Obesity: the role of desynchronosis and genetic factors in mechanisms of its development

- Ризничук, М.О. and Пішак, В.П. (orcid.org/0000-0002-0637-6936) (2017) Obesity: the role of desynchronosis and genetic factors in mechanisms of its development Regulatory mechanisms in biosystems, 1 (8). pp. 1-102. ISSN 2519-8521

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Abstract

Summary. The article highlights the role of desynchronosis and certain genetic factors in the development of obesity. Some pathogenetic links of obesity and the influence of melatonin on them analyzed. Found that desynchronosis is one of the causes of obesity as a result of disregulatory changes in chronoperiodic system – between suprachiasmatic nuclei of the hypothalamus and secretory activity of the pineal gland. In obesity there are some changes in circadian patterns of important physiological parameters. Acrophases of blood pressure; rhythm of hormones secretion, including insulin; electrolytes; sleep-wake cycle displaced for a period of day not characteristic for normal course. Phase discrepancies of established circadian oscillations of physiological processes arises. Gradually emerges preconditions of fat metabolism imbalance, particularly visfatyn, apelin and vaspyn – components of atherosclerotic lesions. Close relationships between metabolism and circadian mechanisms have many evidences. It is proved, that there is a strong direct impact of endogenous circadian rhythms on metabolic pathways that do not depend on food intake or sleep. Identified potential low molecular weight biomarkers of human’s circadian phases. A number of key metabolic enzymes in tissues such as the liver, adipose tissue or the pancreas are chronodependent. Desynchronosis phenomena caused by genetic or environmental factors, can lead to serious metabolic disorders, including obesity, insulin resistance and metabolic syndrome. Genesis of pineal removal-induced insulin resistance and reduced glucose tolerance in cells related to the consequences of melatonin absence, which leads to abnormalities in insulin signaling pathway and reduced GLUT4 gene expression and protein content. Insulin-sensitive tissues (white and brown adipose tissue, skeletal muscle and heart) after pineal removal characterized by a significant reduction of GLUT4 mRNA and the content of microsomal and membrane proteins, which are compensate during treatment by melatonin. Functional synergy between melatonin and insulin exist. Melatonin is able through membrane receptors MT1 to cause rapid tyrosine phosphorylation, activate tyrosine kinase of beta subunit of insulin receptor and mobilize several intracellular stages of insulin-signaling pathway transduction. Thus, the protective effect of melatonin in violation of carbohydrate metabolism manifested in the formation of circadian periodism by modulating the expression of time genes.

Item Type:	Article
Keywords:	melatonin circadian mechanisms, gen, epiphysis
Subjects:	Science and knowledge. Organization. Computer science. Information. Documentation. Librarianship. Institutions. Publications > 6 Applied Sciences. Medicine. Technology > 61 Medical sciences
Divisions:	Institute of Psychology after N.Kostiuk > Department of developmental psychophysiology
Depositing User:	чл.-кор. Василь Павлович Пішак
Date Deposited:	14 Sep 2017 06:51
Last Modified:	14 Sep 2017 06:51
URI:	https://lib.iitta.gov.ua/id/eprint/707647

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