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The present study is significant because it shows that the increase in intestinal NE caused by GLP-1RA is due to the involvement of central nervous system activation in addition to potential peripheral effects of GLP-1

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Further investigations by Moody and Holst indicated that the peptide either was or constituted part of a proglucagon precursor because similar fragments could be found in the pancreas (Moody, Holst, Thim, Lindkaer, Jensen)

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