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Experimental and clinical studies have demonstrated an association between obesity and impaired zinc metabolism, although local effects of zinc in adipose tissue are insufficiently studied. The objective of this study was to review current data on adipotropic effects of zinc and its role in the pathogenesis of obesity. Experimental studies have shown both decreased content of zinc in the adipose tissue in obesity and effects of zinc on adipocyte differentiation and functioning. Therefore, zinc can be considered as a regulator of adipogenesis, and, thus, impaired zinc metabolism may be associated with adipose tissue dysfunction. Modulation of zinc transporters underlies alteration of intracellular zinc levels, whereas further effects of zinc are related with functioning of zinc-containing effector molecules. The zinc transporters known to play a significant role in regulation of adipogenesis include ZIP14 and ZNT7 that are actively expressed during adipocyte maturation. Zinc-α2-glycoprotein is an adipokine acting as an autocrine and paracrine regulator of adipocyte metabolism as well as a lipolytic factor. The effect of zinc on adipose tissuedifferentiation may be also mediated by zinc-finger proteins, primarily Zfp423 and Zfp521. Zfp423 is an adipocyte differentiation factor stimulating the PPARγ expression whereas the antiadipogenic effect of Zfp521 is mediated by Zfp423 down-regulation. Despite a clearly demonstrated effect of Zn-containing metalloproteins a significant part of the effects of zinc may be mediated by biological activity of low-molecular weight zinc compounds or directly by Zn2+ cation. Therefore, improvement of zinc metabolism in the body in general and the adipose tissue in particular can be considered as a strategy for improvement of adipose tissue metabolism in obesity.

Mechanisms of adipotropic effects of zinc and its role in the pathogenesis of obesity