Uteroplacental insufficiency increases visceral adiposity and visceral adipose PPARgamma2 expression in male rat offspring prior to the onset of obesity.

Uteroplacental insufficiency increases visceral adiposity and visceral adipose PPARgamma2 expression in male rat offspring prior to the onset of obesity.
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DOI:
10.1016/j.earlhumdev.2010.02.006
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发表时间:
2010-03
影响因子:
2.5
通讯作者:
Lane, Robert H.
Lane, Robert H.
中科院分区:
医学4区
文献类型:
--
作者:
Joss-Moore, Lisa A.;Wang, Yan;Campbell, Michael S.;Moore, Barry;Yu, Xing;Callaway, Christopher W.;McKnight, Robert A.;Desai, Mina;Moyer-Mileur, Laurie J.;Lane, Robert H.

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子宫胎盘功能不全(UPI)引起的宫内生长受限(IUGR)使个体易于发生成人发病的代谢性疾病,包括胰岛素抵抗和心血管疾病。这些疾病发展的潜在组成部分是脂肪功能障碍;特别是不成比例的丰富内脏脂肪组织。我们推测IUGR会增加大鼠内脏脂肪和内脏脂肪生成的关键调节因子--过氧化物酶体增殖物激活受体γ的表达。为了验证这一假设,我们采用了一个充分描述的UPI诱导的IUGR大鼠模型。皮下和内脏脂肪水平测定青春期对照组和IUGR大鼠使用MRI。检测新生大鼠、青春期大鼠和成年大鼠的PPARγ mRNA和蛋白表达以及PPARγ靶基因的表达。UPI诱导的IUGR增加了雄性(而非雌性)青春期大鼠内脏脂肪组织的相对量,同时增加了雄性内脏脂肪组织中的PPARγ 2 mRNA和蛋白。重要的是,这些影响在明显肥胖症发作之前就已观察到。我们的结论是,增加PPARγ2表达的增值税的IUGR男性与增加内脏脂肪。我们推测,内脏肥胖的增加可能有助于该人群经历的代谢发病率。
Uteroplacental insufficiency (UPI) induced intrauterine growth restriction (IUGR) predisposes individuals to adult onset metabolic morbidities, including insulin resistance and cardiovascular disease. An underlying component of the development of these morbidities is adipose dysfunction; specifically a disproportionately abundant visceral adipose tissue. We hypothesize that IUGR will increase rats visceral adiposity and visceral expression of PPARγ, a key regulator of adipogenesis. To test this hypothesis we employed a well described UPI induced IUGR rat model. Subcutaneous and visceral adipose levels were measured in adolescent control and IUGR rats using MRI. Expression of PPARγ mRNA and protein, as well as PPARγ target genes, was measured in neonatal, adolescent and adult rats. UPI induced IUGR increases the relative amount of visceral adipose tissue in male, but not female, adolescent rats in conjunction with an increase in PPARγ2mRNA and protein in male visceral adipose. Importantly, these effects are seen prior to the onset of overt obesity. We conclude that increased PPARγ2 expression in VAT of IUGR males is associated with increased visceral adiposity. We speculate that the increase in visceral adiposity may contribute to the metabolic morbidities experienced by this population.
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