Abstract

It was recently suggested that the Metabolic Syndrome should be renamed to “Circadian Syndrome”. In this context, we explored the effects of living under standard laboratory conditions, where light is the only cycling variable (relevant to human modern life), in a diurnal mammal, on the relationships between affective-like pathology, type 2 diabetes mellitus (T2DM), and cardiac hypertrophy. After 20 weeks, some of the animals spontaneously developed T2DM, depressive and anxiety-like behavior and cardiac hypertrophy. There were significant correlations between levels of anxiety-like behavior and glucose tolerance, and between heart/total body weight ratio and glucose tolerance. Our data suggest a relationship between the development of T2DM, emotional and cardiac pathology as seen in diurnal humans. Furthermore, our data show a possible relationship between reduced daily cycling cues in the laboratory and what has been regularly termed “Metabolic Syndrome” and recently proposed by us to be renamed to “Circadian Syndrome”.

Highlights

  • The comorbid relationship between depression, cardiovascular diseases (CVD) and type 2 diabetes mellitus (T2DM) is repeatedly described in the literature[1,2,3,4,5,6,7]

  • We recently demonstrated that relatively mild interference with circadian rhythms in the sand rat can accelerate the development of T2DM, obesity and cardiac hypertrophy[37], and suggested that the possible underlying mechanism of this process is related to changes that accompany the switch from the mammalian ancestral nocturnal activity to the current diurnal one[37,44]

  • Studies from the 1960’s onwards show that when sand rats are brought into laboratory conditions and fed standard laboratory food, most, but not all, develop T2DM28,29

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Summary

Introduction

The comorbid relationship between depression, cardiovascular diseases (CVD) and type 2 diabetes mellitus (T2DM) is repeatedly described in the literature[1,2,3,4,5,6,7]. Studies from the 1960’s discovered that when sand rats are held under laboratory conditions and fed standard rodent food they quickly develop diabetes[28,29]. As a result, it has become a frequently used animal model to explore the underlying biology of T2DM30–34. We recently demonstrated that relatively mild interference with circadian rhythms in the sand rat can accelerate the development of T2DM, obesity and cardiac hypertrophy[37], and suggested that the possible underlying mechanism of this process is related to changes that accompany the switch from the mammalian ancestral nocturnal activity to the current diurnal one[37,44]. Similar circadian interventions in nocturnal mice did not result in depressive-like phenotypes[53]

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