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产后母婴分离会改变成年大鼠对致肥胖饮食的反应。

Postnatal maternal separation modifies the response to an obesogenic diet in adulthood in rats.

机构信息

Department of Nutrition and Food Sciences, Physiology and Toxicology, University of Navarra, C/Irunlarrea 1, 31008, Pamplona, Spain.

出版信息

Dis Model Mech. 2012 Sep;5(5):691-7. doi: 10.1242/dmm.009043. Epub 2012 Jul 5.

DOI:10.1242/dmm.009043
PMID:22773756
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3424467/
Abstract

An early-life adverse environment has been implicated in the susceptibility to different diseases in adulthood, such as mental disorders, diabetes and obesity. We analyzed the effects of a high-fat sucrose (HFS) diet for 35 days in adult female rats that had experienced 180 minutes daily of maternal separation (MS) during lactancy. Changes in the obesity phenotype, biochemical profile, levels of glucocorticoid metabolism biomarkers, and the expression of different obesity- and glucocorticoid-metabolism-related genes were analyzed in periovaric adipose tissue. HFS intake increased body weight, adiposity and serum leptin levels, whereas MS decreased fat pad masses but only in rats fed an HFS diet. MS reduced insulin resistance markers but only in chow-fed rats. Corticosterone and estradiol serum levels did not change in this experimental model. A multiple gene expression analysis revealed that the expression of adiponutrin (Adpn) was increased owing to MS, and an interaction between HFS diet intake and MS was observed in the mRNA levels of leptin (Lep) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (Ppargc1a). These results revealed that early-life stress affects the response to an HFS diet later in life, and that this response can lead to phenotype and transcriptomic changes.

摘要

早期生活的不良环境与成年后患各种疾病(如精神障碍、糖尿病和肥胖症)的易感性有关。我们分析了高脂肪蔗糖(HFS)饮食对哺乳期每天接受 180 分钟母婴分离(MS)的成年雌性大鼠的影响,持续 35 天。分析了卵巢周围脂肪组织中肥胖表型、生化特征、糖皮质激素代谢生物标志物水平以及不同肥胖和糖皮质激素代谢相关基因表达的变化。HFS 摄入增加了体重、肥胖和血清瘦素水平,而 MS 降低了脂肪垫的质量,但仅在喂食 HFS 饮食的大鼠中。MS 降低了胰岛素抵抗标志物,但仅在喂食标准饮食的大鼠中。在该实验模型中,皮质酮和雌二醇血清水平没有变化。多重基因表达分析显示,由于 MS,脂联素(Adpn)的表达增加,并且在 HFS 饮食摄入和 MS 之间观察到瘦素(Lep)和过氧化物酶体增殖物激活受体γ共激活因子 1α(Ppargc1a)mRNA 水平的相互作用。这些结果表明,早期生活压力会影响成年后对 HFS 饮食的反应,并且这种反应会导致表型和转录组的变化。

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Prenatal dexamethasone exposure potentiates diet-induced hepatosteatosis and decreases plasma IGF-I in a sex-specific fashion.
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Early Life Stress, Brain Development, and Obesity Risk: Is Oxytocin the Missing Link?早期生活压力、大脑发育与肥胖风险:催产素是缺失的一环吗?
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