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Fetal and infant growth and impaired glucose tolerance in adulthood: the "thrifty phenotype" hypothesis revisited.
Acta Paediatr Suppl 1997; 422:73-7AP

Abstract

The epidemiological links observed between fetal and infant growth and impaired glucose tolerance in adult life that led to the formulation of the "thrifty phenotype" hypothesis have been confirmed by others in widely differing populations. The proposed nutritional basis of these links has been tested in an animal model in which rat dams were fed an isocaloric low-protein diet and the postweaning normally fed offspring were studied. Permanent changes in key hepatic enzymes of glycolysis and gluconeogenesis and reductions in both insulin and glucagon sensitivity of the liver have been observed. Glucose tolerance deteriorated more at age 15 months compared with controls but animals were not frankly diabetic. The longevity of offspring was affected positively when growth was retarded by postnatal protein restriction, but negatively when protein restriction during pregnancy was followed by cross-fostering of pups to normally fed dams with consequent "catch-up" growth. These effects were greatest in males. The thrifty phenotype hypothesis continues to provide a useful conceptual and experimental basis for the study of the aetiology of non-insulin-dependent diabetes.

Authors+Show Affiliations

Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, UK.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

9298798

Citation

Hales, C N.. "Fetal and Infant Growth and Impaired Glucose Tolerance in Adulthood: the "thrifty Phenotype" Hypothesis Revisited." Acta Paediatrica (Oslo, Norway : 1992). Supplement, vol. 422, 1997, pp. 73-7.
Hales CN. Fetal and infant growth and impaired glucose tolerance in adulthood: the "thrifty phenotype" hypothesis revisited. Acta Paediatr Suppl. 1997;422:73-7.
Hales, C. N. (1997). Fetal and infant growth and impaired glucose tolerance in adulthood: the "thrifty phenotype" hypothesis revisited. Acta Paediatrica (Oslo, Norway : 1992). Supplement, 422, pp. 73-7.
Hales CN. Fetal and Infant Growth and Impaired Glucose Tolerance in Adulthood: the "thrifty Phenotype" Hypothesis Revisited. Acta Paediatr Suppl. 1997;422:73-7. PubMed PMID: 9298798.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fetal and infant growth and impaired glucose tolerance in adulthood: the "thrifty phenotype" hypothesis revisited. A1 - Hales,C N, PY - 1997/7/1/pubmed PY - 1997/9/23/medline PY - 1997/7/1/entrez SP - 73 EP - 7 JF - Acta paediatrica (Oslo, Norway : 1992). Supplement JO - Acta Paediatr Suppl VL - 422 N2 - The epidemiological links observed between fetal and infant growth and impaired glucose tolerance in adult life that led to the formulation of the "thrifty phenotype" hypothesis have been confirmed by others in widely differing populations. The proposed nutritional basis of these links has been tested in an animal model in which rat dams were fed an isocaloric low-protein diet and the postweaning normally fed offspring were studied. Permanent changes in key hepatic enzymes of glycolysis and gluconeogenesis and reductions in both insulin and glucagon sensitivity of the liver have been observed. Glucose tolerance deteriorated more at age 15 months compared with controls but animals were not frankly diabetic. The longevity of offspring was affected positively when growth was retarded by postnatal protein restriction, but negatively when protein restriction during pregnancy was followed by cross-fostering of pups to normally fed dams with consequent "catch-up" growth. These effects were greatest in males. The thrifty phenotype hypothesis continues to provide a useful conceptual and experimental basis for the study of the aetiology of non-insulin-dependent diabetes. SN - 0803-5326 UR - https://www.unboundmedicine.com/medline/citation/9298798/Fetal_and_infant_growth_and_impaired_glucose_tolerance_in_adulthood:_the_"thrifty_phenotype"_hypothesis_revisited_ L2 - https://medlineplus.gov/diabetestype2.html DB - PRIME DP - Unbound Medicine ER -