Metabolic syndrome (MetS), characterized by obesity, insulin resistance, dyslipidemia, and hypertension, is a growing global health concern. This review examines the relationship between adipose tissue insulin resistance (AT-IR) and MetS. Adipose tissue functions beyond energy storage as an endocrine organ that regulates metabolism through hormone and cytokine secretion. When adipose tissue becomes insulin resistant, it contributes to systemic metabolic dysfunction through impaired glucose uptake and dysregulated adipokine production. This creates a bidirectional relationship where AT-IR promotes MetS development, while MetS-associated inflammation further worsens adipose insulin sensitivity. Key mechanisms include inflammatory signaling, altered adipokine profile, and mitochondrial dysfunction. Understanding these interactions offers therapeutic opportunities, as targeting adipose tissue function may provide novel approaches for MetS treatment. This review synthesizes current evidence on AT-IR-MetS interactions and discusses therapeutic implications and future research directions.
Rabiee et al. (Sun,) studied this question.