Effects of mercuric chloride on glucose transport in 3T3-L1 adipocytes

Abstract

Mercury, as well as the other Group IIB metals, stimulates glucose transport in adipocytes. Here we characterize the action of mercury on adipocyte glucose transport and examine several potential mechanisms of action. Mercury exposure causes a modest (compared to insulin) 1.8-fold increase in glucose transport. This glucose transport corresponds with an increase in GLUT 1, but not GLUT 4 glucose transporters. Phosphorylation of p38 kinase and c-Jun N-terminal kinase (JNK) were examined as possible mediators of mercury induced GLUT 1 levels. Phosphorylation of p38 kinase, but not JNK, increased with mercury exposure. Activation of p38 and an increase in glucose transport corresponding to an increase in GLUT 1 are indicative the induction of a stress response, which can contribute to the induction of insulin resistance in adipocytes. However, inhibition of p38 by the p38 inhibitor SB203580 did not prevent mercury-mediated glucose uptake. While the magnitude of the action of mercury is modest, its effects were sustained over many days of exposure and impacted subsequent insulin-mediated glucose transport. Pre-treatment with HgCl 2 decreased insulin-mediated glucose transport 1.3-fold suggesting that exposure to mercury may contribute to pathologies associated with glucose homeostasis.