Lund University Diabetes Centre, Malmö, Sweden.
Department of Clinical Pathology, Ryhov Hospital, Jönköping, Sweden.
Mol Cell Endocrinol. 2018 Nov 15;476:8-16. doi: 10.1016/j.mce.2018.04.002. Epub 2018 Apr 6.
Impaired incretin effect is a culprit in Type 2 Diabetes. Cocaine- and amphetamine-regulated transcript (CART) is a regulatory peptide controlling pancreatic islet hormone secretion and beta-cell survival. Here we studied the potential expression of CART in enteroendocrine cells and examined the role of CART as a regulator of incretin secretion and expression. CART expression was found in glucose-dependent insulinotropic polypeptide (GIP)-producing K-cells and glucagon-like peptide-1 (GLP-1)-producing L-cells in human duodenum and jejunum and circulating CART levels were increased 60 min after a meal in humans. CART expression was increased by fatty acids and GIP, but unaffected by glucose in GLUTag and STC-1 cells. Exogenous CART had no effect on GIP and GLP-1 expression and secretion in GLUTag or STC-1 cells, but siRNA-mediated silencing of CART reduced GLP-1 expression and secretion. Furthermore, acute intravenous administration of CART increased GIP and GLP-1 secretion during an oral glucose-tolerance test in mice. We conclude that CART is a novel constituent of human K- and L-cells with stimulatory actions on incretin secretion and that interfering with the CART system may be a therapeutic avenue for T2D.
肠促胰岛素效应受损是 2 型糖尿病的罪魁祸首。可卡因和安非他命调节转录物 (CART) 是一种调节肽,可控制胰岛激素分泌和β细胞存活。在这里,我们研究了 CART 在肠内分泌细胞中的潜在表达,并研究了 CART 作为肠促胰岛素分泌和表达调节剂的作用。在人类十二指肠和空肠中发现 CART 在葡萄糖依赖性胰岛素分泌多肽 (GIP) 产生的 K 细胞和胰高血糖素样肽-1 (GLP-1) 产生的 L 细胞中表达,并且在人类餐后 60 分钟循环 CART 水平增加。脂肪酸和 GIP 增加 CART 表达,但 GLUTag 和 STC-1 细胞中的葡萄糖对其无影响。外源性 CART 对 GLUTag 或 STC-1 细胞中的 GIP 和 GLP-1 表达和分泌没有影响,但 CART 的 siRNA 介导的沉默降低了 GLP-1 的表达和分泌。此外,急性静脉内给予 CART 可在小鼠口服葡萄糖耐量试验中增加 GIP 和 GLP-1 的分泌。我们的结论是,CART 是人类 K 和 L 细胞的新型组成部分,可刺激肠促胰岛素的分泌,干扰 CART 系统可能是 2 型糖尿病的一种治疗途径。