Maternal western diet causes inflammatory milk and TLR2/4-dependent neonatal toxicity
Maternal western diet causes inflammatory milk and TLR2/4-dependent neonatal toxicity
复制标题
DOI：
10.1101/gad.191031.112
复制
发表时间：
2012-06-15
影响因子：
10.5
通讯作者：
Wan, Yihong
中科院分区：
文献类型：
--
作者：
Du, Yang;Yang, Marie;Wan, Yihong
对所有新生哺乳动物来说，母乳是完美的营养品，对它们的产后发育至关重要。在这里，我们报道，出乎意料的是，母鼠的西方饮食摄入会导致含有过量长链和饱和脂肪酸的有毒乳汁的产生，从而引发神经酰胺的积累和哺乳新生儿的炎症，表现为脱发。这种新生儿毒性需要toll样受体（TLR），而不是肠道微生物群，因为TLR2/4缺失或TLR4抑制会产生耐药性，而无菌小鼠仍然敏感。这些发现揭示了母体西方饮食诱导的炎症性乳汁分泌是母体后代界面代谢综合征的一个新方面。
For all newborn mammals, mother's milk is the perfect nourishment, crucial for their postnatal development. Here we report that, unexpectedly, maternal western diet consumption in mice causes the production of toxic milk that contains excessive long chain and saturated fatty acids, which triggers ceramide accumulation and inflammation in the nursing neonates, manifested as alopecia. This neonatal toxicity requires Toll-like-receptors (TLR), but not gut microbiota, because TLR2/4 deletion or TLR4 inhibition confers resistance, whereas germ-free mice remain sensitive. These findings unravel maternal western diet-induced inflammatory milk secretion as a novel aspect of the metabolic syndrome at the maternal offspring interface.