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The long-term consequences of intra-uterine protein malnutrition for glucose metabolism.
Proc Nutr Soc 1999; 58(3):615-9PN

Abstract

Our initial observations, in epidemiological studies, linking indices of poor early (fetal and infant) growth to the subsequent development of poor glucose tolerance and the insulin resistance syndrome in adult life, have been confirmed in studies in a wide variety of populations around the world. These findings led us 5 years ago to propose the 'thrifty phenotype' hypothesis. Tests of this hypothesis in an animal model in which the pregnant and/or lactating rat dams are fed on an isoenergetic diet containing just under half the normal protein content are consistent with the ideas put forward. They have also allowed us to refine the hypothesis in the light of the new data as follows: (1) the growth of the fetus (and possibly infant) is quantitatively and qualitatively altered by its nutritional environment (which may include maternal diet-dependent changes in maternal hormones); (2) these changes serve to select between the growth rates of different tissues according to priorities which differ between males and females (nutritional thrift) and to alter organ function to constitute a thrifty offspring adapted to survival in poor nutritional circumstances (thrifty phenotype); (3) an individual so constituted suffers adverse consequences in adult life if he/she experiences good or supranormal nutrition; (4) both poor insulin secretion and insulin resistance can result from these adaptive processes; (5) the adverse consequences include loss of glucose tolerance and hypertension. The precise outcome of growth retardation during early life may vary according to the type and timing of the factors responsible for the retardation. It remains to be determined to what extent these potentially adverse effects can be delayed or prevented by a suitable postnatal diet. Experiments in animal models are largely consistent with the concepts proposed from human epidemiological studies. They show that the metabolism of the liver, muscle and adipose tissue may be programmed by maternal nutrition during gestation and lactation. The combination of early growth restriction and subsequent adult obesity reproduced in the rat are the main features of the insulin resistance syndrome.

Authors+Show Affiliations

Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, UK.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

10604194

Citation

Ozanne, S E., and C N. Hales. "The Long-term Consequences of Intra-uterine Protein Malnutrition for Glucose Metabolism." The Proceedings of the Nutrition Society, vol. 58, no. 3, 1999, pp. 615-9.
Ozanne SE, Hales CN. The long-term consequences of intra-uterine protein malnutrition for glucose metabolism. Proc Nutr Soc. 1999;58(3):615-9.
Ozanne, S. E., & Hales, C. N. (1999). The long-term consequences of intra-uterine protein malnutrition for glucose metabolism. The Proceedings of the Nutrition Society, 58(3), pp. 615-9.
Ozanne SE, Hales CN. The Long-term Consequences of Intra-uterine Protein Malnutrition for Glucose Metabolism. Proc Nutr Soc. 1999;58(3):615-9. PubMed PMID: 10604194.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The long-term consequences of intra-uterine protein malnutrition for glucose metabolism. AU - Ozanne,S E, AU - Hales,C N, PY - 1999/12/22/pubmed PY - 1999/12/22/medline PY - 1999/12/22/entrez SP - 615 EP - 9 JF - The Proceedings of the Nutrition Society JO - Proc Nutr Soc VL - 58 IS - 3 N2 - Our initial observations, in epidemiological studies, linking indices of poor early (fetal and infant) growth to the subsequent development of poor glucose tolerance and the insulin resistance syndrome in adult life, have been confirmed in studies in a wide variety of populations around the world. These findings led us 5 years ago to propose the 'thrifty phenotype' hypothesis. Tests of this hypothesis in an animal model in which the pregnant and/or lactating rat dams are fed on an isoenergetic diet containing just under half the normal protein content are consistent with the ideas put forward. They have also allowed us to refine the hypothesis in the light of the new data as follows: (1) the growth of the fetus (and possibly infant) is quantitatively and qualitatively altered by its nutritional environment (which may include maternal diet-dependent changes in maternal hormones); (2) these changes serve to select between the growth rates of different tissues according to priorities which differ between males and females (nutritional thrift) and to alter organ function to constitute a thrifty offspring adapted to survival in poor nutritional circumstances (thrifty phenotype); (3) an individual so constituted suffers adverse consequences in adult life if he/she experiences good or supranormal nutrition; (4) both poor insulin secretion and insulin resistance can result from these adaptive processes; (5) the adverse consequences include loss of glucose tolerance and hypertension. The precise outcome of growth retardation during early life may vary according to the type and timing of the factors responsible for the retardation. It remains to be determined to what extent these potentially adverse effects can be delayed or prevented by a suitable postnatal diet. Experiments in animal models are largely consistent with the concepts proposed from human epidemiological studies. They show that the metabolism of the liver, muscle and adipose tissue may be programmed by maternal nutrition during gestation and lactation. The combination of early growth restriction and subsequent adult obesity reproduced in the rat are the main features of the insulin resistance syndrome. SN - 0029-6651 UR - https://www.unboundmedicine.com/medline/citation/10604194/The_long_term_consequences_of_intra_uterine_protein_malnutrition_for_glucose_metabolism_ L2 - https://www.cambridge.org/core/product/identifier/S0029665199000804/type/journal_article DB - PRIME DP - Unbound Medicine ER -