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The results suggest that PCs augment high glucose-induced apoptosis in pancreatic -cells by increasing glucose uptake under high glucose conditions, potentially via a mechanism that downregulates Gck and promotes Bax protein translocation and oligomerization at the mitochondrial membrane

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That modification is the key engineering trick: it makes the molecule more resistant to the enzymes that would normally break GHRH down quickly, giving tesamorelin a longer working window than sermorelin while still acting on the same GHRH receptor

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