A new study at Columbia University Irving Medical Center CUIMC has discovered that the abdominal fat can become dangerous when it becomes inflamed, the inflammation may come from the liver. In obese mice, the liver increases the production DPP4- an enzyme. This enzyme travels through the blood stream to abdominal fat. DPP4 activate inflammatory cells when it gets to liver.

Abdomen or belly fat increases the risk of insulin resistance and type 2 diabetes. The inflammation can be soothed by turning off DPP4 production in the liver, soothing inflamed abdominal fat improved insulin resistance. Targeting liver DPP4 in people may be a new way to treat obesity-induced type 2 diabetes. Inhibiting DPP4 specifically in liver cells attacks insulin resistance. Current DPP4 inhibitors do not reduce inflammation in fat or improve insulin resistance.

Abdomen or belly fat increases the risk of insulin resistance and type 2 diabetes. Patients with type 2 diabetes are given oral DPP4 inhibitors- gliptins to manage their disease. These drugs lower blood sugar by preventing DPP4 from interfering with a hormone that stimulates insulin production. DPP4 inhibitors lower blood sugar by inhibiting DPP4 in the gut. Researchers selectively blocked DPP4 production inside liver cells to reduce fat inflammation, improve insulin resistance and lower blood sugar. DPP4 inhibitors could be more potent if they were redirected to liver cells and away from the gut.
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