Excessive adipose tissue promotes the manifestation of endocrine disorders such as reduction of the secretion of zinc-α2-glycoprotein (ZAG), an adipokine with anti-inflammatory and lipid-mobilizing activity. The molecular structure of this adipokine includes binding sites for zinc, a trace element with important antioxidant and immunological proprieties that also participates in energy metabolism and stimulates the function of ZAG. The objective of this review is to highlight current data on the metabolism of ZAG in obesity and the role of zinc in this process. The identified studies show that subjects with obesity have low serum concentrations of zinc and ZAG, as well as low expression of the genes encoding this protein. Thus, zinc appears to be an important regulator of the homeostasis of ZAG in the body; however, alterations in the metabolism of zinc in obesity appear to compromise the functions of ZAG. Therefore, further studies are needed to clarify the relationship between zinc and ZAG metabolism and its repercussions in obesity.
Keywords: AZGP1; Obesity; Zinc; Zinc-α2-glycoprotein.