The Correlation Between Fecal Amino Acids, Colonic Mucosal Taste Receptors, and Clinical Features and Indicators of Ulcerative Colitis: A Multicenter Exploratory Study

溃疡性结肠炎 内科学 受体 品味 胃肠病学 粪便 医学 排便 钙蛋白酶 味觉感受器 结肠炎 内分泌学 炎症性肠病 化学 生物 食品科学 疾病 微生物学
作者
Yixin Liu,Sumei Sha,Qiuju Ran,Haitao Shi,Juan Ma,Bin Qin,Yingchao Li,Ning Wang,Xin Liu,Jinhai Wang,Li Lu,Na Liu,Xiaojing Quan
出处
期刊:Inflammatory Bowel Diseases [Oxford University Press]
标识
DOI:10.1093/ibd/izae299
摘要

Abstract Background Patients with ulcerative colitis (UC) exhibit abnormal amino acid (AA) metabolism. Taste receptors play a crucial role in the detection of intestinal AAs. Nevertheless, it remains unclear whether UC patients exhibit abnormal expression of these receptors in the colon. Methods An observational, multicenter study was conducted involving adult patients with active UC and healthy controls (HCs), recruited from July 2023 to March 2024. Fresh feces and rectosigmoid mucosal tissues were obtained from each participant. The concentrations of fecal AAs and the expression of taste receptors, including calcium-sensing receptor (CaSR), G protein-coupled receptor family C group 6 member A (GPRC6A), taste receptor type 1 member 1 (T1R1), and metabotropic glutamate receptor 4 (mGLuR4), in the colon were measured. Additionally, the correlation between colonic mucosal taste receptors and clinical characteristics was evaluated. Results Except for GPRC6A, the expression levels of CaSR, mGLuR4, and T1R1 in the colonic mucosa of UC patients were significantly elevated compared to HC. The expression of CaSR was negatively correlated with C-reactive protein and erythrocyte sedimentation rate (ESR). T1R1 expression positively correlated with defecation frequency and an Improved Mayo Endoscopic Score. The total and subtype concentrations of fecal AAs were elevated in UC patients and demonstrated a negative correlation with ESR and fecal calprotectin. Conclusions The increased levels of taste receptors and fecal AAs in the colon of UC patients suggest an abnormal nutrient-sensing mechanism, potentially playing a crucial role in the development of the disease.

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