Cell proliferation in ventromedial hypothalamic lesioned rats inhibits acute gastric mucosal lesions

Noriko Ishizuka; Nobuo Imazeki; Akira Senoo; Junko Sakurai; Masaru Sonoda; Masao Kanazawa; Yoko Suzuki; Yoko Kobayashi; Tosei Takahashi; Ryota Haba; Katsumi Arai; Hiroyuki Shimizu; Kahoru Sasaki; Masako Kako; Kaori Hayashi; Yuichi Suzuki; Shuji Inoue

doi:10.1016/j.orcp.2011.12.003

Cell proliferation in ventromedial hypothalamic lesioned rats inhibits acute gastric mucosal lesions

Obes Res Clin Pract. 2012 Jul-Sep;6(3):e175-262. doi: 10.1016/j.orcp.2011.12.003.

Authors

Noriko Ishizuka¹, Nobuo Imazeki², Akira Senoo³, Junko Sakurai⁴, Masaru Sonoda⁵, Masao Kanazawa⁶, Yoko Suzuki¹, Yoko Kobayashi¹, Tosei Takahashi¹, Ryota Haba¹, Katsumi Arai¹, Hiroyuki Shimizu¹, Kahoru Sasaki³, Masako Kako³, Kaori Hayashi³, Yuichi Suzuki⁷, Shuji Inoue¹

Affiliations

¹ Department of Nutrition, Faculty of Health Care, Kiryu University, Midori City, Gunma 379-2392, Japan.
² Department of Nutrition, Faculty of Health Care, Kiryu University, Midori City, Gunma 379-2392, Japan. Electronic address:imazeki-no@kiryu-u.ac.jp.
³ Department of Nursing, Faculty of Health Care, Kiryu University, Midori City, Gunma 379-2392, Japan.
⁴ FANCL Corporation, Yokohama, Kanagawa 231-0023, Japan.
⁵ Department of Clinical Nutrition, Faculty of Home Economics, Kyoritsu Women's University Chiyoda, Tokyo 101-8437, Japan.
⁶ Division of Diabetology, Metabolism and Endocrinology, The Third Department of Internal Medicine, Tokyo Medical University Shinjuku, Tokyo 160-0023, Japan.
⁷ Department of Nutrition, Faculty of Food and Nutritional Sciences, University of Shizuoka, Shizuoka City, Shizuoka 422-8526, Japan.

PMID: 24331526
DOI: 10.1016/j.orcp.2011.12.003

Abstract

Aim: The role of mucosal layer thickness on prevention of acute gastric mucosal lesions (AGMLs) was examined in ventromedial hypothalamic (VMH)-lesioned rats.

Materials and methods: The incidence of AGMLs after 48-h fasting and 60% ethanol injection into the stomach after 24-h fasting, aggressive factors (gastric acid and serum gastrin) and defensive factors [hexosamine, gastric mucosal blood flow (GMBF), serum thiobarbituric acid reacting substances (TBARS), and thickness of the gastric mucosal layer] were evaluated in VMH-lesioned rats. The effects of cell proliferation on the gastric mucosal layer of these rats were evaluated by H-E staining and immunostaining with proliferating cell nuclear antigen (PCNA).

Results: After 48-h fasting, no AGMLs were observed in VMH-lesioned and sham VMH-lesioned rats (controls). With 60% ethanol administration after 24-h fasting, the numbers of AGMLs were similar in the two groups, but the ulcer index, a marker of ulcer formation, was lower in VMH-lesioned rats compared to that in sham VMH-lesioned rats. VMH-lesioned rats showed increased gastric acid secretion and serum gastrin compared to sham VMH-lesioned rats, indicating an increase in aggressive factors in VMH-lesioned rats. The two groups had similar levels of gastric mucosal hexosamine, GMBF, and gastric mucosal TBARS, but VMH-lesioned rats had an increased thickness of the mucosal cell layer, indicating an increase in defensive factors in these rats. Histologically, VMH-lesioned rats had an increased total mucosal cell layer, especially for the surface epithelial cell layer, and an increased PCNA-labeling index, a marker of cell proliferation, especially in the proliferative zones of gastric mucosa, indicating increased cell proliferation in the proliferative zone of the gastric mucosa.

Conclusion: VMH-lesioned rats are resistant to AGML formation due to increased cell proliferation in gastric mucosa through elevating the levels of defensive factors over those of aggressive factors.