|
|
||||||||
1Research Centre for Reproductive Health, Discipline of Obstetrics and Gynaecology, School of Paediatrics and Reproductive Health, and 2Discipline of Physiology, School of Molecular and Biomedical Sciences, University of Adelaide, Adelaide, South Australia, Australia
Submitted 21 December 2006 ; accepted in final form 24 February 2007
Prenatal and early postnatal life experiences, reflected by size at birth and postnatal catch-up growth, contribute to the risk of developing the metabolic syndrome in adulthood, but their relative importance is unclear. Therefore, we determined the effects of restricted placental and fetal growth on components of the metabolic syndrome in young adult sheep and the relationships of the latter to size at birth and early postnatal growth. Fasting plasma metabolites, glucose tolerance (by intravenous glucose tolerance test, IVGTT), insulin secretion and sensitivity, and resting blood pressure were measured in 22 control and 20 placentally restricted (PR) 1-yr-old sheep. In male sheep, PR increased the initial rise in glucose during an IVGTT and reduced diastolic blood pressure, and small size at birth independently predicted reduced adult size, glucose tolerance, and fasting plasma insulin and insulin disposition of glucose metabolism but increased insulin disposition of circulating FFAs. Also in males, high fractional growth rates in early postnatal life independently predicted impaired early glucose clearance during an IVGTT. In female animals, PR increased insulin sensitivity of glucose metabolism and reduced fasting plasma FFAs, and thinness at birth predicted increased adult size, fasting blood glucose, and pulse pressure. In conclusion, PR and small size at birth are associated with more components of the metabolic syndrome in adult male than in adult female sheep, with few independent effects of early postnatal growth. These sex differences in the onset and extent of adverse metabolic consequences after prenatal restraint in the sheep are consistent with observations in humans.
size at birth; insulin action; blood pressure; glucose metabolism; growth
This article has been cited by other articles:
![]() |
G. D. Wadley, A. L. Siebel, G. J. Cooney, G. K. McConell, M. E. Wlodek, and J. A. Owens Uteroplacental insufficiency and reducing litter size alters skeletal muscle mitochondrial biogenesis in a sex-specific manner in the adult rat Am J Physiol Endocrinol Metab, May 1, 2008; 294(5): E861 - E869. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. L. Hui, C. M. Schooling, S. S. L. Leung, K. H. Mak, L. M. Ho, T. H. Lam, and G. M. Leung Birth Weight, Infant Growth, and Childhood Body Mass Index: Hong Kong's Children of 1997 Birth Cohort Arch Pediatr Adolesc Med, March 1, 2008; 162(3): 212 - 218. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. S. Gilbert, E. Brandon, and T. Vera Fetal insulin secretion in late gestation: does size matter? J. Physiol., December 15, 2007; 585(3): 651 - 652. [Full Text] [PDF] |
||||
![]() |
S. W. Limesand, P. J. Rozance, D. Smith, and W. W. Hay Jr. Increased insulin sensitivity and maintenance of glucose utilization rates in fetal sheep with placental insufficiency and intrauterine growth restriction Am J Physiol Endocrinol Metab, December 1, 2007; 293(6): E1716 - E1725. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |