Division of Nutritional Sciences, Cornell University, Ithaca, NY, USA.
Adv Nutr. 2012 Jul 1;3(4):526-31. doi: 10.3945/an.112.002188.
Childhood stunting is an important and intractable public health problem that underlies ~20% of deaths among children aged <5 y in developing countries. Environmental enteropathy (EE), a subclinical condition of the small intestine characterized by reduced absorptive capacity and increased intestinal permeability, is almost universal among children in developing countries and may mediate stunting. However, the etiology of EE is poorly understood. Mycotoxins are metabolites of fungi that frequently contaminate the staple foods of children living in developing countries. We review evidence from human and animal studies that exposure to mycotoxins, particularly aflatoxin (AF), fumonisin (FUM), and deoxynivaenol (DON), may impair child growth. Although these toxins have distinct actions, they all mediate intestinal damage through: 1) inhibition of protein synthesis (AF, DON); 2) an increase in systemic proinflammatory cytokines (DON); and 3) inhibition of ceramide synthase (FUM). The intestinal pathology that arises from mycotoxin exposure is very similar to that of EE. We propose that future studies should address the role of mycotoxins in the pathogenesis of EE and evaluate interventions to limit mycotoxin exposure and reduce childhood stunting.
儿童发育迟缓是一个重要且棘手的公共卫生问题，它是发展中国家 5 岁以下儿童死亡的 20%左右的主要原因。环境肠病（EE）是一种小肠的亚临床病症，其特征是吸收能力降低和肠道通透性增加，在发展中国家几乎普遍存在于儿童中，并且可能介导发育迟缓。然而，EE 的病因尚不清楚。真菌毒素是真菌的代谢物，经常污染生活在发展中国家的儿童的主食。我们回顾了来自人类和动物研究的证据，表明接触真菌毒素，特别是黄曲霉毒素（AF）、伏马菌素（FUM）和脱氧雪腐镰刀菌烯醇（DON），可能会损害儿童的生长。尽管这些毒素具有不同的作用，但它们都通过以下方式介导肠道损伤：1）抑制蛋白质合成（AF、DON）；2）增加全身促炎细胞因子（DON）；3）抑制神经酰胺合酶（FUM）。真菌毒素暴露引起的肠道病理学与 EE 的非常相似。我们提出，未来的研究应该探讨真菌毒素在 EE 发病机制中的作用，并评估限制真菌毒素暴露和减少儿童发育迟缓的干预措施。
