Zinc: Physiological role and contribution to insulin metabolism and pathogenesis of type II diabetes mellitus

Zinc, as an essential trace element plays a multifaceted role in the human body ensuring cell growth and development, metabolic regulation, cognitive function, and the proper functioning of the reproductive and immune systems. The role of zinc deficiency in development of type 2 diabetes mellitus (T2DM) is being investigated quite actively as zinc is directly involved in crystallization, storage, and release of insulin.

The aim of this review is to summarize current knowledge on the physiological role of zinc as well as environmental and genetic factors influencing its absorption and transport and to examine the contribution made by zinc deficiency to development of various diseases, including glucose metabolism disorders. About 15 % of known genes have been shown to encode proteins capable of binding to zinc (including superoxide dismutase-1, angiotensin converting enzyme, matrix metalloproteinase-3, etc.). Prevalence of zinc deficiency varies across different populations; however, even in developed countries, insufficient zinc intake is observed in at least 10 % of the population. The leading causes of zinc deficiency are its insufficient content in diets as well as a high level of consumption of phytic acid compounds, which is especially significant with a vegetarian diet.

This review discusses studies that have demonstrated an association between the risk of T2DM and zinc bioavailability and intake levels, blood and pancreatic zinc concentrations as well as single-nucleotide polymorphisms in zinc transporter genes (including the rs13266634 variant of the SLC30A8 gene). A number of studies have shown that taking zinc dietary supplements in patients with type 2 diabetes significantly reduced the levels of markers of carbohydrate metabolism disorders (glucose, insulin, insulin resistance index, glycated hemoglobin, etc.).