Overnourishing pregnant adolescent ewes preserves perirenal fat deposition in their growth-restricted fetuses.
Overnourishing the adolescent sheep promotes rapid maternal growth at the expense of the gravid uterus. The growth of the placenta is impaired and results in the premature delivery of low-birthweight lambs. The present study details fetal adipose tissue development in these growth-restricted pregnancies. Singleton pregnancies were established by embryo transfer and, thereafter, adolescent ewes were offered a high (H; n = 12) or moderate (M; n = 14) level of a complete diet until necropsy on Day 131 of gestation. Fetal weight was lower (P < 0.001) in H compared with M groups. High maternal intake preserved brain and perirenal fat weight (P < 0.003), whereas relative weights of the heart, lungs, spleen and liver were unaltered. High nutrient intake resulted in significantly elevated maternal plasma concentrations of insulin, leptin, prolactin and glucose, no significant changes in fetal insulin, leptin or non-esterified fatty acids and attenuated fetal prolactin concentrations. Irrespective of nutritional intake, maternal plasma leptin, prolactin and glucose concentrations were negatively correlated with fetal weight and were positively correlated with fetal perirenal fat proportion (all P < 0.01). The mRNA expression for leptin, prolactin receptor and uncoupling protein (UCP) 1 in fetal perirenal fat was equivalent between groups, but, irrespective of maternal nutrition, UCP1 mRNA levels were negatively correlated with fetal weight (P < 0.01). Thus, overnourishing pregnant adolescent sheep preserves fat deposition in their growth-restricted fetuses, which may have implications for neonatal thermogenesis and for programming of postnatal adiposity.
National Agricultural Research Center for Kyushu Okinawa Region, Nishigoshi-machi, Kumamoto 861-1192, Japan.
Masatoshi
M
Matsuzaki
John S
JS
Milne
Raymond P
RP
Aitken
Jacqueline M
JM
Wallace
D000273:Adipose Tissue / Q000196:embryology* / Q000378:metabolism; D000818:Animals; D001483:Base Sequence; D002352:Carrier Proteins / Q000235:genetics; D018076:DNA, Complementary / Q000235:genetics; D005260:Female; D047109:Fetal Development / Q000235:genetics / Q000502:physiology*; D005317:Fetal Growth Retardation / Q000235:genetics / Q000662:veterinary; D007473:Ion Channels; D007668:Kidney / Q000196:embryology; D020738:Leptin / Q000235:genetics; D008565:Membrane Proteins / Q000235:genetics; D024101:Mitochondrial Proteins; D011247:Pregnancy; D039401:Prenatal Nutritional Physiological Phenomena / Q000502:physiology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011981:Receptors, Prolactin / Q000235:genetics; D012756:Sheep / Q000502:physiology*; D000071256:Uncoupling Protein 1
D002352:Carrier Proteins; D018076:DNA, Complementary; D007473:Ion Channels; D020738:Leptin; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; D011981:Receptors, Prolactin; D000071256:Uncoupling Protein 1