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Prediabetes Patients Improve Fasting Glucose with Zinc

Six-month regimen of 30 mg zinc sulfate once daily found effective compared with those on placebo, according to study.

In Diabetes Research and Clinical Practice, Australian researchers used a cohort of 55 adults, mean age of 44, to assess whether participants would improve fasting glucose with zinc supplementation. Adults with prediabetes randomly assigned daily zinc supplementation saw improved fasting plasma glucose over 6 months vs. those assigned a placebo, study findings show. They found those in the zinc supplement group also had statistically significant improvements in beta-cell function, insulin resistance and insulin sensitivity.

Many genetic variants have been associated with glucose homeostasis and type 2 diabetes in genome-wide association studies. Zinc is an essential micronutrient that is important for β-cell function and glucose homeostasis. So they tested the hypothesis that zinc intake could influence the glucose-raising effect of specific variants.

Chronic elevations in fasting or postprandial glucose levels are the cardinal features of type 2 diabetes (T2D), a common complex disease caused by the interplay of genetic and lifestyle factors. Genome-wide association studies (GWAS) have identified genetic loci reproducibly associated with glycemic traits or T2D. These studies improved our understanding of the mechanisms underlying impaired glucose homeostasis and T2D, potentially aiding the development of novel and individualized medical therapies.

To address these gaps in the literature, they conducted a meta-analysis that included 14 cohorts, totaling up to 45,821 participants, to test the hypothesis that zinc intake modifies the cross-sectional association between fasting glucose levels and genetic variants known to be related to glycemia and zinc metabolism (2) in individuals of European descent without T2D.

They conducted a 14-cohort meta-analysis to assess the interaction of 20 genetic variants known to be related to glycemic traits and zinc metabolism with dietary zinc intake (food sources) and a 5-cohort meta-analysis to assess the interaction with total zinc intake (food sources and supplements) on fasting glucose levels among individuals of European ancestry without diabetes.

They observed a significant association of total zinc intake with lower fasting glucose levels (β-coefficient ± SE per 1 mg/day of zinc intake: −0.0012 ± 0.0003 mmol/L, summary P value = 0.0003), while the association of dietary zinc intake was not significant. They identified a nominally significant interaction between total zinc intake and on fasting glucose levels (β-coefficient ± SE per A allele for 1 mg/day of greater total zinc intake: −0.0017 ± 0.0006 mmol/L, summary interaction P value = 0.005); this result suggests a stronger inverse association between total zinc intake and fasting glucose in individuals carrying the glucose-raising A allele compared with individuals who do not carry it. None of the other interaction tests were statistically significant.

From the results it suggests that higher total zinc intake may attenuate the glucose-raising effect of the rs11558471 SLC30A8 (zinc transporter) variant. The findings also support evidence for the association of higher total zinc intake with lower fasting glucose levels.

Modifiable lifestyle factors, such as diet and physical activity, influence glucose homeostasis and thus represent important targets for T2D prevention and management. Zinc is an essential trace element found in most foods that facilitates catalytic, structural, and transcriptional actions within cells. Zinc is a critical component of the catalytic site of >300 enzymes, including pancreatic carboxypeptidases and RNA polymerases; coordinates with protein domains; facilitates protein folding; produces structures such as zinc fingers; and regulates the expression of metallothioneins. Zinc is necessary in β-cells for insulin crystallization in hexamers. Moreover, it is co-secreted with insulin and exerts insulinomimetic and antioxidant actions and participates in the regulation of β-cell mass. Zinc homeostasis is impaired in animal models of diabetes and in humans with diabetes. Indeed, zinc supplementation studies in animal models support a protective effect of zinc against T2D, and in humans, plasma levels of zinc are inversely associated with the risk of T2D. Nevertheless, a causal link between zinc and T2D in humans is not well-established.

Data from population-based studies indicate that dietary and total zinc intake (food sources and supplements) may reduce T2D risk, but the few intervention studies investigating the effect of zinc supplementation on glucose metabolism, insulin homeostasis, or T2D risk have yielded inconsistent results. Therefore, although zinc supplementation is a potential therapeutic and preventive target for T2D, additional studies are needed before population-wide recommendations regarding zinc intake can be advocated.

Knowledge of gene-environment interactions may enhance our understanding of disease etiology and pathogenesis, as well as help personalize interventions. From the results it was demonstrated that there was a favorable association of whole-grain intake with fasting glucose and insulin, and a potential interaction was observed between the rs780094 GCKR variant and whole-grain intake on fasting insulin concentrations. Zinc intake previously has been shown to interact with genetic variants in relation to chronic diseases and inflammatory biomarkers, but not in the context of glycemic traits.

Despite the small sample size, they “demonstrated a real potential for zinc supplementation to improve glucose handling,” the researchers wrote. This effect may be substantial enough to prevent or, at least, delay progression of prediabetes.

Practice Pearls:

  • Zinc is an essential trace element found in most foods that facilitates catalytic, structural, and transcriptional actions within cells.
  • Zinc supplementation may improve glucose handling.
  • Dietary and total zinc intake (food sources and supplements) may reduce T2D risk.

Researched and prepared by Steve Freed, BPharm, Diabetes Educator, Publisher and reviewed by Dave Joffe, BSPharm, CDE

 

Diabetes September 2011 vol. 60 no. 9 2407-2416