STIMULATORY EFFECTS OF COLD-EXPOSURE AND COLD-ACCLIMATION ON GLUCOSE-UPTAKE IN RAT PERIPHERAL-TISSUES

The effects of cold exposure on the net rates of 2-[H-3]deoxy-D-glucose uptake (K(i)) in rat peripheral tissues wer investigated compratively in warm- and cold-acclimated animals to determine whether cold acclimation induces regulatory alternations in glucose metabolism. Acute exposure of warm-acclimated (25-degrees-C) rats to cold (48 h at 5-degrees-C) markedly increased the K(i) values in red and white skeletal muscles (2-5 times), in the heart (8 times), in several white adipose tissue (WAT) depots (4-20 times), and in brown adipose tissue (BAT) (110 times). After cold acclimation (3 wk at 5-degrees-C), the K(i) values further increased in the heart (15 times) and WAT (up to 29 times) but decreased in BAT (36 times). Remarkably, glucose uptake was still increased in muscles of cold-exposed/cold-acclimated animals (that do not shiver), demonstrating that enhanced glucose uptake may occur in muscles in the absence of shivering thermogenesis (or contractile activity). When cold-acclimated rats were returned to the warm for 18 h, the K(i) values of all tissues, except WAT, returned to control levels. Cold exposure synergistically potentiated the stimulation of tissue glucose uptake induced by a maximal effective dose of insulin (0.5 U/kg iv) in warm- as well as in cold-acclimated animals. The data demonstrate that 1) activation of shivering and/or nonshivering thermogeneses by cold exposure results in a rapid increase of glucose uptake in peripheral tissues; 2) cold acclimation enhances the capacity of heart and WAT for cold-induced glucose uptake, but, with the exception of WAT, it does not induce long-term alternations in glucose metabolism; and 3) cold exposure, but not cold acclimation, increases insulin responsiveness (maximum velocity) in all tissues tested. The results also indicate that activation of nonshivering thermogenesis in BAT and muscles of cold-acclimated animals represents the principal phenomenon explaining the improvement by cold exposure of glucose tolerance and insulin action.