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Evidence was also provided from this study that GLP-1 controls glucose tolerance by extrapancreatic means, as GLP-1R antagonist administration increased plasma glucose levels in these mice during an oral glucose tolerance test

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This, in turn, sequentially activated phosphoinositide 3-kinase (PI3K) and downstream effectors protein kinase B (PKB/Akt), p38 MAPK and PKC contributing to DNA synthesis, gene expression, insulin synthesis and reduced apoptosis (48)