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Description

In osteoblasts specifically, AKT promotes GLUT4 translocation via PI3K signaling to restore glucose uptake under insulin-resistant conditions, securing the carbon substrates needed for collagen glycosylation and ATP-dependent mineralization, a metabolic reprogramming function that extends well beyond the hormone's classical glycemic role

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This mechanism further supports the role of GLP-1RAs in blood pressure regulation and nephroprotection [87]

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