A significantly decreased SSAO activity and plasma ET-1 level, as well as obviously increased plasma levels of MA and NO(x)- were observed in the DM + AG and DM + 2-BEA groups in comparison with the DM group (P < 0.01).
VAP-1 has been strongly implicated in several pathological processes, including diabetes, inflammation, hypertension, hepatic steatosis and renal diseases, and is an important disease marker and therapeutic target.
Vascular adhesion protein-1 (VAP-1) is secreted by vascular smooth muscle cells, adipocytes and endothelial cells with functional monoamine oxidase activity and is elevated in atherosclerosis, diabetes mellitus and obesity.
It is possible that the increased SSAO activity in diabetes may be a result of up-regulation due to increase of SSAO substrates, such as methylamine or aminoacetone.
The increased SSAO activity in diabetes is most likely dependent on post-transcriptional modifications or activation of existing inactive enzyme molecules.
No wild-type animals displayed this phenotype.In conclusion, we suggest that this transgenic mouse model may be of great value for increasing the knowledge about to what extent human SSAO contributes to vascular complications in diabetes, and also to which extent inhibition of SSAO can prevent the development of such complications.