Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 1720 7th Avenue S., Birmingham, AL 35294, USA
Jodi R. Paul
Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 1720 7th Avenue S., Birmingham, AL 35294, USA
Stefani D. Yates
Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 1720 7th Avenue S., Birmingham, AL 35294, USA
Elam J. Cutts
Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 1720 7th Avenue S., Birmingham, AL 35294, USA
Lori L. McMahon
School of Medicine, Department of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, USA
Jennifer S. Pollock
School of Medicine, Division of Nephrology, University of Alabama at Birmingham, Birmingham, AL, USA
David M. Pollock
School of Medicine, Division of Nephrology, University of Alabama at Birmingham, Birmingham, AL, USA
Shannon M. Bailey
School of Medicine, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, Birmingham, AL, USA
Karen L. Gamble
Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 1720 7th Avenue S., Birmingham, AL 35294, USA; Corresponding author
Summary: Feeding rodents a high-fat diet (HFD) disrupts normal behavioral rhythms, particularly meal timing. Within the brain, mistimed feeding shifts molecular rhythms in the hippocampus and impairs memory. We hypothesize that altered meal timing induced by an HFD leads to cognitive impairment and that restricting HFD access to the “active period” (i.e., night) rescues the normal hippocampal function. In male mice, ad-lib access to an HFD for 20 weeks increased body weight and fat mass, increased daytime meal consumption, reduced hippocampal long-term potentiation (LTP), and eliminated day/night differences in spatial working memory. Importantly, two weeks of time-restricted feeding (TRF) at the end of the chronic HFD protocol rescued spatial working memory and restored LTP magnitude, even though there was no change in body composition and total daily caloric intake. These findings suggest that short-term TRF is an effective mechanism for rescuing HFD-induced impaired cognition and hippocampal function.
