ArticleScientific reports2024
Helicobacter pylori components increase the severity of metabolic syndrome and its hepatic manifestations induced by a high fat diet.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- The effect of Hp infection on dyslipidemia in Asia and out of Asia: a systematic review and meta-analysis.Frontiers in medicine · 2025Pooled it
- Diverse high-fat diets drive multi-omic reprogramming that persists after dietary reversal.bioRxiv : the preprint server for biology · 2026Article
- Article
- The Potential Role ofMicroorganisms · 2025Review
- Doxorubicin loaded polylactide nanoparticles functionalized histamine promote apoptosis of human gastric cancer cells AGS.Scientific reports · 2025Article
- Untargeted metabolomic profiling for identifying systemic signatures of helicobacter pylori infection in a guinea pig model.Scientific reports · 2025Article
- Association ofJGH open : an open access journal of gastroenterology and hepatology · 2025Review
- Potential mechanisms and therapeutic prospects of the association betweenWorld journal of hepatology · 2025Article
- A critical review onFrontiers in cellular and infection microbiology · 2025Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The metabolic syndrome, often accompanied by hepatic manifestations, is a high-risk factor for developing cardiovascular disease. Patients with metabolic dysfunction associated with steatohepatic disease (MASDL) are at significant risk of developing coronary artery disease. Atherosclerosis is a systemic inflammatory disorder in which several factors, including dietary or infectious factors, can cause an inflammatory response. Helicobacter pylori (HP) bacteria have been implicated in the progression of proatherogenic vascular endothelial lesions, moreover, our previous study in an experimental in vivo model of Cavia porcellus showed that HP components and high-fat substances acted synergistically in promoting vascular endothelial inflammation, leading to an early onset of a proatherogenic environment. In the present study, our goal was to determine the contribution of HP components to the development of hepatic manifestations of metabolic syndrome in an experimental model. Our results showed that HP infection in animals exposed to a high-fat diet increased oxidative stress and lipid peroxidation, followed by endothelial lipid deposition, impaired endothelial apoptosis, cell lysis, and increased vascular stiffness. Finally, histopathological analysis of liver tissue showed signs of MASLD development in HP-infected animals fed a high-fat diet.
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Registered trials
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