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The nature of this compensatory mechanism in GLP-1 receptor KO mice at high oral glucose load is not known but deserves further studies candidates may be the higher baseline glucose levels or compensatory increase in other gut hormones which may mask the consequence of GLP-1 receptor gene deletion
The expression levels were compared between treated and control groups [2]
The incidence of NAION was 17 events in the semaglutide group compared to 6 in the non-GLP-1 RA group
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