流行病學研究顯示，暴露於細懸浮微粒會導致胰島素阻抗或第二型糖尿病之患病率上升，最近有研究指出半乳糖凝集素-3會直接與胰島素受體做結合，進而導致胰島素阻抗。本研究探討亞慢性呼吸暴露超細微碳黑對胰島素阻抗發生的影響，及Gal-3所可能扮演的角色。
健康雄性Wistar大鼠呼吸暴露電腦程式控制產生的超細微碳黑，數目濃度60萬(顆/立方公分)，6小時/天，5天/週，連續暴露10週或13週，於暴露後24小時犧牲，測量禁食後血糖與胰島素濃度，進行葡萄糖耐受性測試。以H&E染色觀察骨骼肌與脂肪的病理變化，進行CD68與半乳糖凝集素-3的免疫化學染色。以西式墨點法測定骨骼肌與脂肪組織中半乳糖凝集素-3、p-Akt及Akt的表現量。
結果顯示吸入超細微碳黑顆粒10週其禁食血糖無顯著變化，然而禁食胰島素濃度雖有上升之趨勢，但無統計上的差異。而在西式墨點發分析中發現吸入超細微碳黑後會使副睪白色脂肪與骨骼肌組織的半乳糖凝集素-3蛋白表現量增加，以及副睪白色脂肪組織p-Akt/Akt下降。13週呼吸暴露研究顯示，H&E染色中看到吸入超細微碳黑後的骨骼肌橫紋模糊，組織模糊之處常伴隨著脂肪細胞的浸潤，IHC染色發現巨噬細胞包圍脂肪細胞且呈現皇冠形狀，皇冠形狀之巨噬細胞也同時表現半乳糖凝集素-3，西式墨點實驗結果顯示脂肪組織的半乳糖凝集素-3之蛋白表現量也有顯著增加。而在13週白色脂肪與骨骼肌其p-Akt/Akt在吸入超細微碳黑後程度皆顯著下降。
經亞慢性呼吸暴露後，禁食胰島素有上升之趨勢，西式墨點實驗可看出半乳糖凝集素-3的上升，以及p-Akt/Akt的下降。因此，吸入超細微碳黑導致組織發炎及與胰島素阻抗發生相關因子表現的改變，可能會導致日後血糖利用異常。未來將進一步研究乳糖凝集素-3與超細微碳黑暴露造成之胰島素阻抗的關聯。

The purpose of this study is to investigate whether subchronic inhalation exposure to nanoparticles would cause insulin resistance in rats. Healthy Wistar rats were exposed to ufCB at the concentration of 600,000 #/cm3, 6 hour/day, 5 days/week for 10 or 13 consecutive weeks using a computerized nose-only inhalation system. The results show that there was no significant change in blood sugar, but there was an increase trend but no stain fasting insulin after 10 or 13 weeks exposure. However, the expression of Gal-3 was significantly increase and p-Akt/Akt was significantly decrease in eWAT after 10 weeks exposure. Histopathological examination of skeletal muscle showed the loss of the cross striation in ufCB group, and we also found that there were Gal-3+ crown-like structures in eWAT of ufCB and HFD groups. Thus, our results demonstrated that subchronic exposure to ufCB may induce tissue inflammation and Gal-3 might play a key role in the future development of insulin resistance.

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