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Programmierung von kindlichem Übergewicht durch perinatale Überflusssituation

Programming of childhood overweight due to perinatal overnutrition

  • Leitthema
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Zusammenfassung

Kindliches Übergewicht und Adipositas sind dringliche Gesundheitsprobleme mit weitreichenden Folgen bis ins Erwachsenenalter. Durch noch wenig verstandene Mechanismen, die als „fetale Programmierung“ bezeichnet werden, werden in den frühesten Lebensphasen bereits Krankheitsrisiken geprägt, die die kindliche Übergewichtsproblematik zu verstärken scheinen. Eine perikonzeptionelle maternale Adipositas, aber auch weitere perinatale Risikofaktoren, wie disproportional hohe Gewichtszunahme in der Schwangerschaft, Gestationsdiabetes oder eine rasche postnatale Gewichtszunahme des Kindes begünstigen das Risiko für die Entwicklung von Übergewicht und metabolischen Störungen im weiteren Leben. Tierexperimentelle Studien erlauben eine kontrollierte Untersuchung der Folgen einer perinatalen Überflusssituation für die Nachkommen. Verschiedene ungünstige perinatale Ernährungseinflüsse (vermehrte Zufuhr gesättigter Fettsäuren oder zusätzliche Erhöhung des Zuckeranteils in der maternalen Nahrung) haben Auswirkungen auf Körpergewicht und -fettanteil der Nachkommen. Sie verursachen außerdem Störungen der Funktion zahlreicher metabolisch aktiver Organe (Fettgewebe, Gehirn, Leber oder Muskel). Als zugrunde liegende Mechanismen für diesen prägenden Effekt werden proinflammatorische und epigenetische Prozesse diskutiert. Früh ansetzende vorgeburtliche Präventionskonzepte mit positiven Langzeiteffekten auf die Nachkommen stehen derzeit noch aus. Unmittelbar postnatal sind Stillförderung und die Vermeidung einer raschen übermäßigen Gewichtszunahme in den ersten beiden Lebensjahren wichtige Bausteine pädiatrisch-frühpräventiver Maßnahmen.

Abstract

Childhood overweight and obesity are urgent health problems with far-reaching consequences up into adulthood. Based on still poorly defined mechanisms, referred to as fetal programming, the risks of later life health problems are already determined during the earliest prenatal stages of life and appear to aggravate the overweight situation. Periconceptional maternal obesity and additional perinatal risk factors including a disproportionately high gestational weight gain, gestational diabetes and postnatal rapid weight gain in the first 2 years of life, promote the risk of developing overweight and associated metabolic disorders in childhood. Animal experimental studies provide the advantage of studying the consequences of maternal overnutrition for the offspring in a controlled setting. Adverse nutritional exposure, such as a high intake of saturated fatty acids or an additional increase of free sugar in the maternal diet exerts effects on weight status and body fat in the offspring and may result in dysfunction of metabolically active organs including adipose tissue, brain, liver and muscle. Potential underlying mechanisms may involve proinflammatory and epigenetic processes. Whether prenatal prevention concepts may have a beneficial long-term impact on later offspring health is currently unclear. Promotion of breastfeeding and avoidance of rapid postnatal weight gain in the first 2 years of life are essential components of the practicing pediatrician’s efforts for overweight prevention.

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Authors and Affiliations

  1. Experimentelle Pädiatrie m. S. Stoffwechselstörungen, Arbeitsgruppe Molekulare Ernährung, Klinik für Allgemeine Pädiatrie, Neonatologie und Kinderkardiologie, Heinrich-Heine-Universität Düsseldorf, Moorenstr. 5, 40225, Düsseldorf, Deutschland

    V. Brüll &  R. Ensenauer

  2. Klinik und Poliklinik für Kinder- und Jugendmedizin, Universität zu Köln, Köln, Deutschland

    E. Hucklenbruch-Rother

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Correspondence to R. Ensenauer.

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V. Brüll, E. Hucklenbruch-Rother und R. Ensenauer geben an, dass kein Interessenkonflikt besteht.

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J. Dötsch, Köln

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Brüll, V., Hucklenbruch-Rother, E. & Ensenauer, R. Programmierung von kindlichem Übergewicht durch perinatale Überflusssituation. Monatsschr Kinderheilkd 164, 99–105 (2016). https://doi.org/10.1007/s00112-015-0010-x

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