ArticleThe Journal of biological chemistry2010
Involvement of inducible 6-phosphofructo-2-kinase in the anti-diabetic effect of peroxisome proliferator-activated receptor gamma activation in mice.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Targeting adenosine 2A receptor signaling suppresses vascular calcification by restraining smooth muscle osteogenic differentiation.Pharmacological research · 2025Article
- Endothelial adenosine receptor 2A loss alleviates diabetic vascular calcification by blocking CREB1-SNAI1-driven EndMT.Pharmacological research · 2025Article
- Obesity elicits a unique metabolomic signature in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Review
- Methionine- and Choline-Deficient Diet-Induced Nonalcoholic Steatohepatitis Is Associated with Increased Intestinal Inflammation.The American journal of pathology · 2021Article
- Adipocyte inducible 6-phosphofructo-2-kinase suppresses adipose tissue inflammation and promotes macrophage anti-inflammatory activation.The Journal of nutritional biochemistry · 2021Article
- Advances in Unhealthy Nutrition and Circadian Dysregulation in Pathophysiology of NAFLD.Frontiers in clinical diabetes and healthcare · 2021Review
- Article
- Different Effects of Leucine Supplementation and/or Exercise on Systemic Insulin Sensitivity in Mice.Frontiers in endocrinology · 2021Article
- 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
- Adoptive transfer ofLiver research (Beijing, China) · 2020Article
- A locked immunometabolic switch underlies TREM2 R47H loss of function in human iPSC-derived microglia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The Construction and Analysis of the Aberrant lncRNA-miRNA-mRNA Network in Adipose Tissue from Type 2 Diabetes Individuals with Obesity.Journal of diabetes research · 2020Article
- Shift work cycle-induced alterations of circadian rhythms potentiate the effects of high-fat diet on inflammation and metabolism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- PFKFB3 blockade inhibits hepatocellular carcinoma growth by impairing DNA repair through AKT.Cell death & disease · 2018Article
- A role forJournal of molecular endocrinology · 2017Article
- Metabolic and Inflammatory Adaptation of Reactive Astrocytes: Role of PPARs.Molecular neurobiology · 2017Review
- The many ways tissue phagocytes respond to dying cells.Immunological reviews · 2017Review
- Nutrition, microRNAs, and Human Health.Advances in nutrition (Bethesda, Md.) · 2017Review
- Glucose and Palmitate Differentially Regulate PFKFB3/iPFK2 and Inflammatory Responses in Mouse Intestinal Epithelial Cells.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
PFKFB3 is the gene that codes for the inducible isoform of 6-phosphofructo-2-kinase (iPFK2), a key regulatory enzyme of glycolysis. As one of the targets of peroxisome proliferator-activated receptor gamma (PPARgamma), PFKFB3/iPFK2 is up-regulated by thiazolidinediones. In the present study, using PFKFB3/iPFK2-disrupted mice, the role of PFKFB3/iPFK2 in the anti-diabetic effect of PPARgamma activation was determined. In wild-type littermate mice, PPARgamma activation (i.e. treatment with rosiglitazone) restored euglycemia and reversed high fat diet-induced insulin resistance and glucose intolerance. In contrast, PPARgamma activation did not reduce high fat diet-induced hyperglycemia and failed to reverse insulin resistance and glucose intolerance in PFKFB3(+/-) mice. The lack of anti-diabetic effect in PFKFB3(+/-) mice was associated with the inability of PPARgamma activation to suppress adipose tissue lipolysis and proinflammatory cytokine production, stimulate visceral fat accumulation, enhance adipose tissue insulin signaling, and appropriately regulate adipokine expression. Similarly, in cultured 3T3-L1 adipocytes, knockdown of PFKFB3/iPFK2 lessened the effect of PPARgamma activation on stimulating lipid accumulation. Furthermore, PPARgamma activation did not suppress inflammatory signaling in PFKFB3/iPFK2-knockdown adipocytes as it did in control adipocytes. Upon inhibition of excessive fatty acid oxidation in PFKFB3/iPFK2-knockdown adipocytes, PPARgamma activation was able to significantly reverse inflammatory signaling and proinflammatory cytokine expression and restore insulin signaling. Together, these data demonstrate that PFKFB3/iPFK2 is critically involved in the anti-diabetic effect of PPARgamma activation.
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