Here's an interest abstract on Type II diabetes:
Disruption of IRS-2 causes type 2 diabetes in mice
Human type 2 diabetes is characterized by defects in both insulin action and
insulin secretion. It has been difficult to identify a single molecular
abnormality underlying these features. Insulin-receptor substrates (IRS
proteins) may be involved in type 2 diabetes: they mediate pleiotropic signals
initiated by receptors for insulin and other cytokines. Disruption of IRS-1 in
mice retards growth, but diabetes does not develop because insulin secretion
increases to compensate for the mild resistance to insulin. Here the authors
show that disruption of IRS-2 impairs both peripheral insulin signalling and
pancreatic beta-cell function. IRS-2-deficient mice show progressive
deterioration of glucose homeostasis because of insulin resistance in the liver
and skeletal muscle and a lack of beta-cell compensation for this insulin
resistance. Their results indicate that dysfunction of IRS-2 may contribute to
the pathophysiology of human type 2 diabetes.
D J Withers, J S Gutierrez, H Towery, D J Burks, J-M Ren, S Previs,
Y Zhang, D Bernal, S Pons, G I Shulman, S Bonner-Weir
& M F White
Disruption of IRS-2 causes type 2 diabetes in mice
(Letters to Nature)
Nature 391, 900 (1998) |
