This Article Full Text Full Text (PDF) Supplemental Data Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Depke, M. Articles by Kiank, C. Search for Related Content PubMed PubMed Citation Articles by Depke, M. Articles by Kiank, C.

Hypermetabolic Syndrome as a Consequence of Repeated Psychological Stress in Mice

Interfaculty Institute of Genetics and Functional Genomics (M.D., U.V.), Institute of Immunology and Transfusion Medicine, Department of Immunology (C.S., G.D., C.K.) and Department of Neonatology and Pediatric Intensive Care Medicine (G.F.), Ernst-Moritz-Arndt-University D-17487 Greifswald, Germany; and Department of Mucosal Immunity (R.G.), Helmholtz-Centre for Infection Research, D-38124 Braunschweig, Germany

Address all correspondence and requests for reprints to: Cornelia Kiank, Ph.D., Ernst-Moritz-Arndt-University Greifswald, Department of Immunology, Sauerbruchstraβe/DZ, 17487 Greifswald, Germany. E-mail: cornelia.kiank{at}uni-greifswald.de.

Stress is a powerful modulator of neuroendocrine, behavioral, and immunological functions. After 4.5-d repeated combined acoustic and restraint stress as a murine model of chronic psychological stress, severe metabolic dysregulations became detectable in female BALB/c mice. Stress-induced alterations of metabolic processes that were found in a hepatic mRNA expression profiling were verified by in vivo analyses. Repeatedly stressed mice developed a hypermetabolic syndrome with the severe loss of lean body mass, hyperglycemia, dyslipidemia, increased amino acid turnover, and acidosis. This was associated with hypercortisolism, hyperleptinemia, insulin resistance, and hypothyroidism. In contrast, after a single acute stress exposure, changes in expression of metabolic genes were much less pronounced and predominantly confined to gluconeogenesis, probably indicating that metabolic disturbances might be initiated already early but will only manifest in repeatedly stressed mice. Thus, in our murine model, repeated stress caused severe metabolic dysregulations, leading to a drastic reduction of the individual’s energy reserves. Under such circumstances stress may further reduce the ability to cope with new stressors such as infection or cancer.

This article has been cited by other articles:

				M. Dorfman, V. D. Ramirez, E. Stener-Victorin, and H. E. Lara Chronic-Intermittent Cold Stress in Rats Induces Selective Ovarian Insulin Resistance Biol Reprod, February 1, 2009; 80(2): 264 - 271. [Abstract] [Full Text] [PDF]

				K. D. Laugero Filling in the Gaps of Chronic Psychological Stress Disease Models: What's Metabolic Profiling Have to Do with It? Endocrinology, June 1, 2008; 149(6): 2712 - 2713. [Full Text] [PDF]