ArticleMolecular medicine reports2017
Osteopontin deficiency protects mice from cholesterol gallstone formation by reducing expression of intestinal NPC1L1.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Moderate and severe depression increase the incidence of cholelithiasis: Results from Mendelian randomization study and the NHANES 2017-March 2020.Social psychiatry and psychiatric epidemiology · 2025Observational
- NPC1L1 Drives Osteoporosis by Activating the C/EBPα/Cyp27a1/27-Hydroxycholesterol Axis: A Novel Therapeutic Target for Bone Loss.FASEB bioAdvances · 2025Article
- Osteopontin (SPP1) expression on gallstone formation in rabbits fed with a lithogenic diet.Journal of advanced veterinary and animal research · 2023Article
- Article
- Organ Weights inInternational journal of molecular sciences · 2022Article
- Osteopontin Exacerbates High-Fat Diet-Induced Metabolic Disorders in a Microbiome-Dependent Manner.mBio · 2022Article
- An update on the pathogenesis of cholesterol gallstone disease.Current opinion in gastroenterology · 2018Review
- Recent advances in understanding and managing cholesterol gallstones.F1000Research · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homeostasis of cholesterol is regulated by absorption in the intestine and synthesis in the liver. The authors previously demonstrated that OPN (osteopontin) exhibits the ability to alter hepatic cholesterol metabolism, thus affecting cholesterol gallstone formation in mice. The present study investigated the role of OPN in cholesterol gallstone formation, focusing on its effect on intestinal absorption of cholesterol. OPN gene knockout (OPN‑/‑) mice and wild‑type mice were respectively fed with a chow or lithogenic diet (LD) for 8 weeks. Following an 8‑week LD period, the incidence of gallstone, bile composition, level of serum and fecal lipids and the expression of intestinal associated genes were analyzed. OPN‑/‑ mice were protected from gallstone formation induced by 8 weeks' LD‑feeding. This protective effect from OPN deficiency was associated with alterations in bile composition, including a reduced concentration of biliary cholesterol. Additionally, plasma cholesterol level was decreased in LD‑fed OPN‑/‑ mice. The alterations primarily resulted from the decreased expression of intestinal Niemann‑Pick C1‑like (NPC1 L) 1, which is important in the intestinal absorption of cholesterol. The present study demonstrated that OPN deficiency reduced intestinal absorption of cholesterol by suppressing the expression of NPC1L1, thus protecting mice from cholesterol gallstone formation.
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