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Abstract Acute kidney injury (AKI) is a systemic disease that affects energy metabolism in various remote organs in murine models of ischemic AKI

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Four alanine mutated residues, V229A, V160A, I165A, and L401A, caused a significant decrease in GLP-1R internalisation versus WT receptor, with GLP-1R V229A and V160A causing a 40%, and I165A and L401A a 30% decrease in internalisation (Figure 2H, bottom graph)