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Experimental and Clinical Gastroenterology

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Endotoxemia in metabolic syndrome and some mechanisms of its development

https://doi.org/10.31146/1682-8658-ecg-181-9-11-17

Abstract

The aim. Assessment of the relationship between the occurrence of endotoxemia and impaired resorption function of the small intestine, arrhythmia of the motility of the stomach and intestines, and excessive bacterial growth in the metabolic syndrome (MS).

Materials and methods. 62 patients with MS were examined. The average age was 48.62+3.75 years. The motor function of the gastrointestinal tract was studied using peripheral electrogastroenterocolography. To assess the absorption processes in the small intestine, stress tests with glucose and d-xylose were used. Blood endotoxin level, quantitative and& qualitative composition of parietal microbiota of small intestine were determined using an Agilent gas chromatograph with mass-selective and flame-ionization detectors (Agilent Technologies, USA).

Results. 82.9% of the examined patients with MS showed clinical signs of intestinal damage. The electrical activity of& the& small intestine departments in the postprandial period was low in 70% of patients. The electrical activity of& the& colon on an empty stomach was not changed, and after a food load was reduced. Discoordination of motility is observed between small intestine and the colon, aggravated after food stimulation. A significant decrease in the rhythm of contractions is observed at the frequencies of the jejunum, ileum, and colon both on an empty stomach and in the postprandial period, which indicates a weakening of propulsive bowel contractions in patients with MS. In patients with MS, an increase in& the& absorption of glucose and d-xylose was revealed in comparison with the group of healthy individuals. In patients with MS, excessive bacterial growth in small intestine is observed mainly due to conditionally pathogenic microbiota strains. According to the results of the study of blood endotoxin level in patients with MS, a significant increase was revealed in comparison with the control group. Correlation analysis showed a moderate negative relationship between the level of endotoxin and electrical activity of small intestine, between the level of endotoxin and the ratio of the ratio of& the& colon to the ileum. A moderate positive relationship was established between the degree of endotoxemia increase and glucose absorption in small intestine.

Conclusion. A study of the level of endotoxin and indicators of excessive bacterial growth, motor evacuation and resorption functions of small intestine revealed important pathogenetic patterns regarding the contributing role of the latter in& the development of endotoxemia in patients with MS.

About the Authors

M. V. Lyapina
Federal State Budgetary Educational Institution of Higher Education “Tyumen State Medical University” of the Ministry of Health of the Russian Federation
Russian Federation

Mariya V. Lyapina, Candidate of Medical Sciences, Associate Professor of the Department of Propaedeutic and Faculty

625023, st. Odesskaya, 54, Tyumen



A. P. Lukashevich
Federal State Budgetary Educational Institution of Higher Education «Izhevsk State Medical Academy» of the Ministry of Health of the Russian Federation
Russian Federation

Anna P. Lukashevich, Candidate of Medical Sciences, assistent of the Department of Propaedeutics of Internal Medicine with a nursing course

426034, st. Kommunarov, 281, Izhevsk



Ya. M. Vakhrushev
Federal State Budgetary Educational Institution of Higher Education «Izhevsk State Medical Academy» of the Ministry of Health of the Russian Federation
Russian Federation

Yakov M. Vakhrushev, Doctor of Medical Sciences, professor, Head of the Department of Propaedeutics of Internal Medicine with a nursing course

426034, st. Kommunarov, 281, Izhevsk



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Lyapina M.V., Lukashevich A.P., Vakhrushev Ya.M. Endotoxemia in metabolic syndrome and some mechanisms of its development. Experimental and Clinical Gastroenterology. 2020;(9):11-17. (In Russ.) https://doi.org/10.31146/1682-8658-ecg-181-9-11-17

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