AI Article Synopsis

  • Metabolic syndrome (MetS) is increasingly common globally and is complicated by multiple components, affecting diagnosis and treatment.
  • Insulin resistance, primarily triggered by abdominal obesity, plays a central role in MetS development, with lipids, particularly fatty acids (FAs), significantly influencing insulin signaling and inflammation.
  • A deficiency in n-3 polyunsaturated fatty acids (PUFAs) and an excess of free fatty acids (FFAs) can lead to issues like impaired glucose transport and oxidative stress, highlighting the need for deeper understanding in order to improve diagnostics and therapies for MetS.

Article 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.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7491450PMC
http://dx.doi.org/10.1155/2020/5762395DOI Listing

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