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Direct stimulation of β-cell D2R and D3R with dopamine (DA) or D2R/D3R agonists inhibits glucose-stimulated insulin secretion (GSIS) in both human and mouse pancreatic islets 6,7,8,10 , suggesting that β-cell D2R/D3R signaling is an important regulator of GSIS 5,6,8,9

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