De Blasio Miles J, Gatford Kathryn L, Robinson Jeffrey S, Owens Julie A
Discipline of Obstetrics and Gynaecology, School of Paediatric and Reproductive Health, University of Adelaide, Adelaide, SA 5005, Australia.
Am J Physiol Regul Integr Comp Physiol. 2007 Feb;292(2):R875-86. doi: 10.1152/ajpregu.00430.2006. Epub 2006 Oct 5.
Intrauterine growth restriction (IUGR) is associated with accelerated growth after birth. Together, IUGR and accelerated growth after birth predict reduced lean tissue mass and increased obesity in later life. Although placental insufficiency is a major cause of IUGR, whether it alters growth and adiposity in early postnatal life is not known. We hypothesized that placental restriction (PR) in the sheep would reduce size at birth and increase postnatal growth rate, fat mass, and feeding activity in the young lamb. PR reduced survival rate and size at birth, with soft tissues reduced to a greater extent than skeletal tissues and relative sparing of head width (P < 0.05 for all). PR did not alter absolute growth rates (i.e., the slope of the line of best fit for age vs. parameter size from birth to 45 days of age) but increased neonatal fractional growth rates (absolute growth rate relative to size at birth) for body weight (+24%), tibia (+15%) and metatarsal (+18%) lengths, hindlimb (+23%) and abdominal (+19%) circumferences, and fractional growth rates for current weight (P < 0.05) weekly throughout the first 45 days of life. PR and small size at birth reduced individual skeletal muscle weights and increased visceral adiposity in absolute and relative terms. PR also altered feeding activity, which increased with decreasing size at birth and was predictive of increased postnatal growth and adiposity. In conclusion, PR reduced size at birth and induced catch-up growth postnatally, normalizing weight and length but increasing adiposity in early postnatal life. Increased feeding activity may contribute to these alterations in growth and body composition following prenatal restraint and, if they persist, may lead to adverse metabolic and cardiovascular outcomes in later life.
宫内生长受限（IUGR）与出生后生长加速有关。IUGR和出生后生长加速共同预示着后期生活中瘦组织质量减少和肥胖增加。尽管胎盘功能不全是IUGR的主要原因，但它是否会改变出生后早期的生长和肥胖尚不清楚。我们假设，绵羊的胎盘限制（PR）会降低出生时的体型，并提高幼羊的出生后生长速率、脂肪量和摄食活动。PR降低了存活率和出生时的体型，软组织的减少程度大于骨骼组织，且头部宽度相对保留（所有P<0.05）。PR没有改变绝对生长速率（即从出生到45日龄年龄与参数大小的最佳拟合线的斜率），但提高了体重（+24%）、胫骨（+15%）和跖骨（+18%）长度、后肢（+23%）和腹部（+19%）周长的新生儿生长分数率（相对于出生时大小的绝对生长速率），以及生命最初45天内每周当前体重的生长分数率（P<0.05）。PR和出生时的小体型降低了个体骨骼肌重量，并绝对和相对地增加了内脏脂肪量。PR还改变了摄食活动，摄食活动随着出生时体型的减小而增加，并预示着出生后生长和肥胖的增加。总之，PR降低了出生时的体型并诱导了出生后的追赶生长，使体重和长度正常化，但增加了出生后早期的肥胖。摄食活动增加可能导致产前受限后生长和身体成分的这些改变，如果这些改变持续存在，可能会导致后期生活中不良的代谢和心血管结局。
