November 16, 2011

Insulin Sensitivity Boosted By Knocking Out Key Protein In Mice


Researchers were able to dramatically boost insulin sensitivity in lab mice by knocking out a key regulatory protein.

This discovery reevaluates a previously unsuspected role for a nuclear receptor corepressor named NCoR. This specific protein is found in a wide variety of cells. The scientific explanation is intricate but the lay reasoning works here: NCoR does a lot of things in the body by giving a red or green light to different receptors to do different things.

The unique thing about NCoR is that it does many things involving storing fats and metabolizing glucose. It does this by signaling PPARs.  With this understanding – researchers created a knock-out mouse lacking the NCoR in fat cells. Although mice lacking the protein NCoR would be prone to obesity and diabetes – the mice showed to have improved glucose tolerance and had enhanced insulin sensitivity in the liver, muscle and fat, as well as decreased systemic inflammation.

Inflammation is a trademark of insulin resistance. Insulin resistance is a major precursor to type 2 diabetes. In mice with NCoR knocked-out the insulin sensitivity was greatly enhanced. Even though the NCoR manipulation in the knock-out mice was targeted to the fat cells – it translated to all cells in the body that regulate insulin sensitivity. The insulin sensitivity throughout the entire body was improved.

This research proves to open a lot of therapeutic pathways to explore for enhancing insulin sensitivity. However because the vast responsibility of NCoR extends throughout the body and several cells with different functions – the specificity of NCoR needs to be further investigated for use in type 2 diabetes and other insulin-resistant diseases.

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