The rapidly increasing prevalence of type 1 diabetes (T1D) underscores the role of environmental (i.e. non-genetic) determinants of T1D development. Such factors include industrialized diets as well as the intestinal microbiota with which they interact. One component of industrialized diets that deleteriously impact gut microbiota is dietary emulsifiers, which perturb intestinal microbiota to encroach upon their host promoting chronic low-grade intestinal inflammation and metabolic syndrome. Hence, we investigated whether 2 dietary emulsifiers, carboxymethylcellulose (CMC) and polysorbate-80 (P80), might influence the development of T1D in NOD mice, which spontaneously develop this disorder. We observed that chronic emulsifier exposure accelerated T1D development in NOD mice, which was associated with increased insulin autoantibody levels. Such accelerated T1D development was accompanied by compositional and functional alterations of the intestinal microbiota as well as low-grade intestinal inflammation. Moreover, machine learning found that the severity of emulsifier-induced microbiota disruption had partial power to predict subsequent disease development, suggesting that complex interactions occur between the host, dietary factors, and the intestinal microbiota. Thus, perturbation of host–microbiota homeostasis by dietary emulsifiers may have contributed to the post-mid-20th-century increase in T1D.

1 型糖尿病 (T1D) 患病率的迅速增加凸显了环境（即非遗传）决定因素对 T1D 发展的作用。这些因素包括工业化饮食以及与之相互作用的肠道微生物群。工业化饮食中对肠道微生物群产生有害影响的成分之一是膳食乳化剂，它会扰乱肠道微生物群，侵入宿主，从而促进慢性低度肠道炎症和代谢综合征。因此，我们研究了两种膳食乳化剂：羧甲基纤维素 (CMC) 和聚山梨醇酯 80 (P80) 是否可能影响 NOD 小鼠患 T1D 的情况，而 NOD 小鼠会自发患上这种疾病。我们观察到，长期接触乳化剂会加速 NOD 小鼠 T1D 的发展，这与胰岛素自身抗体水平升高有关。这种 T1D 的加速发展伴随着肠道微生物群的组成和功能的改变以及低度肠道炎症。此外，机器学习发现，乳化剂引起的微生物群破坏的严重程度可以部分预测随后的疾病发展，这表明宿主、饮食因素和肠道微生物群之间存在复杂的相互作用。因此，膳食乳化剂对宿主-微生物群稳态的扰动可能导致了 20 世纪中叶后 T1D 发病率的增加。