Related Experiment Video

Updated: Jul 14, 2026

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance
05:23

Gastric Mucosa Quantitative Polymerase Chain Reaction Analysis for Detecting Helicobacter pylori and Antibiotic Resistance

Published on: March 7, 2025

Insulin resistance in children with Helicobacter pylori infection

S Ozdem1, M Akcam, A Yilmaz

  • 1Central Laboratory Clinical Biochemistry Unit, Medical Faculty, Akdeniz University, Antalya, Turkey. ozdem@akdeniz.edu.tr

Journal of Endocrinological Investigation
|May 17, 2007
PubMed

Insights

Helicobacter pylori infection in children is linked to higher insulin resistance. This study found elevated insulin levels and HOMA-IR scores in infected children, suggesting a connection between H. pylori and insulin resistance.

Area of Science:

  • Pediatric Endocrinology
  • Gastroenterology
  • Infectious Diseases

Background:

  • Insulin resistance is a growing concern in pediatric populations.
  • Helicobacter pylori (H. pylori) infection is prevalent in children worldwide.
  • The potential link between H. pylori infection and metabolic disturbances like insulin resistance requires further investigation.

Purpose of the Study:

  • To investigate the association between H. pylori infection and insulin resistance in children.
  • To compare insulin resistance markers between H. pylori-infected children and a control group.

Main Methods:

  • A cohort of 31 H. pylori-infected children and 29 H. pylori-negative controls were studied.
  • Fasting serum insulin and glucose levels were measured in all participants.
  • Insulin resistance was quantified using the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) score.

Main Results:

  • Serum glucose levels showed no significant difference between the infected and control groups.
  • Children with H. pylori infection exhibited significantly higher HOMA-IR scores compared to controls.
  • Elevated fasting serum insulin levels were observed in the H. pylori-infected group.

Conclusions:

  • H. pylori infection in children is associated with increased insulin resistance.
  • The findings suggest a potential relationship between H. pylori and the development of insulin resistance in pediatric patients.
  • Further research is warranted to elucidate the mechanisms underlying this association.

More Related Videos

Profiling Luminal pH in Three-Dimensional Gastrointestinal Organoids Using Microelectrodes08:24

Profiling Luminal pH in Three-Dimensional Gastrointestinal Organoids Using Microelectrodes

Published on: July 5, 2024

Related Concept Videos

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Peptic Ulcer01:27

Peptic Ulcer

Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

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.
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies01:28

Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies

Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.