ReviewJournal of gastroenterology2013
Mechanisms of hepatic triglyceride accumulation in non-alcoholic fatty liver disease.
Review in Journal of gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 489 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
489 citing papers in PubMed, 3 syntheses or guidelines pooled it, 940 citations in OpenAlex.
- Non-HDL-to-HDL-cholesterol ratio and metabolic dysfunction-associated steatotic liver disease: a systematic review and meta-analysis.BMC gastroenterology · 2026Pooled it
- Global research trends on gut microbiota and metabolic dysfunction-associated steatohepatitis: Insights from bibliometric and scientometric analysis.Frontiers in pharmacology · 2024Pooled it
- Pooled it
- Metabolic impact of dietary glycine supplementation in individuals with severe obesity.Scientific reports · 2025Trial
- Changes in abdominal adipose tissue depots assessed by MRI correlate with hepatic histologic improvement in non-alcoholic steatohepatitis.Journal of hepatology · 2023Trial
- Flavonoids for MASLD: Hepatic Lipid Targets, Biopharmaceutic Barriers, and Formulation Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Dyslipidaemia and hepatic steatosis: mechanisms and implications for lipid-lowering therapy.Nature reviews. Cardiology · 2026Review
- Sequential Fractionation ofFoods (Basel, Switzerland) · 2026Article
- E-cigarette vaping is associated with pro-fibrotic gene expression in kidney and liver tissues.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Review
- Integrated Plasma and Tissue Lipid Profiling Demonstrates a Distinctive Metabolic Profile in MAFLD-Associated Non-Cirrhotic Hepatocellular Carcinoma.International journal of molecular sciences · 2026Article
- ER stress-mediated impairment of hepatic lipid export is associated with steatosis in AKI-induced remote liver injury.Scientific reports · 2026Article
- Adipose Tissue Plasticity and Adipogenesis: From Cellular Mechanisms to Therapeutic Targets in Obesity.Current obesity reports · 2026Review
- Article
- Hepatic fat fraction and lipid content of adrenal adenomas: insights from unenhanced CT.Abdominal radiology (New York) · 2026Article
- Therapeutic effects of chitooligosaccharide-epigallocatechin gallate conjugate on NAFLD: impact on gut-liver axis, lipid metabolism, and inflammation in rats fed a high-fat diet.Journal of physiology and biochemistry · 2026Article
- ER Stress-Mediated Impairment of Hepatic Lipid Export Drives Steatosis in AKI-Induced Remote Liver Injury.Research square · 2026Article
- A high-fat diet with vitamin D and propylthiouracil produces a pro-atherogenic phenotype in rats.Animal models and experimental medicine · 2026Article
- Whole-Genome-Guided Functional Characterization ofFoods (Basel, Switzerland) · 2026Article
- APOC3 Promotes DGAT2-Dependent Triglyceride Accumulation in Hepatocytes During Early Metabolic Dysfunction.Biomolecules · 2026Article
429 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Non-alcoholic fatty liver disease (NAFLD) is characterized by hepatic lipid accumulation in the absence of excess alcohol intake. NAFLD is the most common chronic liver disease, and ongoing research efforts are focused on understanding the underlying pathobiology of hepatic steatosis with the anticipation that these efforts will identify novel therapeutic targets. Under physiological conditions, the low steady-state triglyceride concentrations in the liver are attributable to a precise balance between acquisition by uptake of non-esterified fatty acids from the plasma and by de novo lipogenesis, versus triglyceride disposal by fatty acid oxidation and by the secretion of triglyceride-rich lipoproteins. In NAFLD patients, insulin resistance leads to hepatic steatosis by multiple mechanisms. Greater uptake rates of plasma non-esterified fatty acids are attributable to increased release from an expanded mass of adipose tissue as a consequence of diminished insulin responsiveness. Hyperinsulinemia promotes the transcriptional upregulation of genes that promote de novo lipogenesis in the liver. Increased hepatic lipid accumulation is not offset by fatty acid oxidation or by increased secretion rates of triglyceride-rich lipoproteins. This review discusses the molecular mechanisms by which hepatic triglyceride homeostasis is achieved under normal conditions, as well as the metabolic alterations that occur in the setting of insulin resistance and contribute to the pathogenesis of NAFLD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.