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Regarding fibrosis, while direct anti-fibrotic mechanisms are less established, preclinical studies indicate that GLP-1 RAs could suppress fibrogenic cell activation and reduce expression of pro-fibrotic genes encoding extracellular matrix proteins, potentially facilitating fibrosis regression in conjunction with improvements in steatosis and inflammation [29-32]

TZP was well tolerated as an add-on to oral glucose-lowering drugs monotherapy in Japanese diabetic participants and showed development in GC and BW, irrespective of undercurrent glucose-lowering drugs (82)

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The rate of protein synthesis, although somewhat reduced in HLS muscle, was not significantly elevated by IGF-1/BP3 treatment