ArticleThe Journal of nutritional biochemistry2013
Disruption of inducible 6-phosphofructo-2-kinase impairs the suppressive effect of PPARγ activation on diet-induced intestine inflammatory response.
Article in The Journal of nutritional biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Glucose Metabolic Enzyme PFKFB3 in Cardiopulmonary Vascular Health and Disease.Circulation research · 2026Review
- Distinct tumor-TAM interactions in IDH-stratified glioma microenvironments unveiled by single-cell and spatial transcriptomics.Acta neuropathologica communications · 2024Article
- Mini review: STING activation during non-alcoholic fatty liver disease.Frontiers in nutrition · 2023Review
- The Protective Effects of Iron Free Lactoferrin on Lipopolysaccharide-Induced Intestinal Inflammatory Injury via Modulating the NF-κB/PPAR Signaling Pathway.Foods (Basel, Switzerland) · 2022Article
- Obesity elicits a unique metabolomic signature in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Methionine- and Choline-Deficient Diet-Induced Nonalcoholic Steatohepatitis Is Associated with Increased Intestinal Inflammation.The American journal of pathology · 2021Article
- Different Effects of Leucine Supplementation and/or Exercise on Systemic Insulin Sensitivity in Mice.Frontiers in endocrinology · 2021Article
- Parsing the Role of PPARs in Macrophage Processes.Frontiers in immunology · 2021Review
- Sodium Acetate Inhibit TGF-β1-Induced Activation of Hepatic Stellate Cells by Restoring AMPK or c-Jun Signaling.Frontiers in nutrition · 2021Article
- Kinetic Approach to the Influence of Chia Flour on Glucose Bioaccessibility from Hydrothermally Treated Maize and Quinoa Starch.Plant foods for human nutrition (Dordrecht, Netherlands) · 2020Article
- Indole Alleviates Diet-Induced Hepatic Steatosis and Inflammation in a Manner Involving Myeloid Cell 6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase 3.Hepatology (Baltimore, Md.) · 2020Article
- Inhibition of intestinal lipases alleviates the adverse effects caused by high-fat diet in Nile tilapia.Fish physiology and biochemistry · 2020Article
- Regulation of adipose tissue inflammation by adenosine 2A receptor in obese mice.The Journal of endocrinology · 2018Article
- A role forJournal of molecular endocrinology · 2017Article
- Nutritional approaches for managing obesity-associated metabolic diseases.The Journal of endocrinology · 2017Review
- The many ways tissue phagocytes respond to dying cells.Immunological reviews · 2017Review
- Different tissue phagocytes sample apoptotic cells to direct distinct homeostasis programs.Nature · 2016Article
- Glucose and Palmitate Differentially Regulate PFKFB3/iPFK2 and Inflammatory Responses in Mouse Intestinal Epithelial Cells.Scientific reports · 2016Article
- Berberine Ameliorates Hepatic Steatosis and Suppresses Liver and Adipose Tissue Inflammation in Mice with Diet-induced Obesity.Scientific reports · 2016Article
- Myeloid cell-specific disruption of Period1 and Period2 exacerbates diet-induced inflammation and insulin resistance.The Journal of biological chemistry · 2014Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
PFKFB3 is a target gene of peroxisome proliferator-activated receptor gamma (PPARγ) and encodes for inducible 6-phosphofructo-2-kinase (iPFK2). As a key regulatory enzyme that stimulates glycolysis, PFKFB3/iPFK2 links adipocyte metabolic and inflammatory responses. Additionally, PFKFB3/iPFK2 is involved in the effect of active PPARγ on suppressing overnutrition-induced adipose tissue inflammatory response, which accounts for the insulin-sensitizing and antidiabetic effects of PPARγ activation. Using PFKFB3/iPFK2-disrupted mice, the present study investigated the role of PFKFB3/iPFK2 in regulating overnutrition-associated intestine inflammatory response and in mediating the effects of PPARγ activation. In wild-type mice, intestine PFKFB3/iPFK2 was increased in response to high-fat diet (HFD) feeding compared with that in mice fed a low-fat diet. However, intestine PFKFB3/iPFK2 was decreased in PFKFB3/iPFK2-disrupted mice and did not respond to HFD feeding. Furthermore, on an HFD, PFKFB3/iPFK2-disrupted mice displayed a significant increase in major intestine proinflammatory indicators such as toll-like receptor 4 expression, c-Jun N-terminal kinase 1 and nuclear factor kappa B phosphorylation, and proinflammatory cytokine expression compared with wild-type littermates. Upon treatment with rosiglitazone, an agonist of PPARγ, intestine proinflammatory indicators were markedly decreased in wild-type mice, but to a much lesser degree in PFKFB3/iPFK2-disrupted mice. Overall, the status of HFD-induced intestine inflammatory response in all treated mice correlated inversely with systemic insulin sensitivity, indicated by the homeostasis model assessment of insulin resistance data. Together, these results suggest that PFKFB3/iPFK2 is critically involved in the effect of PPARγ activation on suppressing diet-induced intestine inflammatory response.
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Registered trials
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