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Although our data in vivo and in vitro demonstrated that activating GLP-1R inhibited microglial activation, changes in microglia induced by liraglutide can be indirect as well as behavioral effects could be driven by other cells cause our treatments are delivered systemically
However, the magnitude of improvement was significantly greater in the non-cognitive impairment group compared to the cognitive impairment group
This data suggests that proline in position P1 is not sufficient to result in a natural peptide being proteolyzed by DPP4
Glucagon receptor activation adds energy expenditure and hepatic fat oxidation pathways not available with GLP-1 alone
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