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Figure 7 4.1 Hepatocyte-targeted interventions Hepatocytes serve as the central hub of lipid accumulation and metabolic dysregulation in MASH ( de novo lipogenesis (DNL) through modulation of ACLY, ACC1/2, FASN, or DGAT2 effectively reduce hepatic triglyceride content, oxidative stress, and downstream inflammatory signaling ( 4.2 Kupffer cell-targeted interventions Kupffer cells orchestrate hepatic inflammation and contribute to systemic insulin resistance ( 4.3 HSC-targeted interventions HSCs are the principal fibrogenic cells driving ECM deposition and fibrosis in MASH ( 4.4 Pancreatic cells-targeted interventions Pancreatic -cells are essential for maintaining glucose homeostasis, and their dysfunction or loss is a key contributor to T2DM ( 4.5 Combination and multi-target strategies Single-target interventions frequently yield partial therapeutic effects, whereas combinatorial approaches targeting hepatocytes, Kupffer cells, and HSCs demonstrate superior efficacy
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Some patients find their side effect profile worsens at this level and choose to step back to 10mg for maintenance
Our findings indicate that AMPK activation mediates the effects of GLP-1RAs on AD, highlighting the therapeutic potential of GLP-1RAs for the treatment of AD
When a biopsy is performed, partial sampling should be avoided (with the exception of a large lesion in a cosmetically sensitive area)
