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Updated: Feb 17, 2026
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Pathological effects of diabetic mice with Helicobacter pylori infection
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.
Background:
Helicobacter pylori (H. pylori) is widely present in the human gastric mucosa and is closely associated with a variety of gastric diseases. Recent studies have found that H. pylori infection is closely associated with diabetic patients and may adversely affect their glucose metabolism and organ function. However, the effect of H. pylori infection on pathological changes in the body during a diabetic state remains unclear.
Aim:
To investigate the effects of H. pylori infection on the physiology and pathological changes in the organs of diabetic mice.
Methods:
The diabetic mice models were established using streptozotocin (STZ). The mice were infected with H. pylori through oral gavage, with their fasting blood glucose (FBG) and body weight monitored dynamically over a period of 1 to 13 months after infection. Pathological changes in major organs (including the pancreas, stomach, liver, and kidneys) were assessed, along with apoptosis levels in these tissues. The expression of H. pylori virulence factors in the liver and alterations in the intestinal microbiota were also analyzed.
Results:
H. pylori infection led to significant fluctuations in FBG in diabetic mice from the 1st to 9th month, with FBG levels remaining consistently elevated. Body weight increased gradually but remained significantly lower than that of both uninfected diabetic mice and non-diabetic controls. Pancreatic islet cell numbers decreased, accompanied by persistent inflammation and tissue damage for over 9 months. H. pylori colonized the stomach for at least 7 months, causing irreversible gastric mucosal inflammation; by the 13th month, diffuse dense inflammatory infiltration occupying the entire submucosal layer was observed. Progressive damage was observed in liver and kidney tissues, with marked expression of H. pylori virulence factors in the liver by the 9th month. Additionally, significant gut microbiota dysbiosis was observed.
Conclusion:
The STZ-induced diabetic mouse model with H. pylori infection can significantly prolong the colonization time of H. pylori in the stomach and exacerbate the degree of damage to the stomach, liver, and kidney organs.
![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)
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