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Given that insulin signaling activates PI3K-AKT to promote adipogenesis, in part by upregulating adipogenic transcription factors such as PPAR 38,39 , our data suggest that reduced AKT activation underlies the impaired differentiation phenotype observed in GPR146-deficient cells

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In light of this association, one study suggested that butyrate could be responsible for a proliferative effect during in vitro mouse intestinal organoid development due to its interactions with GPR41 and 43 receptors (70)

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IDF Diabetes Atlas, 2024