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In PNA mice, GLP1/E therapy caused upregulation of pathways involved in the metabolism of non-coding RNA, estrogen-dependent gene expression, autophagy, vesicle-mediated transport, and signaling by nuclear receptors, whereas proteins related to inflammation (ROS and RNS production in phagocytes), cellular response to starvation, signaling by insulin receptor, apoptosis, and immune system were downregulated

Additionally, we reported an increase in this immature- PCSK1 -expressing alpha-cell subpopulation in response to intra-islet GLP-1R signaling (13), suggesting that maturity state and GLP-1 production may be related

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