NIH awards $10.8M to Columbia to study connection between diabetes and hea...(in diabetics to atherosclerosis are pres...),Health

Earlier research led by Dr. Tabas explained what causes the death of macrophages, the white blood cells that accumulate in the cholesterol-laden plaques in arteries of patients with atherosclerosis. Those dead macrophages pile up to form what Dr. Tabas calls a macrophage graveyard or necrotic core causing plaque rupture. The rupture can stimulate the formation of clots that can block blood flow and cause heart attacks and strokes. According to Dr. Tabas, the biggest danger in atherosclerosis comes not so much from the plaque growing to a point that it blocks the artery, as is often believed, but rather from smaller plaques becoming unstable and prone to rupture. According to Dr. Tabas, it turns out that plaques from subjects with diabetes have larger necrotic cores, raising the possibility that amplified plaque macrophage death is an important factor in the higher rate of heart disease in diabetics.

Dr. Tall, working with Drs. Tabas and Accili, focused on the fact that macrophages ordinarily contain insulin receptors, but patients with type 2 diabetes are insulin-resistant, meaning these receptors function poorly. The Columbia researchers found in earlier research, published in Cell Metabolism in 2006, that more macrophage death and plaque necrosis occurred in a mouse model of macrophage insulin resistance. This suggests that in patients with type 2 diabetes, insulin resistance promotes macrophage death, which can lead to atherosclerosis.

Dr. Talls laboratory uses molecular, genomic and cellular approaches to investigate basic aspects of the pathogenesis of atheroscler
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