was found that the development of diabetes mellitus is associated with dramatic changes in the metabolism of blood cells and kidney tissue: inhibition of aerobic ATP synthesis, accumulation of lactate, uncoupling of oxidative phosphorylation, and development of lactic acidosis. Diabetes mellitus leads to restructuring of membrane lipids, changes in microviscosity, and suppression of insulin receptors and membrane-bound Na(+), K(+)-ATPase, and Ca(2+)-ATPase. Sharply increased levels of LPO products and lactic acidosis during DM indicate an imbalance in the LPO-antioxidant system and development of oxidative stress.
When metabolic failure in children and adolescents with diabetes, are violations of the structural and functional properties of membrane - the receptor apparatus of cells, accompanied by a decrease in ATP levels, inhibition of activity of membrane-bound enzyme Na+,K+-ATPase, a sharp decrease in insulin binding receptor activity and decrease glucose uptake by cells that indicates a decline in cell sensitivity to insulin.Diabetes in children and adolescents occurs with lipid disorders, activation of the processes of lipid peroxidation, manifested increasing concentrations of both primary and secondary products of lipid peroxidation, changes in structural and functional properties of erythrocyte membranes, as well as disturbances in the antioxidant defense system. Changes in the studied indexes depend on the type of diabetes and duration of the disease.Imbalance in the system LPO-AOD in the background shows the development of dyslipidemia, oxidative stress, particularly pronounced in type 2 diabetes.
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