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These data collectively suggest that intestinal GLP-1 secretion is stimulated by cholinergic and -adrenergic receptor signaling and inhibited by activation of -adrenergic receptors
TLR and NLRP3 inflammasome-dependent innate immune responses to tumor-derived autophagosomes (DRibbles)
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The most relevant results were obtained jointly by the Di Marchi and Tschp groups [33,34], showing promising results in the management of metabolic pathologies such as obesity and diabetes
