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Horm Metab Res 2010; 42(10): 746-753
DOI: 10.1055/s-0030-1261924
Humans, Clinical

© Georg Thieme Verlag KG Stuttgart · New York

Effects of Acute Psychological Stress on Glucose Metabolism and Subclinical Inflammation in Patients with Post-traumatic Stress Disorder

B. Nowotny1 , M. Cavka2 , C. Herder1 , H. Löffler1 , U. Poschen1 , L. Joksimovic2 , K. Kempf1 , A. W. Krug3 , W. Koenig4 , S. Martin1 , J. Kruse5
  • 1Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich-Heine-University, Düsseldorf, Germany
  • 2Clinic for Psychosomatic Medicine and Psychotherapy, Heinrich-Heine University, Düsseldorf, Germany
  • 3Carl Gustav Carus University Hospital, Medical Clinic III, University of Dresden, Dresden, Germany
  • 4Department of Internal Medicine II-Cardiology, University of Ulm Medical Center, Ulm, Germany
  • 5Department for Psychosomatic Medicine and Psychotherapy, Justus-Liebig-University, Giessen, Germany
Further Information

Publication History

received 18.11.2009

accepted 15.06.2010

Publication Date:
27 July 2010 (online)

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Abstract

During acute psychological stress, the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system are activated. The released stress hormones influence glucose metabolism, can activate immune cells, and modulate subclinical inflammation. The aim of our study was to analyze the effect of acute psychological stress on glucose metabolism and the inflammatory status in patients with post-traumatic stress disorder (PTSD). We included 15 overweight male Bosnian war refugees with PTSD into the study (mean age 44±11 years, BMI 29.3±4.3 kg/m2). All subjects underwent an oral glucose tolerance test (OGTT) with either acute stress (trauma script exposure) or a resting period in a cross-over design. Blood was drawn over 2.5 h and metabolic markers were measured. Systemic levels of immune markers were determined using high-sensitive ELISA or bead-based multiplex assay. Immune gene expression was quantified by RT-PCR. After being exposed to acute stress, cortisol levels and heart frequency tended to be increased. Higher blood glucose and insulin levels after stress exposure were observed (p<0.05). Systemic levels of the chemokines interferon-γ-inducible protein-10 and macrophage chemoattractant protein-1 were decreased compared to the control day (both p<0.05) and the expression of the proinflammatory regulator IKKβ was significantly reduced after stress exposure (p<0.001). In conclusion, acute stress induces postprandial blood glucose peaks and elevated insulin levels and a selective decrease of systemic immune markers and the proinflammatory regulator of the NFκB cascade, which are associated with type 2 diabetes. This points towards an independent effect of acute psychological stress on glucose metabolism and inflammation.

Key words

immune marker - psychic stress - metabolism

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Correspondence

B. Nowotny

Institute for Clinical

Diabetology

German Diabetes Center

Leibniz Center at

Heinrich-Heine-University

Auf’m Hennekamp 65

40225 Düsseldorf

Germany

Phone: +49/211/3382 575

Fax: +49/211/3382 592

Email: bettina.nowotny@ddz.uni-duesseldorf.de

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