Proceedings of The Physiological Society

Obesity (2014) Proc Physiol Soc 32, PC020

Poster Communications

Holding mice at an environmental photic cycle that matches their endogenous circadian rhythm period length prevents diet induced obesity

R. Stakler1,3, H. Cohen5, S. Tamir1,4, R. Gutman2,3

1. Department of Nutritional Sciences, Tel-Hai College, Upper Galilee, Israel. 2. Department of Zoology, Tel-Hai College, Upper Galilee, Israel. 3. Unit of Integrative Physiology (LIP), MIGAL - Galilee Research institute, Kiryat Shmona, Israel. 4. Laboratory of Human Health and Nutrition Sciences, MIGAL - Galilee Research institute, Kiryat Shmona, Israel. 5. Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.


  • Figure 1: The effect of feeding on a high-fat diet vs. a low-fat diet on body weight and body fat percentage of newborn FVB/N female mice held under the regular 24 h (half-dark half-light) photic cycle (A) or under their tau-matching 23.7 h (half-dark half-light) photic cycle (B). Each time point represents the mean (

Circadian regulation is responsible for the maintenance of endogenous physiological rhythms, and their temporal organization and entrainment to the environmental (24 h) light-dark photic cycle. Mechanisms underlying circadian regulation and energy homeostasis are interconnected: disruption of the former (i.e., circadian disruption) is accompanied by higher susceptibility to diet-induced obesity (DIO) due to feeding on high-fat diet (HFD). Endogenous circadian rhythms show a period length (tau) that usually deviates from 24 h. Recent descriptive studies have shown that deviation of tau from 24 h is in correlation with mice inter-strain susceptibility to DIO. These studies support our hypothesis that a lack of resonance between tau and environmental period length exacts a metabolic cost increasing susceptibility to DIO. However, this hypothesis has never tested in a controlled setup. Our goal was to conduct controlled animal experiments designed to directly examine whether the deviation of tau from the environmental photic cycle is associated with higher susceptibility to the DIO. This hypothesis was tested by comparing newborn female FVB/N mice rate of obesity, while feeding on a HFD (60% of calories from fat) vs. a low-fat diet (LFD, 10% of calories from fat), under two photic regimes: a 23.7 h photic cycle (half-dark half-light hours) that matches their tau, and a 24 h photic cycle (half-dark half-light hours). Our results show that when raised under a tau-mismatching regular 24 h photic cycle, these female FVB/N mice develop DIO, defined by the difference in body weight and fat % (measured by NMR) under a HFD vs. a LFD (Fig. 1A). However, when raised under their tau-matching 23.7 h photic cycle, DIO was prevented (Fig. 1B). In all, mice fed a HFD had a significantly lower body weight and fat % under a tau-matching 23.7 h photic cycle vs. a tau-mismatching regular 24 h photic cycle. As far as we know, this is the first controlled experiment showing that having a non-24 h period length of the endogenous circadian rhythm enhances the propensity to DIO under the regular 24 h photic cycle. Our results offer a novel risk factor to obesity that justify the identification of biomarkers related to tau for clinical use as a diagnostic risk factor for obesity; and an experimental paradigm for the development of novel, clock-related pharmaceutical prophylactic/therapeutic interventions to reduce the gap between internal and external circadian rhythms, and hence reduce the prevalence of obesity.

Where applicable, experiments conform with Society ethical requirements