ArticleNutrients2023
MicroRNA-34a Mediates High-Fat-Induced Hepatic Insulin Resistance by Targeting ENO3.
Article in Nutrients, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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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.
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.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- The use of circulating miRNAs for the diagnosis, prognosis, and personalized treatment of MASLD.Journal of physiology and biochemistry · 2025Pooled it
- The role of hepatocyte epigenetics in the pathogenesis of metabolic dysfunction-associated steatotic liver disease.Communications medicine · 2026Review
- H19 inhibition orchestrates DNMT3B-dependent epigenetic reprogramming of glycolytic enzymes in the liver during diabetes.Cell communication and signaling : CCS · 2026Article
- Review
- A novel C/EBPα-miR-335-5p-PRKAA2 regulatory axis drives hepatic lipid accumulation in MASLD.Scientific reports · 2026Article
- Role of miRNA signalling in the pathogenesis of MASLD.Frontiers in pharmacology · 2026Review
- ENO3 regulates ferroptosis by interaction with PKM2 to promote the progression of metabolic dysfunction-associated steatotic liver disease.Histology and histopathology · 2026Article
- 1-Deoxynojirimycin Combined with Theaflavins Targets PTGS2/MMP9 to Exert a Synergistic Hypoglycemic Effect.Nutrients · 2025Article
- Expression of Serum and Exosomal microRNA-34a in Subjects with Increased Fat Mass.International journal of molecular sciences · 2025Article
- Bioinformatic identification of signature miRNAs associated with fetoplacental vascular dysfunction in gestational diabetes mellitus.Biochemistry and biophysics reports · 2025Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The etiology of numerous metabolic disorders is characterized by hepatic insulin resistance (IR). Uncertainty surrounds miR-34a's contribution to high-fat-induced hepatic IR and its probable mechanism. The role and mechanism of miR-34a and its target gene ENO3 in high-fat-induced hepatic IR were explored by overexpressing/suppressing miR-34a and ENO3 levels in in vivo and in vitro experiments. Moreover, as a human hepatic IR model, the miR-34a/ENO3 pathway was validated in patients with non-alcoholic fatty liver disease (NAFLD). The overexpression of hepatic miR-34a lowered insulin signaling and altered glucose metabolism in hepatocytes. In contrast, reducing miR-34a expression significantly reversed hepatic IR indices induced by palmitic acid (PA)/HFD. ENO3 was identified as a direct target gene of miR-34a. Overexpression of ENO3 effectively inhibited high-fat-induced hepatic IR-related indices both in vitro and in vivo. Moreover, the expression patterns of members of the miR-34a/ENO3 pathway in the liver tissues of NAFLD patients was in line with the findings of both cellular and animal studies. A high-fat-induced increase in hepatic miR-34a levels attenuates insulin signaling and impairs glucose metabolism by suppressing the expression of its target gene ENO3, ultimately leading to hepatic IR. The miR-34a/ENO3 pathway may be a potential therapeutic target for hepatic IR and related metabolic diseases.
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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 Socratic graph.