1. The potential for renoprotection with incretin-based drugs
Tetsuhiro Tanaka, Yoshiki Higashijima, Takehiko Wada, Masaomi Nangaku 
Kidney International 
Volume 86, Issue 4, Pages (October 2014)
DOI: /ki
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2. Figure 1
Extra pancreatic effects of glucagon-like peptide-1 (GLP-1) and its relationship with dipeptidyl peptidase-4 (DPP-4) inhibitors. Under usual circumstances, the enzyme DPP-4 cleaves an incretin hormone GLP-1 (GLP-1) and removes two amino acids from the N terminus, which converts active GLP-1 (GLP-17–36) to an inactive form (GLP-19–36). Thus, DPP-4 inhibition leads to incretin accumulation. In the pancreas, GLP-1 stimulates insulin release from β-cells and exerts insulinotropic effects. In addition, a growing body of evidence supports the extra pancreatic roles of incretins in the protection of multiple organs of the body, such as the cardiovascular system, lung, and kidney. DPP-4 inhibition is expected to partly, albeit not entirely, phenocopy these pleiotropic effects.
Kidney International  , DOI: ( /ki )
Copyright © 2014 International Society of Nephrology Terms and Conditions

3. Figure 2
DPP-4 substrates and potential consequences of DPP-4 inhibition. (a) Representative DPP-4 substrates are depicted schematically. (b) Upon enzymatic inhibition of DPP-4 by DPP-4 inhibitors, DPP-4 substrates escape from degradation and remain in their active forms, thus exhibiting their respective functions. BNP, brain natriuretic peptide; DPP-4, dipeptidyl peptidase-4; GLP-1, glucagon-like peptide-1; NPY, neuropeptide Y; PYY; peptide YY; SDF-1α, stromal-derived factor-1α.
Kidney International  , DOI: ( /ki )
Copyright © 2014 International Society of Nephrology Terms and Conditions