ArticleScientific reports2016
Glucose and Palmitate Differentially Regulate PFKFB3/iPFK2 and Inflammatory Responses in Mouse Intestinal Epithelial Cells.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- PFKFB3 alleviates the advancement ofFrontiers in cellular and infection microbiology · 2025Article
- Cold Exposure Regulates Hepatic Glycogen and Lipid Metabolism in Newborn Goats.International journal of molecular sciences · 2023Article
- Two weeks of high glucose intake is enough to induce intestinal mucosal damage and disturb the balance of the gut microbiota of rats.Biomedical reports · 2023Article
- Methionine- and Choline-Deficient Diet-Induced Nonalcoholic Steatohepatitis Is Associated with Increased Intestinal Inflammation.The American journal of pathology · 2021Article
- Oleate Prevents Palmitate-Induced Mitochondrial Dysfunction in Chondrocytes.Frontiers in physiology · 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
- Short-Term Diet Induced Changes in the Central and Circulating IGF Systems Are Sex Specific.Frontiers in endocrinology · 2020Article
- PFKFB3, a key glucose metabolic enzyme regulated by pathogen recognition receptor TLR4 in liver cells.Therapeutic advances in endocrinology and metabolism · 2020Article
- Diet Composition for the Management of Obesity and Obesity-related Disorders.Journal of diabetes mellitus and metabolic syndrome · 2018Article
- Nutritional approaches for managing obesity-associated metabolic diseases.The Journal of endocrinology · 2017Review
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
The gene PFKFB3 encodes for inducible 6-phosphofructo-2-kinase, a glycolysis-regulatory enzyme that protects against diet-induced intestine inflammation. However, it is unclear how nutrient overload regulates PFKFB3 expression and inflammatory responses in intestinal epithelial cells (IECs). In the present study, primary IECs were isolated from small intestine of C57BL/6J mice fed a low-fat diet (LFD) or high-fat diet (HFD) for 12 weeks. Additionally, CMT-93 cells, a cell line for IECs, were cultured in low glucose (LG, 5.5 mmol/L) or high glucose (HG, 27.5 mmol/L) medium and treated with palmitate (50 μmol/L) or bovine serum albumin (BSA) for 24 hr. These cells were analyzed for PFKFB3 and inflammatory markers. Compared with LFD, HFD feeding decreased IEC PFKFB3 expression and increased IEC proinflammatory responses. In CMT-93 cells, HG significantly increased PFKFB3 expression and proinflammatory responses compared with LG. Interestingly, palmitate decreased PFKFB3 expression and increased proinflammatory responses compared with BSA, regardless of glucose concentrations. Furthermore, HG significantly increased PFKFB3 promoter transcription activity compared with LG. Upon PFKFB3 overexpression, proinflammatory responses in CMT-93 cells were decreased. Taken together, these results indicate that in IECs glucose stimulates PFKFB3 expression and palmitate contributes to increased proinflammatory responses. Therefore, PFKFB3 regulates IEC inflammatory status in response to macronutrients.
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