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Accumulating evidence implicates visceral hypersensitivity, abnormal gastrointestinal motility, inflammation, and/or infection of the gut in its pathophysiology [53]

That tells us appetite suppression is fundamentally a brain-mediated effect. The brain contains multiple, overlapping circuits that regulate feeding

While LBM loss appears to be less pronounced than FBM loss in many studies, the clinical significance of even modest reductions in skeletal muscle remains uncertain, particularly in older adults or individuals at risk of sarcopenia

In addition to glucose regulation, GLP-1 analogues have additional metabolic action