Chronic social stress lessens the metabolic effects induced by a high fat diet

in Journal of Endocrinology
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  • 1 T Jene, Translational Psychiatry, Leibniz Institute for resilience research, Mainz, Germany
  • 2 I Ruiz de Azua, Institute of Physiological Chemistry, Leibniz Institute for Resilience Research, Mainz, Germany
  • 3 A Hasch, Translational Psychiatry, Johannes Gutenberg Universitat Mainz, Mainz, Germany
  • 4 J Klüpfel, Translational Psychiatry, Johannes Gutenberg Universitat Mainz, Mainz, Germany
  • 5 J Deuster, Translational Psychiatry, Leibniz Institute for resilience research, Mainz, Germany
  • 6 M Maas, Department for Developmental Origins of Disease, University Medical Center Utrecht, Utrecht, Netherlands
  • 7 C Nijboer, Department for Developmental Origins of Disease, University Medical Center Utrecht, Utrecht, Netherlands
  • 8 B Lutz, Leibniz Institute for resilience research, Johannes Gutenberg Universitat Mainz, Mainz, Germany
  • 9 M Müller, Translational Psychiatry, Johannes Gutenberg Universitat Mainz, Mainz, Germany
  • 10 M van der Kooij, Translational Psychiatry, Johannes Gutenberg Universitat Mainz, Mainz, 55099, Germany

Correspondence: Michael van der Kooij, Email: m.vanderkooij@uni-mainz.de
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Stress has a major impact on the modulation of metabolism, as previously evidenced by hyperglycemia following chronic social defeat (CSD) stress in mice. Although CSD-triggered metabolic dysregulation might predispose to pre-diabetic conditions, insulin sensitivity remained intact, and obesity did not develop, when animals were fed with a standard diet (SD). Here, we investigated whether a nutritional challenge, a high fat diet (HFD), aggravates the metabolic phenotype, and whether there are particularly sensitive time windows for the negative consequences of HFD exposure. Chronically stressed male mice and controls (CTRL) were kept under (i) SD-conditions, (ii) with HFD commencing post-CSD, or (iii) provided with HFD lasting throughout, and after CSD. Under SD conditions, stress increased glucose levels early post-CSD. Both HFD regimens increased glucose levels in non-stressed mice, but not in stressed mice. Nonetheless, when HFD was provided after CSD, stressed mice did not differ from controls in long-term body weight gain, fat tissue mass and plasma insulin, and leptin levels. In contrast, when HFD was continuously available, stressed mice displayed reduced body weight gain, lowered plasma levels of insulin, and leptin, and reduced white adipose tissue weights as compared to their HFD-treated non-stressed controls. Interestingly, stress-induced adrenal hyperplasia and hypercortisolemia were observed in mice treated with SD and with HFD after CSD, but not in stressed mice exposed to a continuous HFD treatment. The present work demonstrates that CSD can reduce HFD-induced metabolic dysregulation. Hence, HFD during stress may act beneficially, as comfort food, by decreasing stress-induced metabolic demands.

 

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