Researchers have found that an insulin degrading enzyme inhibitor (IDE inhibitor) improves glucose tolerance after meals.
Insulin degrading enzyme has been known about for decades but its role, particularly with regard to blood glucose levels, has been poorly understood. Researchers from Harvard University have found that using a protein which inhibits the enzymen, an IDE inhibitor improves glucose tolerance.
The researchers tested the IDE inhibitor in lean and obese mice and observed lower blood glucose levels following consumption of glucose by the mice. This raises particular interest as a therapeutic agent for type 2 diabetes therefore. The IDE inhibitor also impairs the action on the blood glucose raising hormone glucagon.
More detailed research will be needed to see whether or not it has significant short or long term complications. The impairment of glucagon, for instance could result in too low blood glucose levels, hypoglycemia, which could present an increased risk of danger.
Possible long term complications could include an increased risk of Alzheimers disease and decreased insulin production in the long term as IDE inhibitors have bee, in previous research, linked with a possible increase in risks of Alzheimer’s disease and beta cell death.
IDE inhibitors prevent degradation of amylin and the amyloid deposits which present an increased risk of Alzheimer’s disease. In addition, amyloid deposits in the pancreas have been linked with increased death of insulin-producing beta cells.
So, whilst IDE inhibitors represent short term improvements in blood glucose levels, the IDE enzyme itself may serve as a therapeutic factor in long term health. The enzyme and its inhibition therefore present an interesting for more research.

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