Impaired Secretion of Glucagon-Like Peptide 1 in Patients with Colorectal Adenoma after an Oral Glucose Load
Impaired Secretion of Glucagon-Like Peptide 1 in Patients with Colorectal Adenoma after an Oral Glucose Load
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口服葡萄糖负荷后结直肠腺瘤患者胰高血糖素样肽 1 的分泌受损
DOI：
10.1159/000486129
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发表时间：
2018
期刊：
影响因子：
3.2
通讯作者：
Ueno Yoshiyuki
中科院分区：
文献类型：
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作者：
Sasaki Yu;Abe Yasuhiko;Takeda Hiroaki;Nishise Shoichi;Yaoita Takao;Yagi Makoto;Sakuta Kazuhiro;Mizumoto Naoko;Shoji Masakuni;Onozato Yusuke;Kawata Sumio;Ueno Yoshiyuki
背景/目的肥胖和胰岛素抵抗与结直肠腺瘤（CRA）风险增加有关。胰高血糖素样肽-1（GLP-1）在葡萄糖稳态中起重要作用，通过其响应于口服营养素而放大胰岛素分泌;然而，其在人类CRA中的作用仍然未知。我们调查了口服葡萄糖介导的GLP-1分泌的患者adenoma.MethodsWe进行了病例对照研究的15例非糖尿病患者病理诊断CRA和10个年龄匹配的健康对照无腺瘤。在75 g口服葡萄糖耐量test.ResultsMean腰围（WC），稳态模型评估的胰岛素抵抗（HOMA-IR）值，葡萄糖和胰岛素的曲线下总面积（AUC）的血浆中活性GLP-1的浓度进行了测定与CRA患者比对照组显着较高。CRA患者的GLP-1总AUC（p= 0.01）低于对照组。此外，GLP-1的总AUC与WC、葡萄糖的总AUC和HOMA-IR呈负相关。多元线性回归分析显示，GLP-1的总AUC与CRA的数量和最大尺寸独立相关。
Background/AimsObesity and insulin resistance are associated with an increased risk of colorectal adenoma (CRA). Glucagon-like peptide-1 (GLP-1) plays an important role in glucose homeostasis through its amplification of insulin secretion in response to oral nutrients; however, its role in human CRA remains unknown. We investigated oral glucose-mediated GLP-1 secretion in patients with adenoma.MethodsWe performed a case-control study of 15 nondiabetic patients with pathologically diagnosed CRA and 10 age-matched healthy controls without adenoma. Plasma concentrations of active GLP-1 were measured during a 75 g oral glucose tolerance test.ResultsMean waist circumference (WC), homeostasis model assessment of insulin resistance (HOMA-IR) values, the total areas under the curve (AUC) of glucose and insulin were significantly higher in patients with CRA than in controls. The total AUC of GLP-1 (p= 0.01) was lower in patients with CRA than in controls. Moreover, the total AUC of GLP-1 showed a negative correlation with WC, total AUC of glucose, and HOMA-IR. Multiple linear regression analyses revealed that the total AUC of GLP-1 was independently correlated with the number and maximum size of CRAs.ConclusionGLP-1 could actively participate in the development of CRA in humans, particularly in patients with metabolic syndrome.