Threshold sensitivity to sodium glutamate receptors («umami taste») and glomerular filtration rate in bronchial asthma

Abstract

Background. In experimental and clinical medicine, new data and ideas on the role of so-called “ectopic” chemosensory receptors expressed outside their canonical localizations have appeared. As for receptors for umami-substances, to date, certain data have been obtained on both receptors in the tongue and extraoral in the kidneys (monosodium glutamate as the best-known ligand). At the same time, the functions of these receptors are still not completely understood. The aim of the study was to assess the sensitivity of glutamate receptors to monosodium glutamate in bronchial asthma using the threshold measurement and to compare it with the glomerular filtration rate in the same patients. Patients and methods . 54 practically healthy individuals, 55 patients with bronchial asthma were examined. To assess the taste sensitivity to monosodium glutamate, solutions of monosodium glutamate were prepared at concentrations of 0.067; 0.1; 0.2; 0.3; 0.4; 0.5%. The concentration at which the taste of meat broth was felt was considered the threshold concentration of the sensation of umami taste. Glomerular filtration rate (eGFR) by CKD-EPI was calculated. Results. In patients with bronchial asthma, a significant direct correlation was found between the threshold measurement and the estimated glomerular filtration rate (high sensitivity to sodium glutamate correlates with a reduced glomerular filtration rate). Sensitivity to sodium glutamate is also directly related to indicators reflecting inflammation (the content of neutrophils, monocytes in peripheral blood, C-reactive protein, erythrocyte sedimentation rate). Conclusion. In bronchial asthma, the use of gustometry measurement has revealed the phenomenon of high sensitivity to monosodium glutamate, which correlates with a reduced glomerular filtration rate and inflammation ndices. It is suggested that the revealed features of glutamatergic signaling may serve as a common pathogenetic mechanism both in bronchial asthma and chronic kidney disease.