Abstract
Metabolic syndrome combines metabolic disorders that lead to weight gain with concomitant systemic inflammation. It is important to identify the pathogenetic links between the disrupted metabolism of glucose, lipids, oxidative stress, inflammation and weight gain, as well as the molecular mechanisms of the circadian clock. The review provides the contemporary data on ensuring the circadian rhythms (CR), involving central and peripheral pacemakers,
their molecular component and hierarchy. The main factors in the CR disruption are changes in the duration of light-dark cycles, disturbance of light regime, duration of sleep, food intake in the afternoon. Disruption of the CR causes a decreased glucose tolerance, an increased insulin resistance of tissues, and impairs absorption, transport and deposition of lipids in the body, leading to the accumulation of excess energy. Such metabolic disorders occur in parallel with an increased level of systemic inflammation: the production of proinflammatory chemo- and cytokines, activation of immune cells. It has been concluded that the CR disorder leads to metabolic disruptions and systemic inflammation, which corresponds to the concept of metabolic syndrome.
References
Haller H. Epidermiology and associated risk factors of hyperlipoproteinemia Z Gesamte Inn Med. 1977 Apr 15;32(8):124-8.
Pucci G, Alcidi R, Tap L, Battista F, Mattace-Raso F, Schillaci G. Sex- and gender-related prevalence, cardiovascular risk and therapeutic approach in metabolic syndrome: A review of the literature. Pharmacol Res. 2017 Jun;120:34-42.
Myers J, Kokkinos P, Nyelin E. Physical Activity, Cardiorespiratory Fitness, and the Metabolic Syndrome. Nutrients. 2019 Jul 19;11(7). pii: E1652.
Oguntibeju OO. Type 2 diabetes mellitus, oxidative stress and inflammation: examining the links. Int J Physiol Pathophysiol Pharmacol. 2019 Jun 15;11(3):45-63.
Кайдашев ИП. Активация NF-kB как молекулярная основа патологического процесса при метаболическом синдроме. Физиологический журнал. 2012, 58(1):93-101. (Kaidashev IP. Activation of NF-kB as the molecular basis of the pathological process in the metabolic syndrome. Physiological Journal. 2012, 58(1):93-101.).
Kaidashev IP. Conception for permanent activation of nuclear factor kbeta as molecular basis for metabolic syndrom pathogenesis. Patologicheskaia fiziologiia i eksperimental’naia terapiia. 3 (2013): 65-72.
Daan S, Aschoff J. Circadian contribution to survival. In: Aschoff J, Daan S, Groos G, editors. Vertebrate Circadian System. Springer-Verlag; Berlin: 1982. pp. 305–21.
Pittendrigh CS. Temporal organization: reflections of a Darwinian clock-watcher. Annu Rev Physiol. 1993;55:16-54.
Hastings MH, Maywood ES, Brancaccio M. The mammalian circadian timing system and the suprachiasmatic nucleus as its pacemaker biology (Basel). 2019 Mar; 8(1): 13.
Berson D.M., Dunn F.A., Taka O.M. Phototransduction by retinal ganglion cells that set the circadian clock. Sciense. 2002; Vol. 295: 1070-1073.
Yamazaki S, Goto M, Menaker M. No evidence for extraocular photoreceptors in the circadian system of the Syrian hamster. J Biol Rhythms. 1999; 14:197-201.
Ketema N. Paul, Talib B. Saafir, and Gianluca Tosini The role of retinal photoreceptors in the regulation of circadian rhythms. Rev Endocr Metab Disord. 2009 Dec; 10(4): 271-278 .
LeGates TA, Fernandez DC, Hattar S. Light as a central modulator of circadian rhythms, sleep and affect. Nat Rev Neurosci. 2014 Jul; 15(7): 443-454.
Dibner C, Schibler U, Albrecht U. The mammalian circadian timing system: organization and coordination of central and peripheral clocks. Annu Rev Physiol. 2010;72:517-49.
Yoo SH, Yamazaki S, Lowrey PL, Shimomura K, Ko CH, Buhr ED, et al. PERIOD2::LUCIFERASE real-time reporting of circadian dynamics reveals persistent circadian oscillations in mouse peripheral tissues. Proc Natl Acad Sci U S A. 2004 Apr 13;101(15):5339-46.