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TMAO promotes macrophage infiltration and activation within adipose tissue, driving a shift in macrophage phenotype toward the pro-inflammatory M1 state, contributing to adipose tissue dysfunction, a key hallmark of obesity-related metabolic dysfunction [30, 75]

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The initial LNP formulations identified in the early to mid-2000s used cationic lipids, which efficiently encapsulated RNA but also caused toxicity and inflammation

Liraglutide, however, does not improve AT dysfunction in subcutaneous tissue or prevent inflammation, and does not improve adipogenesis although it has high homology to native glucagon-like peptide-1 (GLP-1), which was reported to reduce inflammation (Reference Anandhakrishnan and Korbonits5) and increase lipolysis (Reference Sharma, Verma and Vaidya6)