Impact of embryo donor adiposity, birthweight and gender on early postnatal growth, glucose metabolism and body composition in the young lamb

Jacqueline M Wallace, John S Milne, Raymond P Aitken, Clare L Adam

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8 Citations (Scopus)

Abstract

Intrauterine growth restriction (IUGR) is a risk factor for metabolic syndrome, notably when associated with rapid postnatal catch-up growth. A sheep paradigm was used to assess relationships between prenatal and early postnatal growth trajectories, metabolism and body composition. Singletons (single-sire embryo transfer from obese and control donors) were gestated and suckled by overnourished adolescent dams and categorised by birthweight as IUGR or normal (N). Gestation length was equivalent in both categories and all lambs were delivered spontaneously preterm (PT; mean (± s.e.m.) 139.8 ± 1.7 days; term = 145–147 days). The IUGR lambs were smaller at birth, but fractional growth rates (FGR) for eight anthropometry parameters were higher and independent of gender (except thorax girth; males (M) < females (F)). At Day 48, fasting glucose (IUGR > N; M > F) and first-phase insulin response (to 20 min; IUGR < N; M < F) after glucose were influenced by prenatal growth and gender. Embryo donor adiposity influenced glucose tolerance only. Plasma insulin, insulin-like growth factor-1 (M > F) and leptin (M < F) were influenced by gender but not prenatal growth. At necropsy (Day 77), IUGR plus PT lambs had decreased carcass and visceral organ weights, but carcass composition was not different from N plus PT. In contrast, M were heavier, with lower internal fat mass, carcass fat percentage and perirenal fat leptin mRNA than F. Therefore, IUGR was associated with increased postnatal FGR and altered glucose handling, but, without absolute catch-up growth, gender had the predominant influence on postnatal leptinaemia and adiposity.
Original languageEnglish
Pages (from-to)665-681
Number of pages17
JournalReproduction, Fertility and Development
Volume26
Issue number5
Early online date29 May 2013
DOIs
Publication statusPublished - Jun 2014

Fingerprint

Adiposity
adiposity
Body Composition
birth weight
body composition
embryo (animal)
lambs
Embryonic Structures
compensatory growth
Tissue Donors
leptin
Glucose
glucose
metabolism
gender
lipids
Growth
prenatal development
metabolic syndrome
carcass composition

Keywords

  • glucose tolerance
  • insulin
  • insulin-like growth factor-1
  • leptin
  • metabolic syndrome

Cite this

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title = "Impact of embryo donor adiposity, birthweight and gender on early postnatal growth, glucose metabolism and body composition in the young lamb",
abstract = "Intrauterine growth restriction (IUGR) is a risk factor for metabolic syndrome, notably when associated with rapid postnatal catch-up growth. A sheep paradigm was used to assess relationships between prenatal and early postnatal growth trajectories, metabolism and body composition. Singletons (single-sire embryo transfer from obese and control donors) were gestated and suckled by overnourished adolescent dams and categorised by birthweight as IUGR or normal (N). Gestation length was equivalent in both categories and all lambs were delivered spontaneously preterm (PT; mean (± s.e.m.) 139.8 ± 1.7 days; term = 145–147 days). The IUGR lambs were smaller at birth, but fractional growth rates (FGR) for eight anthropometry parameters were higher and independent of gender (except thorax girth; males (M) < females (F)). At Day 48, fasting glucose (IUGR > N; M > F) and first-phase insulin response (to 20 min; IUGR < N; M < F) after glucose were influenced by prenatal growth and gender. Embryo donor adiposity influenced glucose tolerance only. Plasma insulin, insulin-like growth factor-1 (M > F) and leptin (M < F) were influenced by gender but not prenatal growth. At necropsy (Day 77), IUGR plus PT lambs had decreased carcass and visceral organ weights, but carcass composition was not different from N plus PT. In contrast, M were heavier, with lower internal fat mass, carcass fat percentage and perirenal fat leptin mRNA than F. Therefore, IUGR was associated with increased postnatal FGR and altered glucose handling, but, without absolute catch-up growth, gender had the predominant influence on postnatal leptinaemia and adiposity.",
keywords = "glucose tolerance, insulin, insulin-like growth factor-1 , leptin, metabolic syndrome",
author = "Wallace, {Jacqueline M} and Milne, {John S} and Aitken, {Raymond P} and Adam, {Clare L}",
year = "2014",
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T1 - Impact of embryo donor adiposity, birthweight and gender on early postnatal growth, glucose metabolism and body composition in the young lamb

AU - Wallace, Jacqueline M

AU - Milne, John S

AU - Aitken, Raymond P

AU - Adam, Clare L

PY - 2014/6

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N2 - Intrauterine growth restriction (IUGR) is a risk factor for metabolic syndrome, notably when associated with rapid postnatal catch-up growth. A sheep paradigm was used to assess relationships between prenatal and early postnatal growth trajectories, metabolism and body composition. Singletons (single-sire embryo transfer from obese and control donors) were gestated and suckled by overnourished adolescent dams and categorised by birthweight as IUGR or normal (N). Gestation length was equivalent in both categories and all lambs were delivered spontaneously preterm (PT; mean (± s.e.m.) 139.8 ± 1.7 days; term = 145–147 days). The IUGR lambs were smaller at birth, but fractional growth rates (FGR) for eight anthropometry parameters were higher and independent of gender (except thorax girth; males (M) < females (F)). At Day 48, fasting glucose (IUGR > N; M > F) and first-phase insulin response (to 20 min; IUGR < N; M < F) after glucose were influenced by prenatal growth and gender. Embryo donor adiposity influenced glucose tolerance only. Plasma insulin, insulin-like growth factor-1 (M > F) and leptin (M < F) were influenced by gender but not prenatal growth. At necropsy (Day 77), IUGR plus PT lambs had decreased carcass and visceral organ weights, but carcass composition was not different from N plus PT. In contrast, M were heavier, with lower internal fat mass, carcass fat percentage and perirenal fat leptin mRNA than F. Therefore, IUGR was associated with increased postnatal FGR and altered glucose handling, but, without absolute catch-up growth, gender had the predominant influence on postnatal leptinaemia and adiposity.

AB - Intrauterine growth restriction (IUGR) is a risk factor for metabolic syndrome, notably when associated with rapid postnatal catch-up growth. A sheep paradigm was used to assess relationships between prenatal and early postnatal growth trajectories, metabolism and body composition. Singletons (single-sire embryo transfer from obese and control donors) were gestated and suckled by overnourished adolescent dams and categorised by birthweight as IUGR or normal (N). Gestation length was equivalent in both categories and all lambs were delivered spontaneously preterm (PT; mean (± s.e.m.) 139.8 ± 1.7 days; term = 145–147 days). The IUGR lambs were smaller at birth, but fractional growth rates (FGR) for eight anthropometry parameters were higher and independent of gender (except thorax girth; males (M) < females (F)). At Day 48, fasting glucose (IUGR > N; M > F) and first-phase insulin response (to 20 min; IUGR < N; M < F) after glucose were influenced by prenatal growth and gender. Embryo donor adiposity influenced glucose tolerance only. Plasma insulin, insulin-like growth factor-1 (M > F) and leptin (M < F) were influenced by gender but not prenatal growth. At necropsy (Day 77), IUGR plus PT lambs had decreased carcass and visceral organ weights, but carcass composition was not different from N plus PT. In contrast, M were heavier, with lower internal fat mass, carcass fat percentage and perirenal fat leptin mRNA than F. Therefore, IUGR was associated with increased postnatal FGR and altered glucose handling, but, without absolute catch-up growth, gender had the predominant influence on postnatal leptinaemia and adiposity.

KW - glucose tolerance

KW - insulin

KW - insulin-like growth factor-1

KW - leptin

KW - metabolic syndrome

U2 - 10.1071/RD13090

DO - 10.1071/RD13090

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VL - 26

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JO - Reproduction, Fertility and Development

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SN - 1031-3613

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ER -