ArticleThe Journal of biological chemistry2011
Peroxisome proliferator-activated receptor {alpha} is responsible for the up-regulation of hepatic glucose-6-phosphatase gene expression in fasting and db/db Mice.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 62 citations in OpenAlex.
- The physiology of MASLD: molecular pathways between liver and adipose tissues.Clinical science (London, England : 1979) · 2025Review
- Plant miR6262 Modulates the Expression of Metabolic and Thermogenic Genes in Human Hepatocytes and Adipocytes.Nutrients · 2024Article
- Experimental model and novel therapeutic targets for non-alcoholic fatty liver disease development.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Review
- Nutrigenomics in Regulating the Expression of Genes Related to Type 2 Diabetes Mellitus.Frontiers in physiology · 2021Review
- Procyanidin A2, an anti-diabetic condensed tannin extracted fromRSC advances · 2019Article
- Role of ketone signaling in the hepatic response to fasting.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- In utero exposure to di(2-ethylhexyl)phthalate suppresses blood glucose and leptin levels in the offspring of wild-type mice.Toxicology · 2019Article
- A Journey to Understand Glucose Homeostasis: Starting from Rat Glucose Transporter Type 2 Promoter Cloning to Hyperglycemia.Diabetes & metabolism journal · 2018Review
- PPARα-dependent Insig2a overexpression inhibits SREBP-1c processing during fasting.Scientific reports · 2017Article
- Corosolic acid ameliorates acute inflammation through inhibition of IRAK-1 phosphorylation in macrophages.BMB reports · 2016Article
- Metformin stimulates IGFBP-2 gene expression through PPARalpha in diabetic states.Scientific reports · 2016Article
- Hepatic adaptations to maintain metabolic homeostasis in response to fasting and refeeding in mice.Nutrition & metabolism · 2016Article
- Regulation of IGFBP-2 expression during fasting.The Biochemical journal · 2015Article
- Ursolic Acid-Regulated Energy Metabolism-Reliever or Propeller of Ultraviolet-Induced Oxidative Stress and DNA Damage?Proteomes · 2014Review
- Retinoic acid-related orphan receptor γ (RORγ): a novel participant in the diurnal regulation of hepatic gluconeogenesis and insulin sensitivity.PLoS genetics · 2014Article
- Txnip contributes to impaired glucose tolerance by upregulating the expression of genes involved in hepatic gluconeogenesis in mice.Diabetologia · 2013Article
- Metabolite and transcriptome analysis during fasting suggest a role for the p53-Ddit4 axis in major metabolic tissues.BMC genomics · 2013Article
- Adenovirus-mediated overexpression of Tcfe3 ameliorates hyperglycaemia in a mouse model of diabetes by upregulating glucokinase in the liver.Diabetologia · 2013Article
- Hepatic ATGL knockdown uncouples glucose intolerance from liver TAG accumulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Choline metabolism provides novel insights into nonalcoholic fatty liver disease and its progression.Current opinion in gastroenterology · 2012Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose-6-phosphatase (G6Pase) is a key enzyme that is responsible for the production of glucose in the liver during fasting or in type 2 diabetes mellitus (T2DM). During fasting or in T2DM, peroxisome proliferator-activated receptor α (PPARα) is activated, which may contribute to increased hepatic glucose output. However, the mechanism by which PPARα up-regulates hepatic G6Pase gene expression in these states is not well understood. We evaluated the mechanism by which PPARα up-regulates hepatic G6Pase gene expression in fasting and T2DM states. In PPARα-null mice, both hepatic G6Pase and phosphoenolpyruvate carboxykinase levels were not increased in the fasting state. Moreover, treatment of primary cultured hepatocytes with Wy14,643 or fenofibrate increased the G6Pase mRNA level. In addition, we have localized and characterized a PPAR-responsive element in the promoter region of the G6Pase gene. Chromatin immunoprecipitation (ChIP) assay revealed that PPARα binding to the putative PPAR-responsive element of the G6Pase promoter was increased in fasted wild-type mice and db/db mice. These results indicate that PPARα is responsible for glucose production through the up-regulation of hepatic G6Pase gene expression during fasting or T2DM animal models.
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