幽门螺杆菌感染改变蒙古沙鼠的胃和血浆胃饥饿素动态。
Helicobacter pylori infection modifies gastric and plasma ghrelin dynamics in Mongolian gerbils.
作者信息
Suzuki H, Masaoka T, Hosoda H, Ota T, Minegishi Y, Nomura S, Kangawa K, Ishii H
机构信息
Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
出版信息
Gut. 2004 Feb;53(2):187-94. doi: 10.1136/gut.2003.021568.
BACKGROUND
and aim: Although ghrelin, a novel growth hormone releasing peptide localised mainly in the gastric fundus, is reported not only to accelerate food passage and gastrointestinal motility but also to affect appetite and weight control, regulation of gastric ghrelin secretion under the conditions of gastric Helicobacter pylori infection is unknown. The present study was designed to investigate plasma and gastric ghrelin levels in Mongolian gerbils with H pylori colonisation of the gastric mucosa.
METHODS
Gerbils orally inoculated with H pylori were examined after inoculation. To examine preproghrelin mRNA expression in the gastric mucosa, cDNA encoding the gerbil preproghrelin and glyceraldehyde-3-phosphate dehydrogenase homologue was isolated and a quantitative reverse transcription-polymerase chain reaction system was established.
RESULTS
In gerbils showing H pylori colonisation (H pylori group), expression of preproghrelin mRNA and total ghrelin levels were significantly decreased 17 and 23 weeks later (p<0.01). Although the number of ghrelin immunoreactive cells decreased as the stomach weight increased, the gastric contents of total and active ghrelin in this group were the same as those in controls. Gastric myeloperoxidase activity showed a positive correlation with plasma ghrelin levels. On the other hand, at 17 weeks, plasma ghrelin levels were significantly increased in the H pylori group (p<0.05), suggesting a compensatory increase in secretion of the peptide at this time point.
CONCLUSION
The present experimental study demonstrated that gastric and plasma ghrelin dynamics are altered in response to H pylori infection.
背景与目的
尽管胃泌素释放肽（一种主要定位于胃底的新型生长激素释放肽）不仅被报道可加速食物通过和胃肠蠕动，还能影响食欲和体重控制，但幽门螺杆菌感染情况下胃泌素释放肽分泌的调节尚不清楚。本研究旨在调查胃黏膜有幽门螺杆菌定植的蒙古沙鼠的血浆和胃内胃泌素释放肽水平。
方法
给蒙古沙鼠口服接种幽门螺杆菌后进行检查。为检测胃黏膜中胃泌素释放肽原mRNA的表达，分离编码蒙古沙鼠胃泌素释放肽原和甘油醛-3-磷酸脱氢酶同源物的cDNA，并建立定量逆转录-聚合酶链反应系统。
结果
在显示有幽门螺杆菌定植的蒙古沙鼠（幽门螺杆菌组）中，胃泌素释放肽原mRNA表达和总胃泌素释放肽水平在17周和23周后显著降低（p<0.01）。尽管胃泌素释放肽免疫反应性细胞数量随胃重量增加而减少，但该组胃内总胃泌素释放肽和活性胃泌素释放肽含量与对照组相同。胃髓过氧化物酶活性与血浆胃泌素释放肽水平呈正相关。另一方面，在17周时，幽门螺杆菌组血浆胃泌素释放肽水平显著升高（p<0.05），表明此时该肽的分泌有代偿性增加。
结论
本实验研究表明，幽门螺杆菌感染会改变胃和血浆中胃泌素释放肽的动态变化。
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