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The medication works by enhancing insulin secretion in a glucose-dependent manner, suppressing glucagon release, and slowing gastric emptying, which collectively improves glycemic control and promotes weight loss

GHK-Cu operates through a different axis fibroblast activation, copper trafficking, and broad gene modulation without engaging the retinoid receptor family

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A deficiency slows that process, which shows up as fatigue that sleep does not fix

However, unlike pro-fibrotic agents, GHK-Cu also upregulates the activity of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs), facilitating the breakdown of scarred or disorganized collagen

Cobalamin deficiency: clinical picture and radiological findings