Hypermetabolic syndrome as a consequence of repeated psychological stress in mice.
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Authors
Depke, MarenFusch, Gerhard
Domanska, Grazyna
Geffers, Robert

Völker, Uwe
Schuett, Christine
Kiank, Cornelia
Issue Date
2008-06
Metadata
Show full item recordAbstract
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.Citation
Hypermetabolic syndrome as a consequence of repeated psychological stress in mice. 2008, 149 (6):2714-23 EndocrinologyAffiliation
Ernst-Moritz-Arndt-University, Interfaculty Institute of Genetics and Functional Genomics, 17487 Greifswald, Germany.Journal
EndocrinologyPubMed ID
18325986Type
ArticleLanguage
enISSN
0013-7227ae974a485f413a2113503eed53cd6c53
10.1210/en.2008-0038
Scopus Count
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