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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Hexose metabolism in pancreatic islets. Galactose transport, phosphorylation and oxidation.

In rat pancreatic islets, the apparent space of distribution of galactose is not different from that of other hexoses. In homogenates of islets or tumoral insulin-producing cells, galactose is phosphorylated at a very low rate relative to either glucose phosphorylation in the same tissues or galactose phosphorylation by liver homogenates. In intact islets, galactose increases modestly the glucose 6-phosphate content and is oxidized at a much lower rate than glucose. Galactose slightly increases insulin output in the presence of a stimulatory concentration of glucose but fails to provoke insulin release in the absence of glucose, whether in islets removed from rats fed a normal or galactose-rich diet. The low rate of galactose oxidation and its poor insulinotropic capacity appear attributable to the weak activity of galactokinase in pancreatic islets.[1]

References

  1. Hexose metabolism in pancreatic islets. Galactose transport, phosphorylation and oxidation. Giroix, M.H., Malaisse-Lagae, F., Sener, A., Malaisse, W.J. Mol. Cell. Biochem. (1985) [Pubmed]
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