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The Tabas laboratory has made important discoveries in 2012 in two related fields: heart disease and type 2 diabetes. The link is critical because the persistence of heart disease in the current era is driven largely by the epidemic of obesity and type 2 diabetes.

In the heart disease arena, the laboratory discovered two new protective processes that could have important therapeutic implications. Both are related to the process called “atherosclerosis,” which causes clogging of the arteries that feed the heart and brain, leading to heart attacks, sudden cardiac death, and stroke. In one area, the Dr. Xianghai Liao in the Tabas laboratory discovered that a process in which cells clear themselves of harmful debris, called “autophagy,” helps protect against atherosclerosis and its consequences. As such, atophagy was found to go awry in the subpopulations of atherosclerotic lesions that are the most dangerous for clogging the arteries. Therefore, therapeutic attempts to coax this natural process so that it does not fail could help protect against disease-causing atherosclerotic lesions. In another area, Dr. Manikandan Subramanian in the laboratory found that a type of cell that activates the immune system, called “dendritic cells,” primarily activates a type of immune cell called a “regulatory T cell” in the specific setting of atherosclerosis. Regulatory T cells are actually protective against atherosclerosis. The finding that dendritic cells are anti-atherogenic through this mechanisms was very surprising because most investigators thought that dendritic cells primarily activated harmful, pro-atherogenic immune cells. This new discovery gives new promise in the field of atherosclerosis to known therapeutic strategies that are designed to activate dendritic cells.

The Tabas laboratory became interested in type 2 diabetes several years ago because of its importance in driving atherosclerosis. In a new study this year, Drs. Lale Ozcan and Gang Li, in collaboration with Drs. Andrew Marks and Domenico Accili at Columbia, discovered a new pathway in the liver triggered by the hormone called glucagon. Glucagon is known to be excessive in people with type 2 diabetes and to cause the high blood sugar in these patients. The investigators found that glucagon increases blood sugar through a pathway that begins with increasing the mineral calcium in the cell. The increase in calcium activates proteins that induce the expression of genes involved in glucose production. Blocking this pathway using genetic methods or specific drugs lowers blood sugar in mice with type 2 diabetes, and there is evidence that this pathway is active in obese humans. Drs. Ozcan and Tabas are now in the process of translating these findings into the development of a new orally available drug for type 2 diabetes.

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