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Diabetes Med J Br Diabetes Assoc

In this scenario, the traditional concept of a systemic GHK-Cu half life becomes almost irrelevant

It delays stomach emptying, inhibits appetite by activating specific GLP-1 receptors, increases insulin production from pancreatic beta cells, and lowers glucagon secretion from alpha cells

Synthesized in the intestinal L-cells, GLP-1 is secreted in response to food intake, stimulating insulin secretion and inhibiting glucagon release [1]

doi:10.3389/fnut.2023.1152680

The ATF4/CHAC1 pathway is central to this process, with ATF4 upregulating CHAC1 in response to stress signals, thus promoting ferroptosis