GLP-2(3-33), generated naturally by dipeptidylpeptidase IV (DPPIV), acts as a partial agonist on GLP-2 receptor (EC50=5.8 nM)[1][2].
GLP-2 is secreted as a 33-amino acid peptide, but is rapidly degraded at an N-terminus site to GLP-2(3-33) in circulation, in large part, by dipeptidylpeptidase IV (DPPIV). GLP-2 (3-33) acts as a partial agonist with potential competitive antagonistic properties on the GLP-2 receptor. In the GLP-2 receptor-binding assay, the binding IC50 for GLP-2 1-33 was 3.1 nM, and it was 41 nM for GLP-2 3-33. Thus, GLP-2 3-33 had 7.5% binding affinity compared to GLP-2 1-33[1].
GLP-2(3-33) (60 ng; once a day i.p. for 4 weeks) increases dyslipidemia and hepatic lipid accumulation in HFD-fed mice[2]. Animal Model: Male C57BL/6J (B6) mice (HFD)[2]
[1]. Thulesen J, Knudsen LB, Hartmann B, Hastrup S, Kissow H, Jeppesen PB, Ørskov C, Holst JJ, Poulsen SS. The truncated metabolite GLP-2 (3-33) interacts with the GLP-2 receptor as a partial agonist. Regul Pept. 2002 Jan 15;103(1):9-15. [2]. Baldassano S, et al. Influence of endogenous glucagon-like peptide-2 on lipid disorders in mice fed a high-fat diet. Endocr Res. 2016 Nov;41(4):317-324.