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suggested that HQ is a tyrosinase substrate with a poor activity due to the inability to transform met -tyrosinase to oxy -tyrosinase on its own 26
This observation aligns also with a generally lower correlation in gene expression in hypothalamic neurons of both mice treated with the GIPR antagonist or acyl-GLP-1, and further in mice treated with acyl-GIP or MAR709 (Extended Data Fig
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doi: 10.1016/j.neuropharm.2013.08.005 45 KimSMoonMParkS
Ultimately, understanding the nuances of these therapies allows providers to match the right drug to the right patient
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