Abstract
Metabolic syndrome (MetS) has a worldwide tendency to increase and depends on many components, which explains the complexity of diagnosis, approaches to the prevention, and treatment of this pathology. Insulin resistance (IR) is the crucial cause of the MetS pathogenesis, which develops against the background of abdominal obesity. In light of recent evidence, it has been shown that lipids, especially fatty acids (FAs), are important signaling molecules that regulate the signaling pathways of insulin and inflammatory mediators. On the one hand, the lack of n-3 polyunsaturated fatty acids (PUFAs) in the body leads to impaired molecular mechanisms of glucose transport, the formation of unresolved inflammation. On the other hand, excessive formation of free fatty acids (FFAs) underlies the development of oxidative stress and mitochondrial dysfunction in MetS. Understanding the molecular mechanisms of the participation of FAs and their metabolites in the pathogenesis of MetS will contribute to the development of new diagnostic methods and targeted therapy for this disease. The purpose of this review is to highlight recent advances in the study of the effect of fatty acids as modulators of insulin response and inflammatory process in the pathogenesis and treatment for MetS.
Highlights
Metabolic syndrome (MetS) is a complex of several disorders, which together dramatically raise the risk of developing atherosclerotic cardiovascular disease, insulin resistance, and diabetes mellitus [1, 2]
We summarized the molecular mechanisms of the relationship between fatty acids and glucose transport, inflammatory response, mitochondrial dysfunction, and endoplasmic reticulum stress in the development of MetS
Free fatty acids (FFAs), or nonesterified fatty acids (NEFAs), in circulating plasma are derived from the ingestion of dietary fat or from the triglycerides stored in adipose tissue that are distributed to cells to serve as fuel for muscle contraction and systemic metabolism [87]
Summary
Metabolic syndrome (MetS) is a complex of several disorders (abdominal obesity, hyperglycemia, hypertriglyceridemia, and hypertension), which together dramatically raise the risk of developing atherosclerotic cardiovascular disease, insulin resistance, and diabetes mellitus [1, 2]. Lipids play the crucial role in the pathogenesis of IR and the subsequent development of MetS [8,9,10,11,12,13,14,15,16,17,18]. E aim of the review is to analyse the modern views on the role of lipids, PUFAs and FFAs, in the pathogenesis of MetS. We summarized the molecular mechanisms of the relationship between fatty acids and glucose transport, inflammatory response, mitochondrial dysfunction, and endoplasmic reticulum stress in the development of MetS
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
