【Cell 子刊】孕妇高脂肪饮食,祸及子孙三代以上
2016/06/19
一项新研究表明,孕妇高脂肪和高糖饮食容易引发子孙后代的代谢问题,尽管后代健康饮食,这种影响也会存在。相关结论于6月16日发表在《Cell Reports》杂志上。


一项新研究表明,孕妇高脂肪和高糖饮食容易引发子孙后代的代谢问题,尽管后代健康饮食,这种影响也会存在。相关结论于6月16日发表在《Cell Reports》杂志上。

尽管曾有研究将女性孕期的健康状况与后代体重链接起来,华盛顿大学医学院的一项小鼠研究首次表明即使在孕前女性肥胖导致的遗传变异也可通过血液传递至三代以上,从而增加子孙后代与肥胖相关的疾病风险,包括2型糖尿病和心脏病。

“我们的研究表明母亲肥胖会影响后代健康”,本文第一作者Kelle H. Moley医学博士表示,“这是非常重要的,因为在美国超过三分之二的孕龄妇女属于超重或肥胖”。

研究表明,母亲肥胖以及相关代谢问题可通过未受精的卵母细胞或卵子中的线粒体遗传给后代。线粒体被喻为细胞的发电厂,拥有自己的一套基因,遵循母系遗传。“我们的数据首次表明,患有代谢综合征的老鼠可将缺陷线粒体遗传至三代以上,更重要的是,我们的研究表明,卵母细胞或卵子可能携带编码整个机体线粒体功能缺陷的信息。”

从孕前六星期至哺乳期结束,研究人员给小鼠以高脂肪和高糖饮食。“这些饮食模仿了西方的饮食模式,包含60%的脂肪和20%的糖分,从根本上说,就像每天吃快餐一样”,Moley说。

对于后代小鼠,研究人员以普通饲料喂养,这些饮食包含高蛋白和低脂肪、低糖。尽管健康饮食,子代、孙代及曾孙代均出现胰岛素抵抗和其他代谢问题,研究人员还发现这些后代小鼠的肌肉和骨骼组织中出现异常的线粒体。


图片来源:Cell Reports

Moley说,“值得注意的是,对人类而言,后代的饮食方式更接近其父母,因而母体代谢综合征对后代的影响比小鼠模型更加大。”然而,仍需要更多的研究来确定低脂肪和低糖饮食加上定期运动能否扭转这种遗传代谢异常。

“在任何情况下,营养饮食都至关重要”,研究人员表示,“几十年来人们的饮食不断恶化,这在很大程度上取决于加工食品和快餐食品的快速发展。如今,我们看到了肥胖带来的危机。这项研究中,我们看到了孕妇营养不良和肥胖的倾向。”

孕妇肥胖和糖尿病,增加后代自闭症的风险

今年年初,约翰霍普金斯大学公共卫生学院的研究人员在《Pediatrics》杂志上揭示,与正常体重女性的后代相比,患有糖尿病的肥胖女性后代自闭症风险要高4倍。人们知道,肥胖和糖尿病不利于母体的机体健康,这项研究提供证据表明这些因素也影响后代大脑神经的发展。

然而,糖尿病和肥胖是如何导致后代自闭症风险增加,研究人员认为这可能源于肥胖和糖尿病会导致孕妇增加压力和机体的炎症反应,这可能会影响胎儿大脑神经的发育。

相关链接:

Pregnant women's high-fat, high-sugar diets may affect future generations

查看更多
  • The Association of Maternal Obesity and Diabetes With Autism and Other Developmental Disabilities

    BACKGROUND: Obesity and diabetes are highly prevalent among pregnant women in the United States. No study has examined the independent and combined effects of maternal prepregnancy obesity and maternal diabetes on the risk of autism spectrum disorder (ASD) in parallel with other developmental disorders (DDs). METHODS: This study is based on 2734 children (including 102 ASD cases), a subset of the Boston Birth Cohort who completed at least 1 postnatal study visit at Boston Medical Center between 1998 and 2014. Child ASD and other DDs were based on physician diagnoses as documented in electronic medical records. Risks of ASD and other DDs were compared among 6 groups defined by maternal prepregnancy obesity and diabetes status by using Cox proportional hazard regression controlling for potential confounders. RESULTS: When examined individually, maternal prepregnancy obesity and pregestational diabetes (PGDM) were each associated with risk of ASD. When examined in combination, only mothers with obesity and PGDM (hazard ratio 3.91, 95% confidence interval 1.76–8.68) and those with obesity and gestational diabetes (hazard ratio 3.04, 95% confidence interval 1.21–7.63) had a significantly increased risk of offspring ASD. Intellectual disabilities (IDs), but not other DDs, showed a similar pattern of increased risk associated with combined obesity and PGDM. This pattern of risk was mostly accounted for by cases with co-occurring ASD and ID. CONCLUSIONS: Maternal prepregnancy obesity and maternal diabetes in combination were associated with increased risk for ASD and ID. ASD with ID may be etiologically distinct from ASD without ID.

    展开 收起
  • Maternal Metabolic Syndrome Programs Mitochondrial Dysfunction via Germline Changes across Three Generations

    Maternal obesity impairs offspring health, but the responsible mechanisms are not fully established. To address this question, we fed female mice a high-fat/high-sugar diet from before conception until weaning and then followed the outcomes in the next three generations of offspring, all fed a control diet. We observed that female offspring born to obese mothers had impaired peripheral insulin signaling that was associated with mitochondrial dysfunction and altered mitochondrial dynamic and complex proteins in skeletal muscle. This mitochondrial phenotype persisted through the female germline and was passed down to the second and third generations. Our results indicate that maternal programming of metabolic disease can be passed through the female germline and that the transfer of aberrant oocyte mitochondria to subsequent generations may contribute to the increased risk for developing insulin resistance.

    展开 收起
发表评论 我在frontend\modules\comment\widgets\views\文件夹下面 test