Type 2 diabetes is caused by an inability of the beta-cells in the pancreas to produce enough of the hormone insulin to meet the body's needs.
Central to this is a loss of beta-cell function and mass as a result of insulin resistance (the inability of cells in the body to respond appropriately to insulin).
New insight into how insulin resistance leads to loss of beta-cell mass has now been provided by studies in multiple mouse models of type 2 diabetes performed by Randal Kaufman and colleagues, at the University of Michigan Medical School, Ann Arbor.
In the study, in the absence of the protein CHOP, the symptoms of diabetes improved in two mouse models of the disease, and this was associated with increased beta-cell mass. In addition, the structure of the beta-cells appeared to be more normal and they were encouraged to survive.
CHOP is a protein that is involved in promoting the death of a cell that is under stress because it is producing more protein than it is able to handle.
The authors therefore propose that insulin resistance causes beta-cells to make more insulin than they can handle, such that the stress signaling pathways that activate CHOP are initiated and the beta-cells die, thereby decreasing beta-cell mass. Further, it is suggested that drugs that modulate the stress response to over production of insulin might provide a new approach to the treatment of type 2 diabetes.
- Chop deletion reduces oxidative stress, improves beta-cell function, and promotes cell survival in multiple mouse models of diabetes. Journal of Clinical Investigation, September 5, 2008
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