Stressinduzierte Veränderungen des Essverhaltens und gastrointes- tinaler Peptide bei adipösen und normalgewichtigen Frauen

Zusammenfassung

Der vorliegenden Arbeit liegt ein hypothetisches Modell über die Auswirkungen von Stress auf das Essverhalten zugrunde, das biologische, psychologische und verhaltensorientierte Faktoren berücksichtigt. Es wird davon ausgegangen, dass Stress zu einer Beeinträchtigung der Hunger- und Sättigungsregulation führt, indem sowohl die Art des Essverhaltens als auch die Sekretion gastrointestinaler Peptidhormone verändert wird. Basierend auf den Annahmen des Modells wurde ein kontrolliertes Laborexperiment mit 85 adipösen und normalgewichtigen Frauen durchgeführt. Vor und nach einem psychosozialen Stressor wurden Speichel- Kortisol sowie die gastrointestinalen Peptide PYY und Ghrelin gemessen und mit den Werten aus einer Kontrollbedingung und einer normalgewichtigen Kontrollgruppe verglichen. Außerdem wurden zentrale Kenngrößen der Mikrostruktur des Essverhaltens während des Verzehrs einer Labormahlzeit erfasst. Stress führte bei den adipösen Frauen bei der Labormahlzeit zu einer niedrigen anfänglichen Essgeschwindigkeit, die aber nicht beibehalten wurde, sondern sich zum Ende der Mahlzeit hin beschleunigte. Bei den normalgewichtigen Frauen hingegen kam es nach dem Stressor generell zu einer Stimulierung der Nahrungsaufnahme. Die Steuerung des Essverhaltens bei den Frauen mit Adipositas wurde möglicherweise durch Ghrelin beeinflusst, da der zu erwartende postprandiale Abfall der Ghrelin-Werte spezifisch bei der adipösen Gruppe langsamer ausfiel und das demzufolge länger persistierende Hungersignal schneller zur erneuten Kalorienaufnahme beiträgt. Insgesamt sprechen die Ergebnisse für eine Abhängigkeit des laborexperimentellen Essverhaltens adipöser Frauen von externen Reizen wie Stress und für Defizite bei der adäquaten Wahrnehmung des momentanen Hunger- und Sättigungszustandes. Eine Generalisierung auf andere Lebensmittel und Stressoren kann jedoch nur unter Vorbehalt angenommen werden. Als biologische Basis für eine veränderte Hunger-Wahrnehmung deutet sich eine stressspezifisch veränderte Ghrelin-Sekretion an.

Summary

The reported study is based on a hypothetical model of stress-induced eating behaviour, which integrates biological, psychological and behaviourally oriented factors. It is hypothesized that stress leads to a dysregulation of hunger and satiation processes by changing the microstructure of eating behaviour as well as the secretion of gastrointestinal peptides. The model was tested in a controlled laboratory experiment in 85 obese and normal weight women. Before and after a psychosocial stressor, salivary cortisol and the gastrointestinal peptides PYY and ghrelin were measured and compared to a control condition and a normal weight control group. In addition, central parameters of the microstructure of eating behaviour during a laboratory meal where obtained. In the obese women stress induced a slow initial eating rate which was not maintained, but accelerated towards the end of the meal. In the normal weight women, the stressor stimulated intake from the beginning of the meal on. Eating behaviour of the obese women was possibly influenced through ghrelin, because the expected postprandial decrease took place slower specifically in the obese. A persisting hunger signal would then contribute faster to repeated calorie intake. These results show a dependency of the obese from external cues such as stress and point to deficits in the perception of hunger and satiety. As a biological basis for a dysfunctional hunger perception a stress specific change of ghrelin secretion should be taken into account.

Schlüsselwörter

Adipositas - Stress - Gastrointestinale Peptide - Essverhalten - Ghrelin - PYY - Kortisol

Keywords

Obesity - stress - gastrointestinal peptides - eating behaviour - ghrelin - PYY - cortisol

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