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Damaged AECs release pro-inflammatory and pro-fibrotic mediators, including interleukin (IL) -1 and tumor necrosis factor (TNF) -, which promote fibroblast recruitment, inflammatory cell activation (e.g., neutrophils, Th17, gdT cells), and myofibroblast differentiation, ultimately leading to ECM accumulation and fibrotic tissue remodeling [20, 29, 33, 34]

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Research shows that exenatide and liraglutide can activate the AMPK pathway, promoting GLUT4 translocation in an insulin-independent manner, thus increasing glucose uptake in skeletal muscle (168)

That is about as direct as research language gets