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dc.contributor.authorDepke, Maren
dc.contributor.authorFusch, Gerhard
dc.contributor.authorDomanska, Grazyna
dc.contributor.authorGeffers, Robert
dc.contributor.authorVölker, Uwe
dc.contributor.authorSchuett, Christine
dc.contributor.authorKiank, Cornelia
dc.date.accessioned2008-08-21T09:28:28Z
dc.date.available2008-08-21T09:28:28Z
dc.date.issued2008-06
dc.identifier.citationHypermetabolic syndrome as a consequence of repeated psychological stress in mice. 2008, 149 (6):2714-23 Endocrinologyen
dc.identifier.issn0013-7227
dc.identifier.pmid18325986
dc.identifier.doi10.1210/en.2008-0038
dc.identifier.urihttp://hdl.handle.net/10033/36052
dc.description.abstractStress 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.
dc.language.isoenen
dc.subject.meshAcoustic Stimulationen
dc.subject.meshAcute Diseaseen
dc.subject.meshAnimalsen
dc.subject.meshDisease Models, Animalen
dc.subject.meshDrinking Behavioren
dc.subject.meshEnergy Intakeen
dc.subject.meshEnergy Metabolismen
dc.subject.meshFemaleen
dc.subject.meshKineticsen
dc.subject.meshMetabolic Syndrome Xen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred BALB Cen
dc.subject.meshOligonucleotide Array Sequence Analysisen
dc.subject.meshPolymerase Chain Reactionen
dc.subject.meshStress, Psychologicalen
dc.subject.meshWateren
dc.titleHypermetabolic syndrome as a consequence of repeated psychological stress in mice.en
dc.typeArticleen
dc.contributor.departmentErnst-Moritz-Arndt-University, Interfaculty Institute of Genetics and Functional Genomics, 17487 Greifswald, Germany.en
dc.identifier.journalEndocrinologyen
refterms.dateFOA2018-06-13T01:15:47Z
html.description.abstractStress 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.


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