Effects of phlorizin on metabolism and function of pancreatic β-cell
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The effects of phlorizin on several parameters of β-cell function were studied with microdissected islets of obese-hyperglycemic mice. At a concentration of 10 mM, phlorizin significantly depressed insulin release, glucose transport, glucose oxidation, and the level of fructose 1,6-diphosphate, when tested in the presence of 10 mM glucose. Whereas 1 mM phlorizin inhibited glucose transport by about 50%, the glucose-stimulated insulin release remained unaffected by 1-5 mM phlorizin. In the absence of glucose, 10 mM phlorizin significantly stimulated insulin release but had no effect on the islet levels of glucose 6-phosphate or fructose 1,6-diphosphate. The results corroborate our previous hypothesis of a mediated glucose transport into the pancreatic β-cell. Insulin release does not seem to be governed by the glucose transport in toto. Stimulation of insulin release might rather be elicited by the binding of glucose to a distinct membrane receptor, which accounts for but a minor fraction of the total glucose uptake.
|Status||Published - 1972 jan 1|
|Peer review utförd||Ja|