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The binding assays suggested that the N-terminal positions 7, 10, 12, 13 and 15 were important for GLP-1 affinity at rGLP-1R since the substitutions resulted in a 41- to 219-fold increase in IC 50
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in this study, empagliflozin raised the endogenous levels of ketone body (KB) and prevented a reduction in renal ATP levels and organ damage in the mice, an effect abolished by gene deletion of Hmgcs2, a rate-limiting enzyme of ketogenesis [95]
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The half-life of natural GLP-1 is very short
