Altered peripheral taste function in a mouse model of inflammatory bowel disease.

Altered peripheral taste function in a mouse model of inflammatory bowel disease.
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DOI:
10.1038/s41598-023-46244-3
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发表时间:
2023-11-02
期刊:
影响因子:
4.6
通讯作者:
--
中科院分区:
综合性期刊3区
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--
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据报道,炎症性肠病(IBD)患者的糖摄入量增加和味觉障碍,这是一种以腹泻、疼痛、体重减轻和疲劳为特征的慢性疾病。此前尚不清楚IBD小鼠模型的味觉功能是否发生了变化。小鼠在三个7天的周期中摄入葡聚糖硫酸钠(DSS)以诱导慢性结肠炎。DSS治疗的小鼠表现出疾病的迹象,包括显著的体重减轻、腹泻、结肠结构丧失和结肠发炎。在最后一个DSS周期后,我们通过记录鼓索(CT)神经的电生理反应来评估味觉功能,CT神经将舌头味蕾的活动传递到大脑。DSS处理显著降低了神经对天然和人工甜味剂的味觉反应。结肠炎小鼠对碳水化合物、盐、酸或苦味的反应不受影响,但鲜味反应略有升高。DSS处理调节了口腔味蕾中传递甜味和鲜味刺激的受体亚基的表达,作为功能变化的底物。慢性结肠炎期间发生的失调的全身性细胞因子反应或生物失调可能是口腔味蕾变化的上游。我们首次证明结肠炎改变了输入到大脑的味道,这可能会加剧IBD患者的营养不良。
Increased sugar intake and taste dysfunction have been reported in patients with inflammatory bowel disease (IBD), a chronic disorder characterized by diarrhea, pain, weight loss and fatigue. It was previously unknown whether taste function changes in mouse models of IBD. Mice consumed dextran sodium sulfate (DSS) during three 7-day cycles to induce chronic colitis. DSS-treated mice displayed signs of disease, including significant weight loss, diarrhea, loss of colon architecture, and inflammation of the colon. After the last DSS cycle we assessed taste function by recording electrophysiological responses from the chorda tympani (CT) nerve, which transmits activity from lingual taste buds to the brain. DSS treatment significantly reduced neural taste responses to natural and artificial sweeteners. Responses to carbohydrate, salt, sour or bitter tastants were unaffected in mice with colitis, but umami responses were modestly elevated. DSS treatment modulated the expression of receptor subunits that transduce sweet and umami stimuli in oral taste buds as a substrate for functional changes. Dysregulated systemic cytokine responses or dysbiosis that occurs during chronic colitis may be upstream from changes in oral taste buds. We demonstrate for the first time that colitis alters taste input to the brain, which could exacerbate malnutrition in IBD patients.
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