Abstract
Purpose of review
Zinc deficiency is a major modifiable nutritional and public health burden worldwide. Because zinc participates in a wide range of biochemical functions, the physiological consequences of deficiency are diverse and nonspecific, complicating the identification of reliable biomarkers of zinc status. The present review summarizes recent evidence regarding zinc status biomarkers, while integrating the impact of novel findings on the genetics of zinc homeostasis.
Recent findings
Updated assessment of available zinc biomarkers shows that plasma/serum and urinary zinc excretion respond to changes in zinc intake in humans. Despite the impact of inflammation, plasma/serum zinc remains a good indicator of status. Numerous other putative biomarkers do not meet biomarker efficiency criteria. Zinc homeostasis is tightly controlled through the action of more than 20 membrane transporters belonging to two large families (SLC30 and SLC39).
SLC30A2
genetic variants play a key role in controlling urinary zinc excretion, with high geographic variation in allele frequency. The observation from genetic studies that urinary and blood zinc levels are regulated through largely distinct biological pathways suggests that urinary zinc levels may provide relevant complementary information to serum/plasma levels pointing towards urinary-to-plasma ratio as a novel biomarker of human zinc status.
Summary
The combined assessment of serum (or plasma) zinc concentration and urinary zinc excretion appears to be the most sensitive and specific approach for evaluating zinc status in humans.