4.5 Article

The effect of chromium on inflammatory markers, 1st and 2nd phase insulin secretion in type 2 diabetes

Journal

EUROPEAN JOURNAL OF NUTRITION
Volume 53, Issue 1, Pages 127-133

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s00394-013-0508-8

Keywords

Chromium; Insulin sensitivity; Insulin secretion; Interleukin-6; Tumor necrosis factor-alpha

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Impaired insulin sensitivity (SI) and beta-cell function are the two main causes of type 2 diabetes (T2D) and are related to low-grade inflammation status. Trivalent chromium has shown to improve SI in our previous study. This might be due to the ability of decreasing interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) shown in animal studies. In the current study, we measured SI, beta-cell function, and plasma levels of IL-6 and TNF-alpha after treatment of chromium chloride (GaCr) in T2D. Sixty-six patients were randomly assigned to the 20 g of GaCr milk powder studying group or the milk powder placebo group. Oral glucose tolerance test was performed before and after the treatment. The SI and the beta-cell function were measured as well. The SI was significantly improved. At the same time, the static insulin responsivity index (I broken vertical bar(s)) was significantly higher after the treatment (p = 0.003). On the other hand, the dynamic insulin responsivity index (I broken vertical bar(d)) remained unchanged. Interestingly, a significant decrease in the IL-6 level after the treatment (p = 0.015) was noted. Although there was a trend of decreasing in TNF-alpha, it was not statistically significant. Finally, there was no significant correlation between the delta-IL-6, SI, and I broken vertical bar(d) after GaCr treatment. In conclusion, other than the improvement of SI, GaCr could also improve the second phase of insulin responsivity (I broken vertical bar(s)) and IL-6. However, delta-IL-6 was correlated with neither delta-SI nor delta-I broken vertical bar(s) which indicated that the improvement of SI and I broken vertical bar(s) might involve mechanisms other than lower inflammatory effect.

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