Bagley Heidi N, Wang Yan, Campbell Michael S, Yu Xing, Lane Robert H, Joss-Moore Lisa A
Division of Nutrition, University of Utah, Salt Lake City, UT 84158, USA.
J Obes. 2013;2013:312153. doi: 10.1155/2013/312153. Epub 2013 Mar 6.
Intrauterine growth restriction (IUGR) predisposes to obesity and adipose dysfunction. We previously demonstrated IUGR-induced increased visceral adipose deposition and dysregulated expression of peroxisome proliferator activated receptor- γ 2 (PPAR γ 2) in male adolescent rats, prior to the onset of obesity. In other studies, activation of PPAR γ increases subcutaneous adiponectin expression and normalizes visceral adipose deposition. We hypothesized that maternal supplementation with docosahexaenoic acid (DHA), a PPAR γ agonist, would normalize IUGR adipose deposition in association with increased PPAR γ , adiponectin, and adiponectin receptor expression in subcutaneous adipose. To test these hypotheses, we used a well-characterized model of uteroplacental-insufficiency-(UPI-) induced IUGR in the rat with maternal DHA supplementation. Our primary findings were that maternal DHA supplementation during rat pregnancy and lactation (1) normalizes IUGR-induced changes in adipose deposition and visceral PPAR γ expression in male rats and (2) increases serum adiponectin, as well as adipose expression of adiponectin and adiponectin receptors in former IUGR rats. Our novel findings suggest that maternal DHA supplementation may normalize adipose dysfunction and promote adiponectin-induced improvements in metabolic function in IUGR.
宫内生长受限（IUGR）易导致肥胖和脂肪功能障碍。我们之前证明，在肥胖症发作之前，IUGR会导致雄性青春期大鼠内脏脂肪沉积增加以及过氧化物酶体增殖物激活受体γ2（PPARγ2）的表达失调。在其他研究中，PPARγ的激活会增加皮下脂联素的表达，并使内脏脂肪沉积正常化。我们假设，母体补充二十二碳六烯酸（DHA）（一种PPARγ激动剂）会使IUGR脂肪沉积正常化，同时皮下脂肪中PPARγ、脂联素和脂联素受体的表达增加。为了验证这些假设，我们使用了一种经过充分表征的大鼠子宫胎盘功能不全（UPI）诱导的IUGR模型，并对母体补充DHA。我们的主要发现是，在大鼠妊娠和哺乳期补充母体DHA：（1）使IUGR诱导的雄性大鼠脂肪沉积和内脏PPARγ表达的变化正常化；（2）增加血清脂联素，以及 former IUGR大鼠脂肪中脂联素和脂联素受体的表达。我们的新发现表明，母体补充DHA可能使IUGR的脂肪功能障碍正常化，并促进脂联素诱导的IUGR代谢功能改善。
