Effects of postweaning calorie restriction on accelerated growth and adiponectin in nutritionally programmed microswine offspring.
Effects of postweaning calorie restriction on accelerated growth and adiponectin in nutritionally programmed microswine offspring.
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断奶后热量限制对营养计划微型猪后代加速生长和脂联素的影响。
DOI：
10.1152/ajpregu.00162.2017
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发表时间：
2018
期刊：
影响因子：
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通讯作者：
Bagby,SusanP
中科院分区：
文献类型：
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作者：
DuPriest,ElizabethA;Lin,Baoyu;Kupfer,Philipp;Sekiguchi,Kaiu;Bhusari,Amruta;Quackenbush,Alexandra;Celebic,Almir;Morgan,TerryK;Purnell,JonathanQ;Bagby,SusanP
产前发育不良，随后是儿童期快速生长，会在以后的生活中带来更大的心脏代谢风险。围产期母体蛋白限制暴露的微型猪后代“低蛋白后代”（LPO）在胎儿晚期/新生儿阶段生长不良。断奶后，脂联素mRNA水平较低的LPO-AL表现出加速的生长和脂肪沉积速率，尽管正常体脂含量较低且腹腔内脂肪细胞较少。我们研究了热量限制（CR）对LPO和正常蛋白质后代（NPO）生长和代谢状况的影响，这些后代从断奶后随机分配到AL或CR饮食中。CR暂时降低了LPO和NPO的生长，延迟了女性LPO-CR的恢复。在7.5 ~ 12.5周，LPO-CR的线性增长率低于LPO-AL (P< 0.001)，但超过NPO-AL；与NPO-CR相比，LPO-CR组体重增长率下降，但较低。12周后线性加速度停止。16周时，与LPO-AL相比，LPO-CR的追赶率降低（P< 0.001）。LPO组血浆生长激素水平较低（P< 0.02）。CR使脂肪沉积率正常，但脂联素mRNA水平较低（P< 0.001）；脂联素在所有LPO-AL和女性LPO-CR中均较低。我们得出结论，在LPO中：1)尽管生长激素水平较低，但CR延缓了线性生长的开始，但并未消除线性生长的加速；2) CR通过延迟发作导致发育迟缓，加上线性生长加速的有限窗口；3) MPR降低脂联素mRNA，与生长、肥胖或脂肪细胞大小无关；4) MPR降低LPO-AL和女性LPO-CR的循环脂联素，可能增加心脏代谢风险。
Poor prenatal development, followed by rapid childhood growth, conveys greater cardiometabolic risk in later life. Microswine offspring exposed to perinatal maternal protein restriction [MPR; “low protein offspring” (LPO)] grow poorly in late-fetal/neonatal stages. After weaning to an ad libitum (AL) diet, LPO-AL exhibit accelerated growth and fat deposition rates with low adiponectin mRNA, despite low-normal body fat and small intra-abdominal adipocytes. We examined effects of caloric restriction (CR) on growth and metabolic status in LPO and normal protein offspring (NPO) randomized to AL or CR diets from weaning. CR transiently reduced growth in both LPO and NPO, delaying recovery in female LPO-CR. Over 7.5–12.5 weeks, linear growth rates in LPO-CR were slower than LPO-AL (P< 0.001) but exceeded NPO-AL; body weight growth rates fell but were lower in LPO-CR versus NPO-CR. Linear acceleration ceased after 12 weeks. At 16 weeks, percent catch-up in LPO-CR was reduced versus LPO-AL (P< 0.001). Plasma growth hormone was low in LPO (P< 0.02). CR normalized fat deposition rate, yet adiponectin mRNA remained low in LPO-CR (P< 0.001); plasma adiponectin was low in all LPO-AL and in female LPO-CR. Insulin sensitivity improved during CR. We conclude that in LPO:1) CR delays onset of, but does not abolish, accelerated linear growth, despite low growth hormone;2) CR yields stunting via delayed onset, plus a finite window for linear growth acceleration;3) MPR lowers adiponectin mRNA independently of growth, adiposity, or adipocyte size; and4) MPR reduces circulating adiponectin in LPO-AL and female LPO-CR, potentially enhancing cardiometabolic risk.