This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. A number of adverse changes occur to the cardiovascular system (heart and blood vessels) with age-related increases in total and abdominal obesity. For example, blood vessels should dilate or contract in response to different stimuli, such as increased blood pressure, to prevent drastic changes in blood pressure. Age-related increases in total and abdominal obesity are generally associated with an impairment in the blood vessel's ability to dilate. This impairment is due in part to an increase in oxidative stress levels in the body. Oxidative stress is the exposure of the body's cells to molecules (i.e. reactive oxygen species) that are generated continuously in the body as a function of normal metabolism. Reactive oxygen species can produce damage to cells and interfere with the body's normal function, such as the ability of blood vessels to dilate. Additionally, blood vessel function is affected by various proteins (molecules produced from cells that line your blood vessel wall called endothelial cells) that are associated with the destruction of reactive oxygen species as well as the dilation and constriction of a vessel. Importantly, we know that weight loss is associated with improved vascular function as well as reduced oxidative stress. Accordingly, the proposed research will test the hypothesis that the adverse changes in vascular function with age-related increases in total and abdominal obesity can be attributed to changes in the expression of proteins in the vessel wall. Furthermore, diet-induced weight loss may prevent the obesity-related impairments in vascular function by beneficially altering endothelial cell protein expression.
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