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Comment
. 2007 Jun;148(6):2598-600.
doi: 10.1210/en.2007-0336.

G protein-coupled receptors and insulin secretion: 119 and counting

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Comment

G protein-coupled receptors and insulin secretion: 119 and counting

S R Murthy Madiraju et al. Endocrinology. 2007 Jun.
No abstract available

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Figure 1
Figure 1. GPCR-mediated amplification of insulin secretion
Glucose metabolism raises the ATP/ADP ratio, which closes ATP-sensitive potassium channels (KATP channels), depolarizes the cell membrane, activates voltage-gated calcium channels (Ca2+ channels), and results in calcium influx, which in turn triggers the release of insulin. Several extracellular signals can amplify this process through the activation of GPCRs. These include receptors for GLP1, GIP, FFA, acetylcholine, and the newly described GPR119 activated by LPC / OEA. These receptors couple to various downstream signaling pathways in the cell leading to an increase in cyclic AMP levels and / or intracellular calcium and converge to amplify GSIS. Ach, acetylcholine; CPT1, carnitine-palmitoyl transferase 1; DAG, diacylglycerol; ER, endoplasmic reticulum; FA, fatty acid; GIP, glucose-dependent insulinotropic peptide; GLP-1, glucagon-like peptide-1; IP3, inositol triphosphate; LC-CoA: long-chain coenzyme-A; LPC, lysophosphatidylcholine; M3-R, M3-muscarinic receptor; NAPE, N-acylphosphatidylethanolamine; OEA: oleoylethanolamide; PA, phosphatidic acid; PC, phosphatidylcholine; PKA; cyclic AMP-dependent protein kinase; PLA2, phospholipase A2; PLC, phospholipase C; PLD, phospholipase D. Adapted from (13).

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