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Leptin, adiponectin, and resistin are key hormones produced by adipose tissue. In the present study, we have examined the effects of acute cold exposure (18 h at 6 degrees C) on the expression of the genes encoding these hormones in both brown and white fat of rats. Acute cold exposure resulted in a significant (p < 0.001) increase in the level of UCP1 and metallothionein-1 mRNAs in brown adipose tissue, indicative of an activation of thermogenesis. Leptin mRNA was decreased (p < 0.001) in brown fat in the cold, and there was also a small but statistically significant (p < 0.05) decrease in adiponectin mRNA; resistin mRNA did not change significantly (p > 0.05). In white fat, the level of leptin mRNA also fell in the cold (p < 0.05), but there was no significant change (p > 0.05) in either adiponectin or resistin mRNA. The serum concentration of adiponectin was unchanged following acute cold exposure. We conclude that while leptin gene expression is inhibited by exposure to cold, there is no major effect on the expression of either the adiponectin or resistin genes in white or brown fat despite the cold-induced stimulation of sympathetic activity and fatty acid flux. Thus, adiponectin and resistin are unlikely to play a key role in the extensive metabolic adaptations to cold.

Cold acclimation increased the activities of superoxide dismutase, catalase, total and selenium (Se)-dependent glutathione peroxidases (GPx) and glutathione reductase by 2-4-fold in the brown adipose tissue (BAT) of cold-acclimated rats. Nevertheless, when expressed per unit protein, the antioxidant enzyme activities were unaltered. Sensitivity to lipid peroxidation and GSH levels both increased by one order of magnitude in the cold on a per weight basis and were still 3-5 times greater in the cold when expressed per mg of protein. We suggest that activation of BAT leads to a large increase in the potential for lipid peroxidation and that the tissue responds to this challenge by increasing practically all of its antioxidant defences. Nevertheless, GSH, and possibly GPx activity, seem to be the principal defences involved in adaptation of the tissue to a higher sensitivity to peroxidative damage after activation.

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