Adverse effects of nutritional programming during prenatal and early postnatal life, some aspects of regulation and potential prevention and treatments.
Nutritional programming, regulation and some ways for prevention/treatment to ameliorate or normalize adverse outcomes of programming are discussed. Epidemiological studies in human and animal experiments showed that nutrition during fetal and neonatal life may lead to related disorders in adulthood. But several argues may question its validity arising the question of the adequate models used to reproduce human situations. Protein level in milk formula intake by infant during neonatal life is discussed. Body weight at birth reflects the product growth trajectory during fetal life. Low birth weight is considered as the result of an adverse growth trajectory and is often associated with later metabolic diseases in adult age. But, the sum of prenatal growth trajectory, rapid growth in early infancy (catch up growth), early adiposity rebound in childhood must be considered to determine the origins of later diseases in adulthood. The review focuses the regulation of nutritional imprinting on hormonal and epigenetic mechanisms which are complementary. The HPA axis and GH-IGF axis may have a crucial role in the regulation induced by nutritional programming. The persistent alterations seem to be a consequence, at least in part, of elevated insulin levels during "critical periods" of pre- and early postnatal development. Also, leptin seems to play an important role in this complex system. New knowledge about these mechanisms involved suggest the development of new, rational, and effective preventive and/or therapeutic options before and/or after birth. Thus, early infancy may provide an opportunity for intervention aimed at reducing later disease risk.
Guilloteau
P
P
INRA, U1079, Unite Mixte de Recherche - Systeme Elevage, Nutrition Animale et Humaine (UMR SENAH), Domaine de la Prise, 35590 Saint-Gilles, France. Paul.Guilloteau@rennes.inra.fr
Zabielski
R
R
Hammon
H M
HM
Metges
C C
CC
D000328:Adult; D000818:Animals; D002657:Child Development; D002675:Child, Preschool; D002908:Chronic Disease; D044127:Epigenesis, Genetic; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D018507:Gene Expression Regulation, Developmental; D018392:Genomic Imprinting / Q000502:physiology; D006801:Humans; D007223:Infant; D044342:Malnutrition / Q000150:complications / Q000503:physiopathology*; D009747:Nutritional Physiological Phenomena; D009752:Nutritional Status; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D039401:Prenatal Nutritional Physiological Phenomena