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Review
. 2012 Apr;23(4):313-9.
doi: 10.1016/j.jnutbio.2011.11.001.

Molecular Mechanisms of Chromium in Alleviating Insulin Resistance

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Free PMC article
Review

Molecular Mechanisms of Chromium in Alleviating Insulin Resistance

Yinan Hua et al. J Nutr Biochem. .
Free PMC article

Abstract

Type 2 diabetes is often associated with obesity, dyslipidemia and cardiovascular anomalies and is a major health problem approaching global epidemic proportions. Insulin resistance, a prediabetic condition, precedes the onset of frank type 2 diabetes and offers potential avenues for early intervention to treat the disease. Although lifestyle modifications and exercise can reduce the incidence of diabetes, compliance has proved to be difficult, warranting pharmacological interventions. However, most of the currently available drugs that improve insulin sensitivity have adverse effects. Therefore, attractive strategies to alleviate insulin resistance include dietary supplements. One such supplement is chromium, which has been shown to reduce insulin resistance in some, but not all, studies. Furthermore, the molecular mechanisms of chromium in alleviating insulin resistance remain elusive. This review examines emerging reports on the effect of chromium, as well as molecular and cellular mechanisms by which chromium may provide beneficial effects in alleviating insulin resistance.

Figures

Figure 1
Figure 1
Putative mechanisms by which chromium augments cellular glucose uptake. Chromium has been shown to enhance the kinase activity of insulin receptor β, to increase the activity of downstream effectors of insulin signaling pI3-kinase and Akt and to enhance Glut4 translocation to the cell surface. Chromium also down-regulates PTP-1B, the negative regulator of insulin signaling and alleviates ER-stress within the cells, rescuing IRS from JNK-mediated serine phosphorylation and subsequent ubiquitination. Transient upregulation of AMPK by chromium leads to increased glucose uptake. Chromium mediates cholesterol efflux from the membranes causing glut4 translocation and glucose uptake.

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