Hi David ,
this is the next time you provided a link to an article in a news paper.All
the articles refer to the same science.I got the message.I do not need all
the other news papers in the world.Thanks for your concern

Here is the original abstract :

http://www.ncbi.nlm.nih.gov//entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citat
ion&list_uids=16377570

Dietary and genetic control of glucose transporter 2 glycosylation promotes
insulin secretion in suppressing diabetes.

Ohtsubo K, Takamatsu S, Minowa MT, Yoshida A, Takeuchi M, Marth JD.

Pancreatic beta cell-surface expression of glucose transporter 2 (Glut-2) is
essential for glucose-stimulated insulin secretion, thereby controlling
blood glucose homeostasis in response to dietary intake. We show that the
murine GlcNAcT-IVa glycosyltransferase is required for Glut-2 residency on
the beta cell surface by constructing a cell-type- and glycoprotein-specific
N-glycan ligand for pancreatic lectin receptors. Loss of GlcNAcT-IVa, or the
addition of glycan-ligand mimetics, attenuates Glut-2 cell-surface
half-life, provoking endocytosis with redistribution into endosomes and
lysosomes. The ensuing impairment of glucose-stimulated insulin secretion
leads to metabolic dysfunction diagnostic of type 2 diabetes. Remarkably,
the induction of diabetes by chronic ingestion of a high-fat diet is
associated with reduced GlcNAcT-IV expression and attenuated Glut-2
glycosylation coincident with Glut-2 endocytosis. We infer that beta cell
glucose-transporter glycosylation mediates a link between diet and insulin
production that typically suppresses the pathogenesis of type 2 diabetes.

PMID: 16377570

See my comment in one of your other threads : another study linking obesity
to increase in DM

hth
Gys