Abstract 3558: Time of Day: A Vital Determinant in Diet-Induced Cardiometabolic Syndrome Development

Abstract

Excess caloric intake is strongly associated with the development of obesity, type 2 diabetes mellitus, and cardiovascular disease (CVD). Research efforts have focused attention primarily on the quality (i.e., nutritional content) and/or quantity of calories as potential causes for diet-induced pathology. Little is known regarding how the timing of nutrient ingestion influences CVD development, despite growing acceptance that biological rhythms strongly affect cardiovascular physiology and pathophysiology. We therefore hypothesized that the time of day at which dietary fat is consumed profoundly influences the development of the cardiometabolic syndrome. Mice were initially fed either control or high fat diets (10% and 45% calories from fat, respectively) in an ad libitum fashion. As expected, 16 weeks ad libitum high fat feeding resulted in increased body weight gain (13%), increased percent body fat (23%), increased ventricular weight (11%), and myocardial contractile dysfunction (33% decrease in cardiac power, as assessed in ex vivo working mouse heart perfusions), relative to control mice (p<0.05). A separate set of mice were next fed only during the 12hr active/awake/dark phase, and were divided into early fat (EF) and late fat (LF) groups (access to high fat diet only during the first 4 hours versus the last 4 hours of the active phase, respectively; mice were allowed access to control diet for remaining active phase hours). LF feeding resulted in increased body weight gain, increased percent body fat, decreased glucose tolerance, decreased skeletal muscle oxidative capacity, induction of myocardial anf expression, and decreased cardiac power, relative to EF feeding, despite virtually identical quantity and quality of calories consumed (see Table ). These data reveal that the consumption of dietary lipids during the end of the active phase (i.e., dinner for humans) significantly contributes to diet-induced cardiometabolic syndrome development.