Maternal docosahexaenoic acid increases adiponectin and normalizes IUGR-induced changes in rat adipose deposition.
Maternal docosahexaenoic acid increases adiponectin and normalizes IUGR-induced changes in rat adipose deposition.
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DOI：
10.1155/2013/312153
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发表时间：
2013
影响因子：
3.3
通讯作者：
Joss-Moore LA
中科院分区：
文献类型：
--
作者：
Bagley HN;Wang Y;Campbell MS;Yu X;Lane RH;Joss-Moore LA
宫内生长受限（IUGR）易导致肥胖和脂肪功能障碍。我们先前证明了在肥胖发生之前，IUGR诱导雄性青春期大鼠内脏脂肪沉积增加和过氧化物酶体增殖物激活受体γ2（PPARγ2）表达失调。在其他研究中，激活PPARγ可增加皮下脂联素表达并使内脏脂肪沉积正常化。我们假设母亲补充二十二碳六烯酸（DHA），一种过氧化物酶体增殖物激活受体γ激动剂，将使IUGR脂肪沉积正常化，并增加皮下脂肪中的过氧化物酶体增殖物激活受体γ、脂联素和脂联素受体表达。为了验证这些假设，我们使用了一个特征良好的模型，子宫胎盘功能不全（UPI-）诱导IUGR的大鼠与母亲的DHA补充。我们的主要发现是，在大鼠妊娠期和哺乳期补充母亲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，以及前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，母亲补充DHA可以使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。
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-γ2 (PPARγ2) in male adolescent rats, prior to the onset of obesity. In other studies, activation of PPARγ increases subcutaneous adiponectin expression and normalizes visceral adipose deposition. We hypothesized that maternal supplementation with docosahexaenoic acid (DHA), a PPARγ agonist, would normalize IUGR adipose deposition in association with increased PPARγ, 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 PPARγ 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.