Molecular Insights into Adipokines in Metabolic Syndrome: Implications for Novel Therapeutic Strategies
Keywords:
Metabolic Syndrome, Adipokines, Leptin, Adiponectin, Insulin Resistance, PolymorphismAbstract
Background: Adipokines are bio-active peptides released by adipose tissue which control glucose and lipid metabolism, play important roles in pathophysiology of metabolic syndrome (MetS). The main objective of this systematic review was to collect molecular evidence of adipokine dysregulation in MetS and fully evaluate its clinical, genetic, and epigenetic implications. Methodology: Articles published since January 2014 to January 2026 were searched from different databases like PubMed, Scopus, Web of Science, and Google Scholar, by following PRISMA 2020 guidelines. Inclusion criteria were adults, MetS, and quantitative data on adipokines and their association with clinical or genetic variables. The quality was measured using the Newcastle-Ottawa Scale, ROBINS-I tool, and GRADE frameworks. Results: 12 out of 85 records met the inclusion criteria. MetS populations were always associated with an increase in pro-inflammatory adipokines (leptin, resistin, chemerin, visfatin) and a decrease in adiponectin, which are strictly linked to insulin resistance and inflammation. The severity of MetS was more strongly associated with visceral adipose tissue expression as compared to circulating levels alone. Adiponectin and leptin genetic variations (e.g., ADIPOQ, 73 CpG) and epigenetic changes (211 CpGs) controlled the expression of adipokines. The quality was quite average, with observational designs making it hard to make causal inferences. Conclusion: The dysregulation of adipokines is the core of MetS pathophysiology with tissue-specific expression and epigenetic regulation being the factors involved in metabolic dysfunction. Long-term, multi-omics longitudinal studies are necessary in the future to confirm therapeutic targets and allow individual interventions.
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