Furthermore, a previous study has shown in mouse models that N-glycosylation defects, such as those in which N-acetylglucosaminyltransferase-IVa is inactive, can impair insulin release and lead to hyperglycaemia by abnormal N-glycosylation of pancreatic beta-cell glucose transporter-2 (GLUT-2) in T2D. This evidence concerns the gene MGAT4A and type 2 diabetes mellitus.