Avoiding Cesarean-induced Obesity Through Hormone Rescue

项目总结/摘要 通过剖腹产（CS）分娩现在约占美国所有分娩的三分之一。 CS分娩后，新生儿的几种“出生信号激素”水平较低，如催产素， 加压素和皮质类固醇。出生是这些激素信号的敏感时期，所以 它们在出生时水平的变化会影响它们在整个发育过程中的调节。除了参与 出生后，这些激素也调节以后的新陈代谢行为。我们假设这就是为什么 CS与儿童肥胖症的高发病率有关。我们已经开始探索 利用草原田鼠（Microtus）研究生育方式与随后代谢调节之间的联系 赭色胃）。草原田鼠是为数不多的啮齿动物模型之一， 潜在的能量调节，而不受传统的室内空调带来的慢性冷应激的影响。 温度外壳。我们最近的研究结果表明，通过CS分娩的草原田鼠在 他们的体温调节、社会行为和代谢调节足以产生增加的体重增加 跨越发展。在本研究中，我们将进一步调查这一点，以评估是否田鼠交付的 CS是在增加内脏肥胖的风险-在人类肥胖的最危险的方面之一。我们 将充分表征受试者的能量预算以及大脑功能，代谢的基础， 从解剖学、连接性和生育信号激素的调节方面来说。最后，我们测试是否 取代CS新生儿中缺失的激素激增可以避免通常在 CS分娩的儿童和田鼠。在这样做的时候，我们希望提供一个简单，直接，和成本效益 减少这一人群儿童肥胖症的战略。我们假设CS分娩代表分娩 如果没有出生信号激素的完整补充， 神经内分泌学和新陈代谢在整个发展。

Project Summary / Abstract Delivery via cesarean section (CS) now makes up roughly one third of all births in the United States. After CS delivery, newborns experience lower levels of several ‘birth signaling hormones’ such as oxytocin, vasopressin, and corticosteroids. Birth is a sensitive period for the signaling of these hormones, and so changes in their levels at birth can affect their regulation throughout development. Besides being involved in birth, these same hormones also regulate metabolism behavior in later life. We hypothesize this is why delivery by CS is associated with substantially higher rates of childhood obesity. We have begun to explore the connections between birth mode and subsequent metabolic regulation using the prairie vole (Microtus ochrogaster). The prairie vole is one of the few rodent models that allows us to examine the physiology underlying energy regulation without the burden of chronic cold stress brought on by conventional, room temperature housing. Our recent findings suggest that prairie voles delivered via CS experience changes in their thermoregulation, social behavior, and metabolic regulation sufficient to produce increased weight gain across development. In the present study, we will investigate this further to assess whether voles delivered by CS are at increased risk for visceral adiposity -one of the most dangerous aspects of obesity in humans. We will fully characterize subjects’ energy budgets as well as the brain functioning that underlies metabolism in terms of anatomy, connectivity and the regulation of the birth signaling hormones. Finally, we test whether replacing the missing hormone surge in CS newborns can avoid the metabolic outcomes typically seen in children and voles delivered by CS. In so doing, we hope to offer a simple, straightforward, and cost-effective strategy to reduce childhood obesity in this population. We hypothesize that a CS delivery represents delivery without the full complement of birth signaling hormones and as such will result differences in neuroendocrinology and metabolism throughout development.