Postnatal Stress Produces Hyperglycemia in Adult Rats Exposed to Hypoxia-Ischemia
Postnatal Stress Produces Hyperglycemia in Adult Rats Exposed to Hypoxia-Ischemia
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DOI：
10.1203/pdr.0b013e3181b1bd1b
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发表时间：
2009-09-01
影响因子：
3.6
通讯作者：
Juul, Sandra E.
中科院分区：
文献类型：
--
作者：
McPherson, Ronald J.;Mascher-Denen, Marcella;Juul, Sandra E.
胎儿或出生后早期应激源可能使婴儿易患糖尿病、代谢综合征或中风。我们假设，出生后应激将使动物容易发展为代谢综合征，并损害对缺氧缺血性脑损伤的生理反应。我们通过检测新生大鼠和成年大鼠暴露于缺氧缺血(H-I)中的皮质酮(CS)、葡萄糖代谢和脑损伤来表征出生后应激的短期和长期生理反应。从出生后第3天至第7天，将大鼠幼鼠分为三个水平的出生后应激。所有大鼠均于P7或P134进行单侧脑损伤。观察缺氧前后的脑损伤、生长发育、血压、尿/血浆CS、血浆瘦素、胰岛素和血糖。出生后应激增加了新生儿CS的产生，加重了新生儿脑白质损伤，并与成人H-I后的高血糖有关，尽管胰岛素的产生增加了。在成人体重、血压或瘦素方面没有组间差异。出生后应激加剧了脑损伤并导致成人高血糖，在低氧暴露后触发，这与早期暴露于低氧的新生儿更容易受到缺氧的假设一致，并可能在成年后容易发展为代谢综合征。与每天短暂的处理相比，长时间的母体分离会产生更多的高血糖。(儿科研究66：278-282,2009)
Fetal or early postnatal stressors may predispose infants to develop diabetes, metabolic syndrome, or stroke. We hypothesized that postnatal stress will predispose animals to develop metabolic syndrome and impair the physiologic response to hypoxic-ischemic brain injury. We characterized the short- and long-term physiologic responses to postnatal stress by examining corticosterone (CS), glucose metabolism, and brain injury in neonatal and adult rats exposed to hypoxia-ischemia (H-I). Rat pups were divided into three levels of postnatal stress from postnatal day (P) 3 to P7. All rats underwent unilateral brain injury on either P7 or P134. We measured brain injury, growth, blood pressure, urine/plasma CS, plasma leptin, insulin, and glucose before and after H-I. Postnatal stress increased neonatal CS production, exacerbated neonatal white matter injury, and was associated with adult hyperglycemia after H-I despite increased insulin production. There were no group differences in adult weight, blood pressure, or leptin. Postnatal stress exacerbated brain injury and produced adult hyperglycemia, triggered after hypoxia exposure, consistent with the hypotheses that neonates exposed to early stress are more vulnerable to hypoxia and may be predisposed to develop metabolic syndrome in adulthood. Prolonged maternal separation produced more hyperglycemia than did brief daily handling. (Pediatr Res 66: 278-282, 2009)