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THE level of glucose in the blood perfusing the islets of Langerhans is thought to regulate the secretion of insulin by the β-cells<sup>1</sup>. At present nothing is known about the mechanism of this regulation or even about the way in which the β-cells metabolize glucose. Studies designed to provide information about these problems are hampered by the fact that the pancreatic islets are rather diffusely scattered throughout the entire exocrine portion of the gland and comprise only about 2 per cent of the total pancreatic tissue<sup>2</sup>. Even if one were successful in obtaining islet tissue free of exocrine pancreas, the β-cells represent only 60â 90 per cent of the total cell population<sup>3</sup>. However, in humans there are insulin-producing tumours of the pancreas which are usually composed of only β-cells and such tissue does afford an opportunity to study β-cell metabolism. A ratio greater than unity for the amount of carbon dioxide labelled with carbon-14 derived from glucose-1-<sup>14</sup>C as compared to that from glucose-6-<sup>14</sup>C has been taken as evidence for the existence of the hexose monophosphate pathway in the tissue under study<sup>4</sup>. The present report concerns studies using a β-cell tumour and indicates that there is an active hexose monophosphate pathway in these cells (this patient was studied through the kindness of the National Institute of Neurological Diseases and Blindness, National Institutes of Health, Bethesda, Md.). It is realized that the metabolism in these benign tumours may not be completely analogous to that of β-cells in normal islets. |
