Placental restriction of fetal growth increases insulin action, growth, and adiposity in the young lamb

De Blasio, Miles J., Gatford, Kathryn L., McMillen, I. Caroline, Robinson, Jeffrey S. and Owens, Julie A. 2007, Placental restriction of fetal growth increases insulin action, growth, and adiposity in the young lamb, Endocrinology, vol. 148, no. 3, pp. 1350-1358, doi: 10.1210/en.2006-0653.

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Title Placental restriction of fetal growth increases insulin action, growth, and adiposity in the young lamb
Author(s) De Blasio, Miles J.
Gatford, Kathryn L.
McMillen, I. Caroline
Robinson, Jeffrey S.
Owens, Julie A.ORCID iD for Owens, Julie A.
Journal name Endocrinology
Volume number 148
Issue number 3
Start page 1350
End page 1358
Total pages 9
Publisher Oxford University Press
Place of publication Oxford, Eng.
Publication date 2007-03
ISSN 0013-7227
Keyword(s) Adiposity
Animals, Newborn
Birth Weight
Blood Glucose
Body Size
Fetal Growth Retardation
Glucose Tolerance Test
Insulin Resistance
Pregnancy, Animal
Science & Technology
Life Sciences & Biomedicine
Endocrinology & Metabolism
Summary Most children who are short or light at birth due to intrauterine growth restriction (IUGR) exhibit accelerated growth in infancy, termed "catch-up" growth, which together with IUGR, predicts increased risk of type 2 diabetes and obesity later in life. Placental restriction (PR) in sheep reduces size at birth, and also causes catch-up growth and increased adiposity at 6 wk of age. The physiological mechanisms responsible for catch-up growth after IUGR and its links to these adverse sequelae are unknown. Because insulin is a major anabolic hormone of infancy and its actions are commonly perturbed in these related disorders, we hypothesized that restriction of fetal growth would alter insulin secretion and sensitivity in the juvenile sheep at 1 month, which would be related to their altered growth and adiposity. We show that PR impairs glucose-stimulated insulin production, but not fasting insulin abundance or production in the young sheep. However, PR increases insulin sensitivity of circulating free fatty acids (FFAs), and insulin disposition indices for glucose and FFAs. Catch-up growth is predicted by the insulin disposition indices for amino acids and FFAs, and adiposity by that for FFAs. This suggests that catch-up growth and early-onset visceral obesity after IUGR may have a common underlying cause, that of increased insulin action due primarily to enhanced insulin sensitivity, which could account in part for their links to adverse metabolic and related outcomes in later life.
Language eng
DOI 10.1210/en.2006-0653
Field of Research 07 Agricultural And Veterinary Sciences
11 Medical And Health Sciences
06 Biological Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2007, The Endocrine Society
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Document type: Journal Article
Collection: Office of the Deputy Vice-Chancellor (Research)
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