Tahara Tomomitsu, Arisawa Tomiyasu, Shibata Tomoyuki, Nakamura Masakatsu, Wang Fangyu, Yoshioka Daisuke, Okubo Masaaki, Maruyama Naoko, Kamano Toshiaki, Kamiya Yoshio, Nakamura Masahiko, Fujita Hiroshi, Nagasaka Mitsuo, Iwata Masami, Takahama Kazuya, Watanabe Makoto, Yamashita Hiromi, Nakano Hiroshi, Hirata Ichiro
Department of Gastroenterology, Fujita Health University School of Medicine, Japan.
Hepatogastroenterology. 2009 Jul-Aug;56(93):1245-8.
BACKGROUND/AIMS: The role of genetics in the susceptibility to functional dyspepsia (FD) is not well established. Cholecystokinin (CCK) is released from enteroendocrine cells in the duodenal mucosa after food ingestion and signals satiation through peripheral or central actions. A common polymorphisms of CCK and it's receptor gene has been shown to be associated with panic disorder and schizophrenia. It was investigated the prevalence of CCK polymorphism in dyspeptic patients in a Japanese population.
A total of 124 dyspeptic patients, 119 non-symptomatic healthy controls participated in this study. Dyspeptic patients were also classified by Rome III criteria. T779C of Cholecystokinin (CCK)-1 intron 1, by polymerase chain reaction-restriction fragment length polymorphism. H. pylori infection status was examined by histology or antibody against H. pylori.
Although frequency of CCK-1 polymorphisms in overall dyspeptic patients, subgroups by Roma III criteria and non-symptomatic healthy controls did not show any significant differences, 779 T carriers significantly increased the risk of postprandial syndrome (PDS) in male subjects (53.5% vs, 84.2; OR = 4.63, 95% CI = 1.24-17.31, p = 0.018). This significant association was also remained after logistic regression analysis with adjustment for age and H. pylori infection status (OR = 4.99, 95% CI = 1.31-18.95, p = 0.018). In female and different H. pylori infection status, no significant association was observed between CCK-1 polymorphisms and dyspepsia.
Our data suggest that the 779 T carriers of CCK-1 intron 1 is associated with an increased risk of PDS in Japanese male subjects.
背景/目的：遗传学在功能性消化不良（FD）易感性中的作用尚未完全明确。进食后，十二指肠黏膜中的肠内分泌细胞会释放胆囊收缩素（CCK），其通过外周或中枢作用发出饱腹感信号。CCK及其受体基因的一种常见多态性已被证明与惊恐障碍和精神分裂症有关。本研究调查了日本人群中消化不良患者CCK多态性的患病率。
共有124例消化不良患者和119例无症状健康对照参与本研究。消化不良患者也根据罗马III标准进行分类。采用聚合酶链反应-限制性片段长度多态性方法检测胆囊收缩素（CCK）-1内含子1的T779C。通过组织学或抗幽门螺杆菌抗体检测幽门螺杆菌感染状况。
尽管总体消化不良患者、按罗马III标准分类的亚组以及无症状健康对照中CCK-1多态性的频率没有显著差异，但779T携带者显著增加了男性受试者餐后综合征（PDS）的风险（53.5%对84.2%；OR = 4.63，95%CI = 1.24 - 17.31，p = 0.018）。在对年龄和幽门螺杆菌感染状况进行调整的逻辑回归分析后，这种显著关联仍然存在（OR = 4.99，95%CI = 1.31 - 18.95，p = 0.018）。在女性和不同幽门螺杆菌感染状况下，未观察到CCK-1多态性与消化不良之间的显著关联。
我们的数据表明，CCK-1内含子1的779T携带者与日本男性受试者PDS风险增加有关。
