THE SYSTEM OF SEROTONIN METABOLISM IN THE BRAIN OF RATS IN THE DEVELOPMENT OF GLUTAMATEINDUCED OBESITY AND ITS CORRECTION WITH NANOCRYSTALLINE CERIUM DIOXIDE

One of the causes of obesity is the body’s energy imbalance. The aim of our work was to investigate the serotonin system in the brain tissue of rats with glutamate-induced obesity and its correction with nanocrystalline cerium dioxide. The research was conducted on 30 white rats, divided into 3 groups of 10 animals each: 1st − intact control, 2nd − simulation of obesity by administration of monosodium glutamate to neonatal animals, 3rd − correction of obesity using nanocrystalline cerium dioxide against the background of neonatal administration of monosodium glutamate. To confirm the presence of obesity, at 4 months of age, rats were weighed, naso-anal length was measured, and Lee’s index was calculated. It was found that rats after neonatal administration of monosodium glutamate developed obesity, and the content of serotonin in the brain decreased by 72.9% compared to the control. The content of tryptophan, a precursor in the synthesis of serotonin, in rats with glutamate-induced obesity was 93.3% lower compared to controls. Tryptophan hydroxylase activity in the brain of rats with glutamate-induced obesity tended to decrease, and tryptophan decarboxylase activity increased by 65.9% compared to the controls. The activity of monoamine oxidase in the brain of rats after neonatal administration of monosodium glutamate increased by 41.7% compared to the control, which indicates enhanced degradation of serotonin. Indoleamine-2,3-dehydrogenase activity in the brain of rats with glutamate-induced obesity increased by 122.2%, this evidences activation of the alternative kynurenine pathway of tryptophan metabolism in the brain. This may also be one of the reasons for the reduced serotonin content in the brains of rats with glutamate-induced obesity. Periodic administration of nanocrystalline cerium dioxide to rats after neonatal sodium glutamate administration prevented obesity and led to an increase in serotonin and tryptophan content in the brain by 171.6% and 72.7%, respectively, a decrease in tryptophan decarboxylase activity by 15.1%, an increase in monoamine oxidase activity by 60.7% and a decrease in indoleamine2,3-dihydrogenase activity by 17.7% compared to rats after neonatal sodium glutamate administration. We conclude that the serotonin system is involved in the development of glutamate-induced obesity, and that periodic administration of nanocrystalline cerium dioxide significantly improves serotonin metabolism parameters.