Abstract
Zinc is an essential component of the insulin granule and it possibly modulates insulin secretion and signaling. Since insulin resistance is a hallmark in the development of type 2 diabetes mellitus, this study aimed at investigating if zinc supplementation is able to improve glucose tolerance and β-cell function in a model of insulin resistance. Male C57BL/6 mice were distributed in four groups according to the diet: normal fat (NF); normal fat supplemented with ZnCl2 (NFZ); high-fat (HF); and, high-fat chow supplemented with ZnCl2 (HFZ). Intraperitoneal glucose (ipGTT) and insulin (ipITT) tolerance, glycemia, insulinemia, HOMA-IR, and HOMA-β were determined after 15 weeks in each diet. Glucose-stimulated insulin secretion (GSIS) was investigated in isolated islets. The insulin effect on glucose uptake, metabolism, and signaling was investigated in soleus muscle. ZnCl2 did not affect body mass or insulin sensitivity as assessed by ipITT, HOMA-IR, muscle glucose metabolism, and Akt and GSK3-β phosphorylation. However, glucose tolerance, HOMA-β, and GSIS were significantly improved by ZnCl2 supplementation. Therefore, ZnCl2 supplementation improves glucose homeostasis in high fat-fed mice by a mechanism that enhances β-cell function, rather than whole-body or muscle insulin sensitivity.
Highlights
Diabetes mellitus is a growing public health problem affecting approximately 9% of the adult population worldwide [1]
We have investigated in this study the effect of ZnCl2 in the control of insulin secretion and glycemia in a mouse model of glucose intolerance induced by high-fat chow
The ZnCl2 supplementation was reflected in increased Zn2+ daily intake in the supplemented groups, while no effect of chow was observed on Zn2+ intake
Summary
Diabetes mellitus is a growing public health problem affecting approximately 9% of the adult population worldwide [1]. While type 1 diabetes mellitus (T1DM) predominantly results from autoimmune destruction of pancreatic β-cells, with little or no insulin synthesis, type 2 diabetes mellitus (T2DM) develops due to the installation of insulin resistance in target tissues (reviewed in [2]), and high circulating insulin levels. An ancillary effect of zinc supplementation has been previously proposed to treat T2DM and its complications. Those studies have reported better glycemic control associated with the administration of this mineral [4,5,6], suggesting that zinc is a potential therapeutic agent for the treatment of diabetes
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