Centre for Neuroscience, Surgery and Trauma, Blizard Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, London E1 2AT, UK.
Division of Gastroenterology and Hepatology, Department of Internal Medicine, School for Nutrition and Translational Research in Metabolism, Maastricht University Medical Centre, 6229 Maastricht, The Netherlands.
Nutrients. 2021 Apr 13;13(4):1271. doi: 10.3390/nu13041271.
Receptors located on enteroendocrine cells (EECs) of the colon can detect nutrients in the lumen. These receptors regulate appetite through a variety of mechanisms, including hormonal and neuronal signals. We assessed the effect of obesity on the expression of these G-protein coupled receptors (GPCRs) and hormones at both mRNA and protein level.
qPCR and immunohistochemistry were used to examine colonic tissue from cohorts of patients from the Netherlands (proximal and sigmoid tissue) and the United Kingdom (tissue from across the colon) and patients were grouped by body mass index (BMI) value (BMI < 25 and BMI ≥ 25).
The mRNA expression of the hormones/signaling molecules serotonin, glucagon, peptide YY (PYY), CCK and somatostatin were not significantly different between BMI groups. GPR40 mRNA expression was significantly increased in sigmoid colon samples in the BMI ≥ 25 group, but not proximal colon. GPR41, GPR109a, GPR43, GPR120, GPRC6A, and CaSR mRNA expression were unaltered between low and high BMI. At the protein level, serotonin and PYY containing cell numbers were similar in high and low BMI groups. Enterochromaffin cells (EC) showed high degree of co-expression with amino acid sensing receptor, CaSR while co-expression with PYY containing L-cells was limited, regardless of BMI.
While expression of medium/long chain fatty acid receptor GPR40 was increased in the sigmoid colon of the high BMI group, expression of other nutrient sensing GPCRs, and expression profiles of EECs involved in peripheral mechanisms of appetite regulation were unchanged. Collectively, these data suggest that in human colonic tissue, EEC and nutrient-sensing receptor expression profiles are not affected despite changes to BMI.
位于结肠肠内分泌细胞（EEC）上的受体可以检测腔道中的营养素。这些受体通过多种机制调节食欲，包括激素和神经元信号。我们评估了肥胖对这些 G 蛋白偶联受体（GPCR）和激素在 mRNA 和蛋白水平上的表达的影响。
使用 qPCR 和免疫组织化学方法检查了来自荷兰（近端和乙状结肠组织）和英国（整个结肠的组织）患者队列的结肠组织，患者按体重指数（BMI）值分组（BMI<25 和 BMI≥25）。
在 BMI 组之间，激素/信号分子 5-羟色胺、胰高血糖素、肽 YY（PYY）、胆囊收缩素和生长抑素的 mRNA 表达没有显著差异。GPR40mRNA 表达在 BMI≥25 组的乙状结肠样本中显著增加，但在近端结肠中没有。GPR41、GPR109a、GPR43、GPR120、GPRC6A 和 CaSR 的 mRNA 表达在低和高 BMI 之间没有改变。在蛋白水平上，高和低 BMI 组之间 5-羟色胺和 PYY 含量细胞的数量相似。肠嗜铬细胞（EC）与氨基酸感应受体 CaSR 的共表达程度较高，而与 PYY 含量 L 细胞的共表达程度有限，无论 BMI 如何。
虽然中/长链脂肪酸受体 GPR40 在高 BMI 组的乙状结肠中表达增加，但其他营养感应 GPCR 的表达谱以及参与外周食欲调节机制的 EEC 的表达谱没有改变。总的来说，这些数据表明，尽管 BMI 发生了变化，但人类结肠组织中 EEC 和营养感应受体的表达谱不受影响。
