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[10] In dogs, an ancient mutation in IGF1 is the primary cause of the toy phenotype

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After the knockout of the GLP-1R gene, in transgenic mice expressing human GLP-1R in pancreatic islets and pancreatic ductal cells restored cAMP and serine threonine kinase (Akt) phosphorylation levels in isolated islets, increased GLP-1-stimulated insulin secretion and GLP-1R-dependent -cell proliferation, and promoted transgenic mice for glucose regulation in response to feeding (Lamont et al., 2012)

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