Neonatal Nutrition and Gastroenterology Program, Department of Pediatrics, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 2T9, Canada.
Nutrition Services, Alberta Health Services, Calgary, AB T2N 2T9, Canada.
Nutrients. 2021 Dec 29;14(1):145. doi: 10.3390/nu14010145.
Necrotizing enterocolitis (NEC) is a significant cause of mortality and morbidity in preterm infants. The pathogenesis of NEC is not completely understood; however, intestinal immaturity and excessive immunoreactivity of intestinal mucosa to intraluminal microbes and nutrients appear to have critical roles. Dietary fats are not only the main source of energy for preterm infants, but also exert potent effects on intestinal development, intestinal microbial colonization, immune function, and inflammatory response. Preterm infants have a relatively low capacity to digest and absorb triglyceride fat. Fat may thereby accumulate in the ileum and contribute to the development of NEC by inducing oxidative stress and inflammation. Some fat components, such as long-chain polyunsaturated fatty acids (LC-PUFAs), also exert immunomodulatory roles during the early postnatal period when the immune system is rapidly developing. LC-PUFAs may have the ability to modulate the inflammatory process of NEC, particularly when the balance between n3 and n6 LC-PUFAs derivatives is maintained. Supplementation with n3 LC-PUFAs alone may have limited effect on NEC prevention. In this review, we describe how various fatty acids play different roles in the pathogenesis of NEC in preterm infants.
坏死性小肠结肠炎（NEC）是早产儿死亡和发病的重要原因。NEC 的发病机制尚未完全阐明；然而，肠道不成熟和肠黏膜对腔内微生物和营养素的过度免疫反应似乎起着关键作用。膳食脂肪不仅是早产儿的主要能量来源，而且对肠道发育、肠道微生物定植、免疫功能和炎症反应也有很强的作用。早产儿消化和吸收甘油三酯脂肪的能力相对较低。脂肪可能因此在回肠中积累，并通过诱导氧化应激和炎症而导致 NEC 的发展。一些脂肪成分，如长链多不饱和脂肪酸（LC-PUFAs），在免疫系统迅速发育的出生后早期也具有免疫调节作用。LC-PUFAs 可能具有调节 NEC 炎症过程的能力，特别是当 n3 和 n6 LC-PUFAs 衍生物之间的平衡得以维持时。单独补充 n3 LC-PUFAs 对预防 NEC 的作用可能有限。在这篇综述中，我们描述了各种脂肪酸如何在早产儿 NEC 的发病机制中发挥不同的作用。
