Does leptin-mediated inflammatory signaling crucially link visceral fat inflammation to obesity-associated β-cell dysfunction?
A markedly elevated leptin production from inflamed visceral fat could deteriorate β-cell function via leptin receptor-mediated oxidative stress and cyclooxygenase-2 activation in the development of obesity.
Although alpha galactosidase and alpha 1,2 fucosyltransferase had different biochemical properties, they could inhibit the expression of Gal alpha 1,3 Gal synergistically, leading to stronger resistance of xenograft against cytolysis.