Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland; Unit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland.
Department of Public Health and Welfare, Finnish Institute for Health and Welfare, Helsinki, Finland; Unit of Health Sciences, Faculty of Social Sciences, Tampere University, Tampere, Finland; Tampere University Hospital, Wellbeing Services County of Pirkanmaa, Tampere, Finland.
J Nutr. 2024 Jul;154(7):2244-2254. doi: 10.1016/j.tjnut.2024.05.015. Epub 2024 May 23.
Gut dysbiosis and increased intestinal permeability have been reported to precede type 1 diabetes-related autoimmunity. The role of gut inflammation in autoimmunity is not understood.
This study aimed to assess whether gut inflammation markers are associated with risk of islet autoimmunity and whether diet is associated with gut inflammation markers.
A nested case-control sample of 75 case children with islet autoimmunity and 88 control children was acquired from the Finnish Type 1 Diabetes Prediction and Prevention cohort. Diet was assessed with 3-d food records, and calprotectin and human β-defensin-2 (HBD-2) were analyzed from stool samples at 6 and 12 mo of age. Conditional logistic regression analysis was used in a matched case-control setting to assess risk of autoimmunity. Analysis of variance, independent samples t test, and a general linear model were used in secondary analyses to test associations of background characteristics and dietary factors with inflammation markers.
In unadjusted analyses, calprotectin was not associated with risk of islet autoimmunity, whereas HBD-2 in the middle (odds ratio [OR]: 3.23; 95% confidence interval [CI]: 1.03, 10.08) or highest tertile (OR: 3.02; 95% CI: 1.05, 8.69) in comparison to the lowest at 12 mo of age showed borderline association (P-trend = 0.063) with higher risk of islet autoimmunity. Excluding children with cow milk allergy in sensitivity analyses strengthened the association of HBD-2 with islet autoimmunity, whereas adjusting for dietary factors and maternal education weakened it. At age 12 mo, higher fat intake was associated with higher HBD-2 (β: 0.219; 95% CI: 0.110, 0.328) and higher intake of dietary fiber (β: -0.294; 95% CI: -0.510, -0.078), magnesium (β: -0.036; 95% CI: -0.059, -0.014), and potassium (β: -0.003; 95% CI: -0.005, -0.001) with lower HBD-2.
Higher HBD-2 in infancy may be associated with higher risk of islet autoimmunity. Dietary factors play a role in gut inflammatory status.
据报道，肠道菌群失调和肠道通透性增加先于 1 型糖尿病相关的自身免疫。肠道炎症在自身免疫中的作用尚不清楚。
本研究旨在评估肠道炎症标志物是否与胰岛自身免疫的风险相关，以及饮食是否与肠道炎症标志物相关。
从芬兰 1 型糖尿病预测和预防队列中获取了 75 名胰岛自身免疫患儿的病例对照样本和 88 名对照儿童。通过 3 天的食物记录评估饮食情况，并在 6 和 12 个月时分析粪便样本中的钙卫蛋白和人β-防御素-2（HBD-2）。在匹配的病例对照研究中，使用条件逻辑回归分析评估自身免疫的风险。在二次分析中，使用方差分析、独立样本 t 检验和一般线性模型来测试背景特征和饮食因素与炎症标志物的关系。
在未调整的分析中，钙卫蛋白与胰岛自身免疫的风险无关，而在 12 个月时中值（比值比 [OR]：3.23；95%置信区间 [CI]：1.03，10.08）或最高三分位（OR：3.02；95%CI：1.05，8.69）与最低三分位相比，与更高的胰岛自身免疫风险呈边缘关联（P 趋势=0.063）。在敏感性分析中排除牛乳过敏的儿童后，HBD-2 与胰岛自身免疫的关联增强，而调整饮食因素和母亲教育后则减弱。在 12 个月时，较高的脂肪摄入量与较高的 HBD-2（β：0.219；95%CI：0.110，0.328）和较高的膳食纤维摄入量（β：-0.294；95%CI：-0.510，-0.078）、镁（β：-0.036；95%CI：-0.059，-0.014）和钾（β：-0.003；95%CI：-0.005，-0.001）呈负相关。
婴儿期较高的 HBD-2 可能与更高的胰岛自身免疫风险相关。饮食因素在肠道炎症状态中起作用。
