A new study suggests that inflammation may be the driving force behind damage to blood vessels caused by elevated blood glucose levels, with the potential for the use of anti-inflammatory medications in reducing the risk of blood vessel disease in patients with diabetes. These findings were presented at the American Heart Association’s High Blood Pressure Research Scientific Sessions 2014.
Researchers from the Universidad Autónoma de Madrid examined cultured smooth muscle cells from the aorta and discovered that excess glucose in the culture fluid did not enter the cells in the absence of inflammation; no harm was done when extra glucose was forced into the cells in the absence of inflammation. Following the introduction of inflammation-stimulating protein interleukin-1 (IL-1), an increased amount of glucose entered the cells. The glucose was metabolized via chemical pathways spurring escalating inflammation, overwhelming the ability of the cells’ to counteract. In the presence of the IL-1-blocker anakinra, which blocks the activity of IL-1, these changes did not occur.
Further studies will test if the effect is similar in cultured cells from the lining of blood vessels and explore the glucose/inflammation link in animals.
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