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Rats were acclimated to cold at 4 degrees C for a period of 42 days. Pancreases of normal and cold-acclimated rats were isolated and perfused with a Krebs-Henseleit bicarbonate medium containing dextran, adenosine, glucose, and a fluorocarbon as oxygen carrier. The biphasic secretion pattern of insulin in response to glucose stimulation was evident in both groups. Both basal and glucose-induced insulin release from pancreases of cold-acclimated rats exhibited a very significant reduction in comparison with controls (p less than 0.001). These observations are interpreted as indicating that cold-acclimation, an altered steady state of metabolism, is characterized by enhanced sympathetic activity which reduces insulin availability and release. Consequently enhanced free fatty acid mobilization resulting from reduced inhibition by insulin of lipolysis in the peripheral fat depots and increased lipolysis resulting from sympathetic activation are seen.

Arginine-stimulated insulin and glucagon outputs from isolated perfused pancreata of warm-acclimated and 2-, 4-, and 6-wk cold-acclimated rats (4 degrees C) were determined to assess whether observed changes in these parameters were a result of cold exposure per se or a part of the adaptive process of cold acclimation. Progressive and sequential changes were seen in both insulin and glucagon outputs. At 2 wk cold acclimation, glucagon rose and insulin output tended to fall, at 4 wk, glucagon output remained elevated and insulin output was further reduced, and at 6 wk, glucagon output had returned to control levels, whereas insulin output was substantially further reduced. These changes resulted in reduction of the insulin-to-glucagon molar ratio of the total arginine-induced output from 7.27 +/- 1.76 (SE) in the warm acclimate to 2.31 +/- 0.79 (SE) at 2 wk, 1.42 +/- 0.29 (SE) at 4 wk, and 1.26 +/- 0.21 (SE) at 6 wk cold acclimation. The data do not provide in vitro support for the hypothesis that changes in pancreatic hormone secretion in vivo are a consequence of cold exposure and not cold acclimation.

Administration of glucagon to rats at 25 degrees C had no effect upon their VO2, while administration of noradrenaline or noradrenaline plus glucagon raised the VO2. At 5 degrees C, noradrenaline had no effect upon the cold-enhanced VO2, while glucagon caused a rise of 13.7%, implying increased glucagon sensitivity at 5 degrees C. The glucagon-induced enhancement of VO2 was abolished by concurrent administration of noradrenaline.