Gemma Enrique-Tarancón

TL;DR: It is proposed that SSAO activity might contribute through hydrogen peroxide production to the in vivo regulation of GLUT4 trafficking in adipose cells.

TL;DR: It is proposed that SSAO activity regulates glucose transport in adipocytes via the translocation of GLUT4 carriers to the cell surface, resulting from a potent tyrosine phosphorylation of IRS-1 and IRS-3 and phosphoinositide 3-kinase activation.

TL;DR: Tyramine is readily oxidized by adipocytes and potentiates the effects of vanadium on glucose transport through release of hydrogen peroxide, showing the role of the amine oxidases allows them to be considered as more than mere scavengers of circulating amines.

TL;DR: Different mechanisms were responsible for GLUT4 repression in response to high-fat feeding or aging in skeletal muscles and adipose tissue, which was additive to the reduction inGLUT4 protein content detected in aged rats.

TL;DR: Mafenide could not be considered as an antidiabetic drug despite being oxidized and exhibiting insulin-mimicking effects in rat and mouse adipocytes, and the endogenous substrate methylamine improved glucose utilization in all in vitro and in vivo models, leading to consider novel SSAO substrates as drugs with potential anti-hyperglycaemic properties.