Neonatal and fetal exposure to trans-fatty acids retards early growth and adiposity while adversely affecting glucose in mice.
Neonatal and fetal exposure to trans-fatty acids retards early growth and adiposity while adversely affecting glucose in mice.
复制标题
DOI：
10.1016/j.nutres.2010.06.006
复制
发表时间：
2010-06
期刊：
影响因子：
--
通讯作者：
Rudel LL
中科院分区：
文献类型：
--
作者：
Kavanagh K;Sajadian S;Jenkins KA;Wilson MD;Carr JJ;Wagner JD;Rudel LL
西方饮食中消耗的工业生产的反式脂肪酸（TFA）被纳入母体和胎儿组织，并通过母乳线性传递给后代。我们假设，与未修饰的脂肪酸相比，婴儿在子宫内和哺乳期暴露于TFA会促进肥胖和血糖控制不良。我们进一步假设，仅在子宫内暴露可能会导致成年后的这些结果。为了验证这一假设，我们给雌性C57/BL 6小鼠喂食相同的西方饮食，这些饮食仅在C18：1的顺式或反式异构体上不同，然后旨在确定通过妊娠和哺乳期母体转移TFA是否会改变生长、身体组成和葡萄糖代谢。小鼠未暴露于TFA，在妊娠期间、哺乳期间或整个妊娠和哺乳期间暴露于TFA。我们在断奶和成年时评估了体重和组成（通过计算机断层扫描）以及葡萄糖代谢。通过母乳接触TFA会导致显著的早期生长迟缓（p<0.001）和较高的空腹血糖（p=0.01），但胰岛素敏感性没有差异。食用富含TFA的牛奶的小鼠中血浆胰岛素样生长因子-1升高（p=0.02）可能有助于在这些小鼠中观察到的后期追赶生长、消瘦和外周胰岛素敏感性保持。在子宫内暴露于TFA的小鼠在无TFA母乳的情况下经历了快速的早期新生儿生长，并且具有显著受损的胰岛素敏感性（p<0.05）和更大的腹部脂肪（p=0.01）。我们的结论是，非常早期的追赶性生长导致外周胰岛素敏感性受损，在这个模型的饮食相关的胎儿和新生儿编程。令人惊讶的是，TFA延缓了生长和肥胖，同时仍然对葡萄糖代谢产生不利影响。
Industrially produced trans fatty acids (TFAs) consumed in western diets are incorporated into maternal and fetal tissues, and are passed linearly to offspring via breast milk. We hypothesized that TFA exposure in utero and during lactation in infants would promote obesity and poor glycemic control as compared to unmodified fatty acids. We further hypothesized that in utero exposure alone may program for these outcomes in adulthood. To test this hypothesis we fed female C57/BL6 mice identical western diets that differed only in cis- or trans-isomers of C18:1 and then aimed to determine whether maternal transfer of TFAs through pregnancy and lactation alters growth, body composition and glucose metabolism. Mice were unexposed, exposed during pregnancy, during lactation, or throughout pregnancy and lactation to TFA. Body weight and composition (by computed tomography), and glucose metabolism we assessed at weaning and adulthood. TFA exposure through breast milk caused significant early growth retardation (p<0.001) and higher fasting glucose (p=0.01) but insulin sensitivity was not different. Elevated plasma insulin-like growth factor-1 in mice consuming TFA-enriched milk (p=0.02) may contribute to later catch-up growth, leanness and preserved peripheral insulin sensitivity observed in these mice. Mice exposed to TFA in utero underwent rapid early neonatal growth with TFA-free breast milk and had significantly impaired insulin sensitivity (p<0.05) and greater abdominal fat (p=0.01). We conclude that very early catch-up growth resulted in impaired peripheral insulin sensitivity in this model of diet-related fetal and neonatal programming. TFA surprisingly retarded growth and adiposity while still adversely affecting glucose metabolism.
登录
查看更多内容
DOI：
10.1038/oby.2005.48
发表时间：
2005-02-01
期刊：
OBESITY RESEARCH
影响因子：
--
作者：
Li, CY;Kaur, H;Ahluwalia, JS
通讯作者：
Ahluwalia, JS
影响因子：
7
作者：
Dunger, D. B.;Salgin, B.;Ong, K. K.
通讯作者：
Ong, K. K.
影响因子：
7.1
作者：
Mozaffarian, D;Pischon, T;Rimm, EB
通讯作者：
Rimm, EB
影响因子：
7.1
作者：
Mosley, EE;Wright, AL;McGuire, MA
通讯作者：
McGuire, MA
影响因子：
1.6
作者：
Aoki, N;Yamaguchi, Y;Matsuda, T
通讯作者：
Matsuda, T