The role of the renin angiotensin system in vascular and renal responses to severe food restriction

Project: Research

Investigators

  • Aline Maria Arlindo De Souza (PI)

Description

Approximate 5% of the U.S. population (>16 million people) lived with 'very low food security' in 2016 according to the U.S. Department of Agriculture (USDA). This category is defined as having insufficient quantities of food for at least one period during the year. Black and Hispanic households and individuals living below the poverty level continue to be disproportionately represented in this category. Numerous studies show food insecurity is an independent risk factor for cardio-metabolic diseases including obesity, cardiovascular disease, insulin resistance, and type 2 diabetes mellitus. Most of these studies, however, include USDA categories of food insecurity that are based on food quality and not quantity (i.e., marginal and low food security). Thus, it is difficult to differentiate the role of diet from the role of food insufficiency in the long-term adverse consequences to cardiovascular health. Therefore, there is a critical need to elucidate the mechanisms underlying the link between food insecurity and cardio-metabolic disease. My recent studies using an animal model of severe food restriction (sFR) that mimics very low food security showed that three months after refeeding, these rats had increased pressor responses to angiotensin II (Ang II) and more visceral fat than the control animals even though body weights were indistinguishable between the two groups. Thus, both up-regulation of the vasoconstrictor arm of the renin angiotensin system (RAS) and increased visceral fat deposition may contribute to the pathophysiological consequences of individuals living with very low food security. Aim 1 will elucidate the mechanisms underlying increased pressor responses to Ang II. Aim 2 will investigate the role of RAS up-regulation in the increased visceral fat deposition. Throughout these studies, we will test strategies for reversing the allostatic mechanisms leading to increased Ang II pressor responses and greater visceral fat deposition. Research into the mechanisms underlying the link between sFR and long-term dysregulation of blood pressure and fat deposition will inform clinical trials focusing on new therapeutic options for preventing cardio-metabolic disease in individuals who have experienced very low food security and on strategies to reduce health disparities in cardio-metabolic disease. A greater understanding of the association between very low food security and chronic disease will also inform public policy options.
Award amount$104,060.00
Award date01/01/2019
Program typePostdoctoral Fellowship
Award ID19POST34380744
Effective start/end date01/01/201912/31/2020
StatusActive