Update on Zinc Biology

Abstract

Zinc has become a prominent nutrient of clinical and public health interest in the new millennium. Functions and actions for zinc emerge as increasingly ubiquitous in mammalian anatomy, physiology and metabolism. There is undoubtedly an underpinning in fundamental biology for all of the aspects of zinc in human health (clinical and epidemiological) in pediatric and public health practice. Unfortunately, basic science research may not have achieved a full understanding as yet. As a complement to the applied themes in the companion articles, a selection of recent advances in the domains homeostatic regulation and transport of zinc is presented; they are integrated, in turn, with findings on genetic expression, intracellular signaling, immunity and host defense, and bone growth. The elements include ionic zinc, zinc transporters, metallothioneins, zinc metalloenzymes and zinc finger proteins. In emerging basic research, we find some plausible mechanistic explanations for delayed linear growth with zinc deficiency and increased infectious disease resistance with zinc supplementation.

Effect of zinc supplementation on bone formation in hemodialysis patients with normal or low turnover bone

“…It seems to be elucidated why the long-term Zn supplementation was required for the increase of serum BAP in this study. Because the diverse transcription factors and the signals that regulate their activity form a highly interconnected, cooperative network in osteoblasts, 1 the effects of Zn might be the sum of opposing actions which offset each other, resulting in the slow promotion of bone formation and a time-consuming increase in serum BAP. We measured serum BAP by mass concentration, but not by enzyme activity.…”

“…Since Zn is the most abundant trace element in bone, it may induce the increase in ALP-related DNA synthesis and stimulate bone growth. 1,2 Bone ALP (BAP) catalyzes the hydrolysis of pyrophosphate and provides the extracellular phosphate pool, which determines the rate of hydroxyapatite crystal formation in bone. In vitro, Zn has been shown to stimulate osteoblastic bone formation by activation of ALP, 3,4 while Zn deficiency reduced bone mineralization by decreasing synthesis of ALP.…”

Trace element status and zinc homeostasis differ in breast and formula-fed piglets

“…Over 50 different enzymes in mammals necessitate zinc directly as a cofactor in the reaction they catalyze. 7 Zinc also has a structural function, as it contributes to the shaping of zinc finger motifs in hundreds of proteins. Severe zinc deficiency in infants causes growth retardation, dermatitis, alopecia, diarrhea, and immune deficiency.…”

“…7,17 Under low zinc conditions, the expression of these transporters is modulated to increase zinc uptake from diet and minimize losses in urine and feces. In the small intestine, the transporter Zip4 is expressed on the apical membrane and is responsible for the import of dietary zinc into enterocytes.…”

“…Zip4 is mainly expressed in the liver, the digestive tract, the uterus, and placenta. 7 Mutations in this gene are responsible for the autosomal recessive disorder acrodermatitis enteropathica. Zinc absorption is severely reduced in these patients and the symptoms are similar to dietary zinc deficiency.…”