Abstract
Neurodegenerative disorders in the cerebral cortex and hippocampus are one of the most common causes of disability and mortality in patients with diabetes. Excessive glucose concentration causes a toxic effect due to an increased amount of glycolysis products, lipid and protein peroxide oxidation, decreased membranous potential of the mitochondria and deficiency of neuron energy supply due to mitochondrial dysfunction. Gammaamino butyric acid is known to localize to the mitochondria, and its functional cycle is closely linked to glucose metabolism. Objective of the study: experimental investigation of сarbacetam effect with cerebral mitochondrial dysfunction of rats with type 2 diabetes mellitus. The experiments were conducted on laboratory nonlinear albino male rats with the body weight 0.18–0.20 kg. Type 2 diabetes is modeled on streptozotocin and a high-fat diet. Carbacetam was administered intraperitoneally at a dose of 5 mg/kg, once daily for 14 days. Under conditions of central nervous system damage induced by type 2 diabetes mellitus, lipid and protein peroxide oxidation increases in the mitochondrial fraction of the cerebral cortex and hippocampus of rats; activity of superoxide dismutase, catalase, α-ketoglutarate dehydrogenase, succinate dehydrogenase decreases; a relative rate of mitochondrial swelling increases. After carbacetam administration during 14 days the content of products reacting with 2-thiobarbituric acid and protein oxidation modification decrease in the mitochondria of the brain and hippocampus of rats with type 2 diabetes mellitus; activity of catalase in the cerebral cortex and α-ketoglutarate dehydrogenase in the hippocampus increases, activity of succinate dehydrogenase increases in both structures examined which is indicative of its antioxidant properties. Decrease of a relative rate of mitochondrial swelling in the cerebral cortex and hippocampus of rats confirms a protective effect of carbacetam under conditions of mitochondrial dysfunction.
Highlights
IntroductionGlucose is the main source of energy for the brain
Considering cerebroprotective effect of gamma-aminobutyric acid (GABA) agents in case of functionalorganic disorders of the central nervous system (CNS), the issue concerning carbacetam effect, a new modulator of GABA-ergic system, is of a certain interest [5], under conditions of functional disorders of the cerebral mitochondria state caused by type 2 diabetes mellitus (DM)
The obtained result correlates with the conclusions drawn by other scientists who stated that TBA AP content increased due to the effect of highly reactive oxygen forms acting on polyunsaturated fatty acids, components of phospholipids of all the cellular membranes; this parameter is a marker of mitochondrial membrane damage [16]
Summary
Glucose is the main source of energy for the brain. The brain containing the largest amount of mitochondria is a regulation center of the body energy homeostasis. The authors guarantee absence of competing interests and their own financial interest when carrying out the research and writing the article. Клінічна ендокринологія mitochondrial dysfunction of the brain and decrease of energy deficiency is a topical area of pharmacological protection. According to the latest scientific data mitochondria contain gamma-aminobutyric acid (GABA) — an inhibitor neurotransmitter of the CNS and trophic factor of synaptogenesis. It functional cycle is closely associated with glucose metabolism. Objective of the study: experimental investigation of carbacetam effect with cerebral mitochondrial dysfunction of rats with type 2 diabetes mellitus
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