ArticleMetabolites2022
A Potential Role for Bile Acid Signaling in Celiac Disease-Associated Fatty Liver.
Article in Metabolites, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- Patients with Celiac Disease Have High Prevalence of Fatty Liver and Metabolic Syndrome.Digestive diseases and sciences · 2024Pooled it
- Modulation of metabolic parameters among obese diabetic individuals through a gluten-free diet.BMC nutrition · 2026Article
- Revolutionising portal hypertension diagnosis: the rise of non-invasive techniques in liver cirrhosis.Frontiers in medicine · 2025Review
- Gluten-Free Diet-What's Good for Celiac Disease Can Be Bad for Metabolism.Digestive diseases and sciences · 2024Article
- MAFLD and Celiac Disease in Children.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
23 authors at 9 institutions in 5 countries.
Funding
Abstract
Celiac disease (CeD) is a chronic autoimmune disorder characterized by an intolerance to storage proteins of many grains. CeD is frequently associated with liver damage and steatosis. Bile acid (BA) signaling has been identified as an important mediator in gut-liver interaction and the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Here, we aimed to analyze BA signaling and liver injury in CeD patients. Therefore, we analyzed data of 20 CeD patients on a gluten-free diet compared to 20 healthy controls (HC). We furthermore analyzed transaminase levels, markers of cell death, BA, and fatty acid metabolism. Hepatic steatosis was determined via transient elastography, by MRI and non-invasive scores. In CeD, we observed an increase of the apoptosis marker M30 and more hepatic steatosis as compared to HC. Fibroblast growth factor 19 (FGF19) was repressed in CeD, while low levels were associated with steatosis, especially in patients with high levels of anti-tissue transglutaminase antibodies (anti-tTG). When comparing anti-tTG-positive CeD patients to individuals without detectable anti-tTG levels, hepatic steatosis was accentuated. CeD patients with significant sonographic steatosis (defined by CAP ≥ 283 db/m) were exclusively anti-tTG-positive. In summary, our results suggest that even in CeD patients in clinical remission under gluten-free diet, alterations in gut-liver axis, especially BA signaling, might contribute to steatotic liver injury and should be further addressed in future studies and clinical practice.
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