Presenter: heba sultan
Authors: Heba Sultan, Sohom Mookherjee, Jae Min Cho, Seul-Ki Park, Paul E Bourrant, Caitlin S. Peterson, Lori J. Begaye, Amandine Chaix, J. David Symons
Faculty Advisor: John David Symons
Institution: University of Utah
Endothelial dysfunction resulting from systemic inflammation and / or metabolic disruption precipitates age and obesity-associated vascular complications. Time-restricted feeding (TRF) prevents metabolic diseases in mice fed an obesogenic diet, but its effect on endothelial function in the context of obesity and / or aging is unknown. Here we tested the hypothesis that TRF attenuates age and obesity-induced vascular dysfunction. Three-month old C57BL/6J male mice consumed high-fat high sucrose (HFHS) chow ad-libitum for 10-months. At 13-months of age arterial function was assessed in carotid arteries using isometric procedures, and middle cerebral arteries (MCAs) using isobaric techniques. HFHS feeding was offered to additional mice in an ad libitum manner, or between 0800-1700 only (i.e., TRF). Importantly, all mice were familiarized with and maintained on an altered light : dark cycle such that the dark phase occurred between 0800 and 1700. At 19-months of age, carotid artery and MCA function was evaluated in both groups. Endothelium-dependent dysfunction was more severe (p<0.05) at 19 vs. 13-months in MCAs from mice that consumed HFHS chow ad-libitum. Of interest, endothelial dysfunction was attenuated (p=NS) in TRF vs. ad- libitum fed mice at 19 months. Carotid arterial function was not different at 19 vs. 13-months in mice that consumed HFHS diet in an ad-libitum manner. Likewise, vascular function was similar in carotid arteries from ad-libitum and TRF mice at 19-months. This study is ongoing and MCA and carotid artery structure, function, and intravascular signaling pathways will be evaluated in additional ad-libitum and TRF mice at 25-months. Our results will reveal whether TRF is an efficacious lifestyle modification strategy to lessen obesity and / or age-associated arterial dysfunction.