Affiliations: Postgraduiertenstudium Psychobiologie, Abteilung
für Theoretische und Klinische Psychobiologie, Universität
Trier | Postgraduiertenstudium Psychobiologie, Abteilung
für Verhaltensgenetik, Universität Trier | Department of Psychology and Social Behavior,
University of California, Irvine, 3340 Social Ecology II, Irvine, CA
92697-7085
Note: [] Korrespondenzadresse: Stefan Wüst, Postgraduiertenstudium
Psychobiologie, Abteilung für Theoretische und Klinische Psychobiologie,
Universität Trier
Abstract: Association of a polymorphism in the H6PD gene and basal cortisol
secretion, body fat mass and leptin level The hypothalamus-pituitary-adrenal (HPA) axix is vital for an
organism's response to physical or psychosocial stimulation. Chronic
dysregulation of HPA axis activity is related to several psychiatric and
psychosomatic disorders. Cortisol, the end product of this endocrine system,
affects a multitude of systems in the body, including the HPA axis itself and
it also has an influence on behavior. The intracellular availability of
cortisol is crucial for the regulation of this endocrine system. The enzyme
hexose-6-phosphat-dehydrogenase (H6PDH) affects cortisol availability via its
influenec on 11β-hydroxysteroid dehydrogenase type I
(11β-HSDI)-activity, which regenerates cortisol from inactive cortisone.
116 healthy males (33 monozygotic & 25 dizygotic twin pairs) were studied
to estimate the association between a polymorphism in the exon 5 of the H6PD
gene (R435Q, GA) and adrenocortical responses to psychosocial stress, basal
salivary cortisol levels and body composition. Compared with subjects with the
more frequent H6PD genotypers the homozygous AA-carriers displayed a
significantly decreased cortisol awakening rise (CAR) as well as lower daytime
cortisol levels. In response to stress, the AA-carriers exhibited a trend
towards lower cortisol and ACH responses compared with GG- and GA-carriers. In
addition, significantly higher levels of leptin and amount of body fat were
observed in AA-carriers. We hypothesize that the R453Q polymorphism in the H6PD
gene might influence intracellular cortisol availability and thus affect HPA
axis regulation.
