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Human thyroid C-cells express GLP-1 receptors at much lower levels than rodent C-cells, and there is no established causal relationship between GLP-1 receptor agonists and MTC in humans
Similarly, another interesting study revealed that Rbpj deficiency in myeloid cells decreased experimental MASH by increasing the expression of genes related to fatty acid degradation and peroxisomal fatty acid oxidation [128], suggesting that targeting Notch signaling in macrophages may constitute a novel therapeutic strategy for MASH treatment
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