Osawa Hiroyuki, Kita Hiroto, Ohnishi Hirohide, Nakazato Masamitsu, Date Yukari, Bowlus Christopher L, Ishino Yumiko, Watanabe Eiko, Shiiya Tomomi, Ueno Hiroaki, Hoshino Hiroko, Satoh Kiichi, Sugano Kentaro
Department of Internal Medicine, Division of Gastroenterology, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke, Japan.
J Gastroenterol. 2006 Oct;41(10):954-61. doi: 10.1007/s00535-006-1880-4. Epub 2006 Nov 9.
Ghrelin is a body weight-regulating peptide produced and secreted primarily by the gastric mucosa. Helicobacter pylori infection impairs gastric ghrelin production, leading to a lower plasma ghrelin concentration. However, the effect of H. pylori eradication on plasma ghrelin levels and its relation to body weight change after H. pylori cure are still uncertain. We examined the association of plasma ghrelin levels with gastric ghrelin production and body weight change before and after H. pylori eradication.
Plasma ghrelin concentrations, gastric ghrelin expression, and body weight were determined in a total of 134 consecutive individuals before and 12 weeks after successful H. pylori eradication. Gastric ghrelin expression was evaluated by determining mRNA expression levels and the number of ghrelin-producing cells in gastric mucosa biopsy specimens by real-time reverse transcriptase-polymerase chain reaction and immunohistochemistry, respectively.
Plasma ghrelin concentration increased in 50 patients and decreased in 84 patients after H. pylori eradication. After H. pylori cure, however, gastric preproghrelin mRNA expression was increased nearly fourfold (P < 0.0001), and the number of ghrelin-positive cells was increased or unchanged. In contrast, plasma ghrelin changes after H. pylori cure were inversely correlated with both body weight change (P < 0.0001) and initial plasma ghrelin levels (P < 0.0001).
Changes in plasma ghrelin concentrations before and after H. pylori cure were inversely correlated with body weight change and initial plasma ghrelin levels but not with gastric ghrelin production in Japanese patients.
胃饥饿素是一种主要由胃黏膜产生和分泌的体重调节肽。幽门螺杆菌感染会损害胃饥饿素的产生,导致血浆胃饥饿素浓度降低。然而,幽门螺杆菌根除对血浆胃饥饿素水平的影响及其与幽门螺杆菌治愈后体重变化的关系仍不确定。我们研究了幽门螺杆菌根除前后血浆胃饥饿素水平与胃饥饿素产生及体重变化之间的关联。
对134例连续患者在成功根除幽门螺杆菌之前及之后12周测定血浆胃饥饿素浓度、胃饥饿素表达及体重。分别通过实时逆转录聚合酶链反应和免疫组织化学测定胃黏膜活检标本中胃饥饿素mRNA表达水平及胃饥饿素产生细胞数量,以评估胃饥饿素表达。
根除幽门螺杆菌后,50例患者血浆胃饥饿素浓度升高,84例患者降低。然而,幽门螺杆菌治愈后,胃前胃饥饿素mRNA表达增加近四倍(P < 0.0001),胃饥饿素阳性细胞数量增加或未改变。相比之下,幽门螺杆菌治愈后血浆胃饥饿素变化与体重变化(P < 0.0001)和初始血浆胃饥饿素水平(P < 0.0001)均呈负相关。
在日本患者中,幽门螺杆菌治愈前后血浆胃饥饿素浓度变化与体重变化和初始血浆胃饥饿素水平呈负相关,但与胃饥饿素产生无关。