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Insulin stimulates its own secretion from pancreatic ? cells through rapid nitrosylation of glucokinase (GK), according to results by Rizzo and Piston on page 243.
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: f+ ^8 S$ ?0 V r3 ]When glucose levels are low, an inhibited form of GK associates with insulin-containing granules in pancreatic ? cells. Rizzo and Piston have determined that this localization is mediated through interaction with neuronal nitric oxide synthase (nNOS). Insulin treatment disrupted this association through nitrosylation of a GK cysteine residue. Activation of nNOS and the resulting nitrosylation of GK may be mediated through a rise in intracellular calcium, a known response of ? cells to insulin treatment. Release of the enzyme into the cytoplasm and the accompanying conformational change—both of which required NO production— activated GK.0 w) R# c8 s* u8 H/ |% e$ l5 \
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GK induces secretion of the granules, thus promoting local increases in insulin levels. A recently developed drug for the treatment of type II diabetes is a GK activator. The new results suggest that the drug may activate GK by preventing granule binding. Piston plans to test this possibility in the near future.(NO regulates association of GK (yellow) ) |
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发表于 2009-3-6 00:39
发表于 2015-5-26 19:39
