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Nutrients, growth, and the development of programmed metabolic function.

Abstract

For each individual, the genetic endowment at conception sets the limits on the capacity or metabolic function. The extent to which this capacity is achieved or constrained is determined by the environmental experience. The consequences of these experiences tend to be cumulative throughout life and express themselves phenotypically as achieved growth and body composition, hormonal status and the metabolic capacity for one or other function. At any time later in life the response to an environmental challenge, such as stress, infection or excess body weight is determined by an interaction amongst these factors. When the metabolic capacity to cope is exceeded, the limitation in function is exposed and expresses itself as overt disease. During early life and development the embryo, fetus and infant are relatively plastic in terms of metabolic function. The effect of any adverse environmental exposure is likely to be more marked than at later ages and the influence is more likely to exert a fundamental effect on the development of metabolic capacity. This has been characterised as "programming" and has come to be known as "the Barker hypothesis" or "the fetal origins hypothesis". Barker has shown that the size and shape of the infant at birth has considerable statistical power to predict the risk of chronic disease in later life. These relationships are graded and operate across a range of birth weight, which would generally be considered to be normal, and are not simply a feature of the extreme of growth retardation. The first evidence showed strong relations between birth weight and heart disease, the risk factors for heart disease, diabetes and hypertension, and the intermediary markers for heart disease, blood cholesterol and fibrinogen. Strong associations have also been found for bone disease, allergic disease and some aspects of brain function. In experimental studies in animals it is possible to reproduce all of the metabolic features predicted from this hypothesis by moderating the consumption of food, or its pattern during pregnancy, and determining metabolic behaviour in the offspring. It has been shown that aspects of maternal diet exert an influence on fetal growth, especially the dietary intake of carbohydrate, protein and some micronutrients. However, these relationships are less strong than might have been predicted, especially when compared with the associations which can be drawn with maternal shape, size and metabolic capacity. Maternal height, weight and body composition relate to the metabolic capacity of the mother and her ability to provide an environment in which the delivery of nutrients to the fetus is optimal. Current evidence suggests that the size of the mothers determines her ability to support protein synthesis, and that maternal protein synthesis, especially visceral protein synthesis, is very closely related to fetal growth and development. It is not clear the extent to which the effect of an adverse environment in utero can be reversed by improved conditions postnatally, but some care is needed in exploring this area, as the evidence suggests that "catch-up" growth imposes its own metabolic stress and may in itself exert a harmful effect.

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  • Publisher Full Text
  • Authors+Show Affiliations

    Institute of Human Nutrition, Fetal Origins of Adult Disease Division, University of Southampton, UK.

    Source

    MeSH

    Adaptation, Biological
    Amino Acids
    Animals
    Birth Weight
    Body Composition
    Child Development
    Chronic Disease
    Embryonic and Fetal Development
    Energy Metabolism
    Female
    Growth
    Humans
    Infant Nutritional Physiological Phenomena
    Infant, Newborn
    Models, Animal
    Nutritional Physiological Phenomena
    Pregnancy

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    11065059

    Citation

    Jackson, A A.. "Nutrients, Growth, and the Development of Programmed Metabolic Function." Advances in Experimental Medicine and Biology, vol. 478, 2000, pp. 41-55.
    Jackson AA. Nutrients, growth, and the development of programmed metabolic function. Adv Exp Med Biol. 2000;478:41-55.
    Jackson, A. A. (2000). Nutrients, growth, and the development of programmed metabolic function. Advances in Experimental Medicine and Biology, 478, pp. 41-55.
    Jackson AA. Nutrients, Growth, and the Development of Programmed Metabolic Function. Adv Exp Med Biol. 2000;478:41-55. PubMed PMID: 11065059.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Nutrients, growth, and the development of programmed metabolic function. A1 - Jackson,A A, PY - 2000/11/7/pubmed PY - 2001/10/12/medline PY - 2000/11/7/entrez SP - 41 EP - 55 JF - Advances in experimental medicine and biology JO - Adv. Exp. Med. Biol. VL - 478 N2 - For each individual, the genetic endowment at conception sets the limits on the capacity or metabolic function. The extent to which this capacity is achieved or constrained is determined by the environmental experience. The consequences of these experiences tend to be cumulative throughout life and express themselves phenotypically as achieved growth and body composition, hormonal status and the metabolic capacity for one or other function. At any time later in life the response to an environmental challenge, such as stress, infection or excess body weight is determined by an interaction amongst these factors. When the metabolic capacity to cope is exceeded, the limitation in function is exposed and expresses itself as overt disease. During early life and development the embryo, fetus and infant are relatively plastic in terms of metabolic function. The effect of any adverse environmental exposure is likely to be more marked than at later ages and the influence is more likely to exert a fundamental effect on the development of metabolic capacity. This has been characterised as "programming" and has come to be known as "the Barker hypothesis" or "the fetal origins hypothesis". Barker has shown that the size and shape of the infant at birth has considerable statistical power to predict the risk of chronic disease in later life. These relationships are graded and operate across a range of birth weight, which would generally be considered to be normal, and are not simply a feature of the extreme of growth retardation. The first evidence showed strong relations between birth weight and heart disease, the risk factors for heart disease, diabetes and hypertension, and the intermediary markers for heart disease, blood cholesterol and fibrinogen. Strong associations have also been found for bone disease, allergic disease and some aspects of brain function. In experimental studies in animals it is possible to reproduce all of the metabolic features predicted from this hypothesis by moderating the consumption of food, or its pattern during pregnancy, and determining metabolic behaviour in the offspring. It has been shown that aspects of maternal diet exert an influence on fetal growth, especially the dietary intake of carbohydrate, protein and some micronutrients. However, these relationships are less strong than might have been predicted, especially when compared with the associations which can be drawn with maternal shape, size and metabolic capacity. Maternal height, weight and body composition relate to the metabolic capacity of the mother and her ability to provide an environment in which the delivery of nutrients to the fetus is optimal. Current evidence suggests that the size of the mothers determines her ability to support protein synthesis, and that maternal protein synthesis, especially visceral protein synthesis, is very closely related to fetal growth and development. It is not clear the extent to which the effect of an adverse environment in utero can be reversed by improved conditions postnatally, but some care is needed in exploring this area, as the evidence suggests that "catch-up" growth imposes its own metabolic stress and may in itself exert a harmful effect. SN - 0065-2598 UR - https://www.unboundmedicine.com/medline/citation/11065059/full_citation L2 - https://dx.doi.org/10.1007/0-306-46830-1_4 DB - PRIME DP - Unbound Medicine ER -