相关实验视频
Updated: Feb 17, 2026
07:43
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
22.6K
糖尿病小鼠患有Helicobacter pylori感染的病理影响
Wan-Ping Yang1, Jin-Hai Zeng1,2, Biao-Liang Wu1,3
1Guangxi Technology Innovation Cooperation Base of Prevention and Control Pathogenic Microbes with Drug Resistance, Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China.
World journal of diabetes
|February 16, 2026
概括
在糖尿病小鼠中,Helicobacter pylori感染会使胃,肝脏和脏损伤恶化,延长细菌殖民的时间. 这项研究强调了H. pylori对糖尿病人器官功能的有害影响.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 内分泌学 在内分泌学.
背景情况:
- 杆菌 (H. pylori) 在胃粘膜中普遍存在,并与胃疾病有关.
- H. pylori 感染越来越多地与糖尿病有关,可能会损害葡萄糖代谢和器官功能.
- 对于H. pylori对糖尿病器官病理学的特定影响尚不清楚.
研究的目的:
- 研究H. pylori感染对糖尿病小鼠器官的生理和病理影响.
- 在糖尿病模型中分析H. pylori对葡萄糖代谢,体重和组织损伤的影响.
主要方法:
- 糖尿病小鼠模型被诱导使用链毒素 (STZ).
- 鼠被口服感染了H. pylori;禁食血糖 (FBG) 和体重被监测了13个月.
- 评估了关键器官 (胰腺,胃,肝脏,脏) 的病理变化,亡,H. pylori毒性因子表达和肠道微生物群.
主要成果:
- 在糖尿病小鼠中,H. pylori感染引起了显著的FBG波动和持续的升高,并降低了体重.
- 胰腺小岛细胞减少,持续炎症和损伤观察到超过9个月.
- 发现了不可逆转的胃炎症,进展性肝脏和脏损伤,肝脏中的H. pylori毒性因子表达,以及肠道失生症.
结论:
- 杆菌感染显著延长其在STZ诱导的糖尿病小鼠的胃中的定居时间.
- 同时感染加剧了糖尿病小鼠的胃,肝脏和脏的病理损伤.
- 这些发现强调了H. pylori和糖尿病对器官健康的协同负面影响.
![Assessment of Gastric Emptying in Non-obese Diabetic Mice Using a [13C]-octanoic Acid Breath Test](/_next/image?url=https%3A%2F%2Fcloudfront.jove.com%2FCDNSource%2Fteasers%2F50301.jpg&w=3840&q=50)
相关概念视频
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
1.3K
Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
1.3K
01:17Gastritis-II: Pathophysiology
1.4K
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
1.4K
01:24Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
1.3K
Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI) tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
1.3K
01:20Pathophysiology of Diabetes
3.8K
Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...
3.8K
01:30Peptic Ulcer Disease I: Introduction
900
Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
900
01:28Peptic Ulcer Disease II: Pathophysiology
2.3K
Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
2.3K