ArticleJournal of hepatology2013
Post-transcriptional activation of PPAR alpha by KLF6 in hepatic steatosis.
Article in Journal of hepatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 52 citations in OpenAlex.
- Identification of Foxm1 as a critical regulator for metabolic dysfunction-associated steatotic liver disease by epigenomic and transcriptional profiling.Cell insight · 2026Article
- Coagulation protease-activated receptor-2 (PAR2) promotes dyslipidemia, obesity and MASLD through repression of the hepatic pioneer factor HNF4α.JHEP reports : innovation in hepatology · 2026Article
- The possible renoprotective effect of denatonium benzoate in a rat model of type 2 diabetes: role of Krüppel-like factor 6 (KLF6).Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Liver Metabolism at the Crossroads: The Reciprocal Control of Nutrient-Sensing Nuclear Receptors and Autophagy.International journal of molecular sciences · 2025Review
- Identification of genetic associations and functional SNPs of bovine KLF6 gene on milk production traits in Chinese holstein.BMC genomic data · 2023Article
- Specificity Proteins (SP) and Krüppel-like Factors (KLF) in Liver Physiology and Pathology.International journal of molecular sciences · 2023Review
- Mechanistic insights into the peroxisome proliferator-activated receptor alpha as a transcriptional suppressor.Frontiers in medicine · 2022Review
- Article
- PVT1 knockdown inhibited the biological behavior of LPS-induced cardiac fibroblasts by regulating miR-24.Genes & genomics · 2021Article
- The Emerging Factors and Treatment Options for NAFLD-Related Hepatocellular Carcinoma.Cancers · 2021Review
- Current Options and Future Directions for NAFLD and NASH Treatment.International journal of molecular sciences · 2021Review
- Non-coding RNA crosstalk with nuclear receptors in liver disease.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- TransSynW: A single-cell RNA-sequencing based web application to guide cell conversion experiments.Stem cells translational medicine · 2021Article
- The Role and Mechanism of Oxidative Stress and Nuclear Receptors in the Development of NAFLD.Oxidative medicine and cellular longevity · 2021Review
- Review
- MCD diet-induced steatohepatitis generates a diurnal rhythm of associated biomarkers and worsens liver injury in Klf10 deficient mice.Scientific reports · 2020Article
- Klf6 protects β-cells against insulin resistance-induced dedifferentiation.Molecular metabolism · 2020Article
- The Krüppel-Like Factors and Control of Energy Homeostasis.Endocrine reviews · 2019Review
- Podocyte-Specific Loss of Krüppel-Like Factor 6 Increases Mitochondrial Injury in Diabetic Kidney Disease.Diabetes · 2018Article
- Neurotensin contributes to pediatric intestinal failure-associated liver disease via regulating intestinal bile acids uptake.EBioMedicine · 2018Article
Corrections and comments
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Authors and funding
24 authors at 6 institutions in 5 countries.
Funding
Abstract
BACKGROUND &
aimsDysregulated glucose homeostasis and lipid accumulation characterize non-alcoholic fatty liver disease (NAFLD), but underlying mechanisms are obscure. We report here that Krüppel-like factor 6 (KLF6), a ubiquitous transcription factor that promotes adipocyte differentiation, also provokes the metabolic abnormalities of NAFLD by post-transcriptionally activating PPARα-signaling.
methodsMice with either hepatocyte-specific depletion of KLF6 ('ΔHepKlf6') or global KLF6 heterozygosity (Klf6+/-) were fed a high fat diet (HFD) or chow for 8 or 16 weeks. Glucose and insulin tolerance tests were performed to assess insulin sensitivity. Overexpression and knockdown of KLF6 in cultured cells enabled the elucidation of underlying mechanisms. In liver samples from a cohort of 28 NAFLD patients, the expression of KLF6-related target genes was quantified.
resultsMice with global- or hepatocyte-depletion of KLF6 have reduced body fat content and improved glucose and insulin tolerance, and are protected from HFD-induced steatosis. In hepatocytes, KLF6 deficiency reduces PPARα-regulated genes (Trb3, Pepck) with diminished PPARα protein but no change in Pparα mRNA, which is explained by the discovery that KLF6 represses miRNA 10b, which leads to induction of PPARα. In NAFLD patients with advanced disease and inflammation, the expression of miRNA 10b is significantly downregulated, while PEPCK mRNA is upregulated; KLF6 mRNA expression also correlates with TRB3 as well as PEPCK gene expression.
conclusionsKLF6 increases PPARα activity, whereas KLF6 loss leads to PPARα repression and attenuation of lipid and glucose abnormalities associated with a high fat diet. The findings establish KLF6 as a novel regulator of hepatic glucose and lipid metabolism in fatty liver.
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