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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
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Likewise, they can increase insulin secretion by improving beta-cell survival and suppressing glucagon secretion by improving alpha-cell health and glucose sensing ability
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