Relationship between Zinc-Alpha-2-Glycoprotein, Obesity, And Metabolic Syndrome

Abstract

Zinc-alpha-2-glycoprotein (ZAG) is a 40–43 kDa soluble glycoprotein first identified in human plasma and secreted by various tissues, particularly adipose tissue. It plays a significant role in lipid mobilization, energy homeostasis, and regulation of metabolic processes. ZAG acts as an adipokine—a cytokine secreted by fat tissue—implicated in the modulation of body fat and insulin sensitivity. Obesity is characterized by excess adipose tissue and is often accompanied by metabolic disturbances. Numerous studies have shown that ZAG expression is downregulated in obese individuals compared to lean individuals. Lower levels of ZAG in adipose tissue and circulation are associated with increased fat accumulation, reduced lipolytic activity, and impaired energy metabolism. Experimental models have demonstrated that ZAG overexpression or administration can reduce fat mass and enhance glucose tolerance, suggesting a protective role against obesity and insulin resistance. Metabolic syndrome is a cluster of conditions—including central obesity, insulin resistance, hypertension, and dyslipidemia—that increase the risk of cardiovascular disease and type 2 diabetes. ZAG has been proposed as a potential biomarker for metabolic syndrome, due to its inverse correlation with several metabolic syndrome components such as waist circumference, triglycerides, and insulin resistance markers.