Sandbox Reserved 1170: Difference between revisions
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=== Mechanism of Insulin Secretion === | === Mechanism of Insulin Secretion === | ||
One proposed pathway of insulin secretion by hGPR40 involves the activation of the Gaq/11 protein complex. This complex then activates phospholipase C (PLC) which in turn phosphorylates phosphatidylinositol 4,5-bisphosphate to inositol 1,4,5-triphosphate (IP3) and diacylglycerol (DAG). IP3 can then mediate the influx of Ca2+ caused by the binding of free fatty acids to hGPR40 by moving into the cytoplasm, binding to the endoplasmic reticulum, and allowing for the release of | One proposed pathway of insulin secretion by hGPR40 involves the activation of the Gaq/11 protein complex. This complex then activates phospholipase C (PLC) which in turn phosphorylates phosphatidylinositol 4,5-bisphosphate to inositol 1,4,5-triphosphate (IP3) and diacylglycerol (DAG). IP3 can then mediate the influx of Ca2+ caused by the binding of free fatty acids to hGPR40 by moving into the cytoplasm, binding to the endoplasmic reticulum, and allowing for the release of Ca<sup>2+</sup> into the cytosol.<ref name="Burant"/> This increase in [Ca<sup>2+</sup>] amplifies the similar increase in [Ca<sup>2+</sup>] that results from high concentrations of glucose. In this way, hGPR40 mimics glucose dependent insulin secretion.<ref name="Itoh">PMID:12629551</ref> | ||
Another pathway through which hGPR40 induces insulin expression is through phospholipase D1 (PKD1). When free fatty acids bind to hGPR40, it is able to phosphorylate and therefore activate PKD1. The PKD1 plays a role in controlling the organization of an actin network that lays in role in insulin secretion.<ref name="Burant"/> | Another pathway through which hGPR40 induces insulin expression is through phospholipase D1 (PKD1). When free fatty acids bind to hGPR40, it is able to phosphorylate and therefore activate PKD1. The PKD1 plays a role in controlling the organization of an actin network that lays in role in insulin secretion.<ref name="Burant"/> | ||
