Abstract

Type 1 diabetes (T1D) is an autoimmune disorder caused by the destruction of insulin-secreting β-cells.T1D is on the rise around the world. Exposure to polycyclic aromatic hydrocarbons (PAHs) including 2-aminoanthracene (2AA) is considered a contributor to TID increase. The contribution of the ingestion of 2AA toward T1D vulnerability is examined. 2AA is found in a variety of household products. Juvenile male Sprague Dawley rats ingested various amounts of 2AA contaminated diet for 12 weeks. Results showed marginal reduction in body weight gain for the 100 mg/kg treated animals. Glucose tolerance test (GTT) indicated no changes at six weeks. However, at week 12, both treated groups had higher levels of blood glucose than the control group. Serum insulin concentration was elevated in the 50 mg/kg group while reduced in the 100 mg/kg animals. Serum lactate dehydrogenase activity was elevated in treated groups. Evaluation of pancreatic inflammatory cytokines revealed overexpression of IL-1B, IL-6, and IL-7. Apoptotic genes in the pancreas of exposed rats were overly expressed. Histopathology and insulin immunohistochemistry data showed the presence of mesenteric vessels surrounded by lymphocyte and enlarged size of islet cells respectively in the high dose group. These results suggest 2AA ingestion may enhance T1D development.

摘要

1型糖尿病（T1D）是由分泌胰岛素的β细胞破坏引起的自身免疫性疾病.T1D在世界范围内呈上升趋势。暴露于包括2-氨基蒽（2AA）的多环芳烃（PAH）被认为是TID增加的原因。研究了摄入2AA对T1D脆弱性的贡献。2AA存在于各种家用产品中。幼龄的雄性Sprague Dawley大鼠摄食了各种数量的2AA污染饮食，持续12周。结果表明，对于100 mg / kg治疗的动物，体重增加略有减少。葡萄糖耐量试验（GTT）表明六周没有变化。但是，在第12周时，两个治疗组的血糖水平均高于对照组。50 mg / kg组的血清胰岛素浓度升高，而100 mg / kg组的血清胰岛素浓度降低。治疗组血清乳酸脱氢酶活性升高。胰腺炎性细胞因子的评估显示IL-1B，IL-6和IL-7的过度表达。暴露大鼠胰腺中的凋亡基因过度表达。组织病理学和胰岛素免疫组化数据表明，高剂量组分别存在被淋巴细胞包围的肠系膜血管和胰岛细胞增大。这些结果表明，摄入2AA可能会增强T1D的发育。组织病理学和胰岛素免疫组化数据表明，高剂量组分别存在被淋巴细胞包围的肠系膜血管和胰岛细胞增大。这些结果表明，摄入2AA可能会增强T1D的发育。组织病理学和胰岛素免疫组化数据表明，高剂量组分别存在被淋巴细胞包围的肠系膜血管和胰岛细胞增大。这些结果表明，摄入2AA可能会增强T1D的发育。