Low-grade chronic inflammation in obesity impairs the interplay between adiponectin and high-density lipoproteins, contributing to endothelial dysfunction and increased cardiovascular risk.
This review highlights the interdependent role of dysfunctional HDLs and reduced adiponectin in promoting endothelial dysfunction and increasing cardiovascular risk in obesity.
Obesity is an epidemic public health problem that has progressively worsened in recent decades and is associated with low-grade chronic inflammation (LGCI) in metabolic tissues and an increased risk of several diseases. In particular, LGCI alters metabolism and increases cardiovascular risk by impairing endothelial function and altering the functions of adiponectin and high-density lipoproteins (HDLs). Adiponectin is an adipokine involved in regulating energy metabolism and body composition. Serum adiponectin levels are reduced in obese individuals and negatively correlate with chronic sub-clinical inflammatory markers. HDLs are a heterogeneous and complex class of lipoproteins that can be dysfunctional in obesity. Adiponectin and HDLs are strictly interdependent, and the maintenance of their interplay is essential for vascular function. Since such a complex network of interactions is still overlooked in clinical settings, this review aims to highlight the mechanisms involved in the impairment of the HDLs/adiponectin axis in obese patients to predict the risk of cardiovascular diseases and activate preventive countermeasures. Here, we provide a narrative review of the role of LGCI in altering HDLs, adiponectin and endothelial functions in obesity to encourage new studies about their synergic effects on cardiovascular health and disease.
Zocchi et al. (Tue,) conducted a review in Obesity. Low-grade chronic inflammation was evaluated. Low-grade chronic inflammation in obesity impairs the interplay between adiponectin and high-density lipoproteins, contributing to endothelial dysfunction and increased cardiovascular risk.