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In a 2023 animal model, GHK-Cu accelerated diabetic wound closure by 40% via PI3K/Akt signaling (Zhang et al., 2023)

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Direct stimulation of -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 -cell D2R/D3R signaling is an important regulator of GSIS 5,6,8,9