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What they found (summary): Amylin is a critical partner of insulin in metabolism, the loss of amylin in T2DM is as significant as the loss of insulin The AMY1 receptor in the area postrema is the primary target for the appetite effect Amyloid aggregation is the main problem with native amylin, proline substitutions (the Pramlintide strategy) are essential The half-life of native amylin is only 13 minutes, that is why lipidated analogs like Cagrilintide are necessary Perspective: amylin + GLP-1 combinations are the natural evolution of metabolic pharmacotherapy Why it matters: This is the reference article for amylin pharmacology
The crosstalk between distinct RCDs is well documented and can be interpreted through the lens of the cell death-governing intracellular system with multiple redundant backup pathways [20, 142]
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So when it comes to safely decreasing androgen receptors, please consider all other options aside from reducing total testosterone production
