METABOLIC SYNDROME, CHRONIC LOW-GRADE INFLAMMATION, AND MELATONIN

Abstract

The metabolic syndrome (MetS) is a combination of cardiovascular disease factors, including obesity, insulin resistance (IR), and chronic low-grade inflammation (CLGI). Therefore, successful treatment of MetS requires a potential drug that has antagonistic effects on MetS-triggering factors. Currently, the relationship between circadian disorders, glucose metabolism, and other components of MetS is being intensively studied, as the circadian system is one of the main regulators of metabolism. Deficiency of melatonin (MEL) production or impaired expression of neurohormone receptors is associated with obesity, MetS, IR, hypertension, and type 2 diabetes mellitus. MEL is a potential candidate for the treatment of obesity in MetS due to its biological effects on insulin and adipose tissue metabolism, lipolysis, and mitochondrial processes. In particular, there is a significant correlation between MEL and insulin levels in patients with MetS, as well as between the MEL/insulin ratio and changes in blood lipid profile. It is likely that the most important function of MEL is the antioxidant protection of cells. At the same time, MEL is known for its anti-inflammatory properties, which obviously occur at different levels. In particular, it is the correction of metabolic dysregulation, including the IR state; processes that contribute to CLGI, and autocrine and paracrine effects on immune cells. Thus, MEL can provide an innovative strategy for the treatment of MetS by combining its effect on the circadian rhythm with cytoprotective properties. However, there is little data on the relationship between MetS, CLGI and MEL. This review aims to discuss the significance and specifics of the relationship between MetS and CLGI. Particular attention is paid to describing the specific mechanisms of action of MEL on CLGI as well as to analyzing the evidence from experimental and clinical trials of MEL. Search strategy. The search was conducted in Scopus, Science Direct (from Elsevier), and PubMed, including Medline databases.