Abstract
This investigation was based on the hypothesis that long term cold exposure (cold-acclimation) reduces the overall amounts of insulin secreted by the pancreatic islets of Langerhans of the rat and possibly also reduces insulin synthesis. Evidence was obtained indicating that this effect was mediated through the sympathetic postganglionic terminals at the pancreatic beta-cells. The study was made on isolated perfused pancreases in a purpose-built perfusion system, and an artificial perfusion medium with a fluorocarbon as oxygen carrier were used. It was confirmed that insulin secretion from the isolated perfused pancreas, in response to glucose stimulation follows a biphasic secretion pattern. Cold-acclimation reduces insulin secretion as a result of alpha-adrenergic activity. This effect was reversed by the action of the alpha-adrenergic antagonist phento-lamine. A similar inhibitory effect on insulin release was achieved by perfusion with noradrenaline (40 ng/100 ml), although not to the same extent of inhibition which prevailed during cold-acclimation. The results suggested that the demonstrated alpha-adrenergic inhibition is directly effected by the pancreatic sympathetic fibres rather than by adrenal medullary secretion of catecholamines. Insulin output was measured by radioimmunoassay and the results were statistically analysed and discussed. It was concluded that during cold-acclimation, inhibition of insulin secretion and enhancement of catecholamine secretion enabled the cold-acclimated rat to maintain an adequate supply of thermogenic substrates for peripheral metabolism.