Premature Death of Sleep Fragmented Males is Associated With An Accumulation of Reactive Oxygen Species In The Gut

Abstract 70 million Americans report insufficient sleep due to work or lifestyle choices. Decreased duration and poor quality are associated with high rates of CVD is strongly increased risk all-cause mortality. The effects gender have been studied in CVD, but the impact sexual dimorphism Sleep Fragmented (SF)-associated atherogenesis not known. Recently, we found that fat diet (HFD) fed male Apoe −/−mice on SF experienced premature death. 80% males did survive past week 2 SF, while females survived 8 under same conditions. We sought identify a cause death HFD following fragmentation. Interestingly, Ldlr −/−mouse experience when suggesting ApoE absence, hyperlipidemia, plays an essential function induction Furthermore, oral 17β-Estradiol was able rescue from induced Compared controls, had decreased body weight circulating LPS, ROS cell-free dsDNA at Finally, small intestines tight junction protein (Tjp1) expression, compromised intestinal barrier function. Our data suggests combination known factors for (male sex, genotype, HFD) results combined inadequate sleep. our this specific co-factors might result systemic increase oxidative stress, possibly caused by leakage LPS gut, which may be alleviated through administration 17β-Estradiol. Supported project–initiation funds Center Integrative Neuroscience Inflammatory Diseases AHA Predoctoral (20PRE35180156)