title: Hexose metabolism in pancreatic islets. Galactose transport, phosphorylation and oxidation.
abstract: 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.
mesh_terms: D000818:Animals; D001692:Biological Transport; D005690:Galactose / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D007515:Islets of Langerhans / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D010084:Oxidation-Reduction; D010766:Phosphorylation; D051381:Rats
chemical_list: D007328:Insulin; D005947:Glucose; D005690:Galactose