ArticleJournal of gastroenterology2017
Fatty acids in a high-fat diet potentially induce gastric parietal-cell damage and metaplasia in mice.
Article in Journal of gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 29 citations in OpenAlex.
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- Dietary Stearic Acid Accelerates Intestinal Tumorigenesis via Fatty Acid-binding Protein 5 Without Promoting Obesity.Cellular and molecular gastroenterology and hepatology · 2026Article
- Lipidomics and single-cell transcriptomics uncover aberrant lipid metabolism in metaplasia lesions during gastric carcinogenesis.Journal of gastroenterology · 2026Article
- Mitochondria-Associated Pathways in Cancer and Precancerous Conditions: Mechanistic Insights.International journal of molecular sciences · 2025Review
- High fat diet induces gastric production of fibroblast growth factor 23 (FGF23).International journal of obesity (2005) · 2025Article
- Translational Utility of Organoid Models for Biomedical Research on Gastrointestinal Diseases.Stem cell reviews and reports · 2024Review
- Gastric intestinal metaplasia: progress and remaining challenges.Journal of gastroenterology · 2024Review
- Association of plasma lipid metabolism profiles with overall survival for patients with gastric cancer undergoing gastrectomy based onNutrition & metabolism · 2023Article
- Immunohistochemical determination of somatostatin release in gastric tissue of rats fed with a high-fat and cholesterol diet.Veterinary research forum : an international quarterly journal · 2023Article
- The Role of Lipid Metabolism in Gastric Cancer.Frontiers in oncology · 2022Review
- Obesity-associated up-regulation of lipocalin 2 protects gastric mucosa cells from apoptotic cell death by reducing endoplasmic reticulum stress.Cell death & disease · 2021Article
- Article
- Efficacy and Mechanism of a Chinese Classic Prescription of Yueju in Treating Nonalcoholic Steatohepatitis and Protecting Hepatocytes from Apoptosis.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Paradoxical Roles of Oxidative Stress Response in the Digestive System before and after Carcinogenesis.Cancers · 2019Review
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundObesity is associated with risk of adenocarcinoma in the proximal stomach. We aimed to identify the links between dietary fat and gastric premalignant lesions.
methodsC57BL/6 mice were fed high fat diet (HFD), and gastric mucosa was histologically analysed. Morphological changes were also analysed using an electron microscope. Transcriptome analysis of purified parietal cells was performed, and non-parietal gastric corpus epithelial cells were subjected to single-cell gene-expression profiling. Composition of gastric contents of HFD-fed mice was compared with that of the HFD itself. Lipotoxicity of free fatty acids (FFA) was examined in primary culture and organoid culture of mouse gastric epithelial cells in vitro, as well as in vivo, feeding FFA-rich diets.
resultsDuring ~8-20 weeks of HFD feeding, the parietal cells of the stomach displayed mitochondrial damage, and a total of 23% of the mice developed macroscopically distinct metaplastic lesions in the gastric corpus mucosa. Transcriptome analysis of parietal cells indicated that feeding HFD enhanced pathways related to cell death. Histological analysis and gene-expression profiling indicated that the lesions were similar to previously reported precancerous lesions identified as spasmolytic polypeptide-expressing metaplasia. FFAs, including linoleic acid with refluxed bile acids were detected in the stomachs of the HFD-fed mice. In vitro, FFAs impaired mitochondrial function and decreased the viability of parietal cells. In vivo, linoleic acid-rich diet, but not stearic acid-rich diet induced parietal-cell loss and metaplastic changes in mice.
conclusionsDietary lipids induce parietal-cell damage and may lead to the development of precancerous metaplasia.
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