ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2015
Fructose-induced increases in expression of intestinal fructolytic and gluconeogenic genes are regulated by GLUT5 and KHK.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Chronic Fructose Substitution for Glucose or Sucrose in Food or Beverages and Metabolic Outcomes: An Updated Systematic Review and Meta-Analysis.Frontiers in nutrition · 2021Pooled it
- Dietary Fructose and Palmitic Acid Induce Shared and Divergent Transcriptional Responses in the Larval Midgut ofCurrent issues in molecular biology · 2026Article
- The association between high fructose corn syrup and the development of type-2 diabetes.Frontiers in clinical diabetes and healthcare · 2026Review
- Fructose uptake by brown adipose tissue is independent of carbohydrate response element-binding protein and does not cause elevatedActa biochimica et biophysica Sinica · 2025Article
- Fructose catabolism and its metabolic effects: Exploring host-microbiota interactions and the impact of ethnicity.The Journal of physiology · 2025Review
- Fructose Malabsorption, Gut Microbiota and Clinical Consequences: A Narrative Review of the Current Evidence.Life (Basel, Switzerland) · 2025Review
- Fructose metabolism and its roles in metabolic diseases, inflammatory diseases, and cancer.Molecular biomedicine · 2025Review
- Mindful Eating: A Deep Insight Into Fructose Metabolism and Its Effects on Appetite Regulation and Brain Function.Journal of nutrition and metabolism · 2025Review
- Fructose Metabolism in Cancer: Molecular Mechanisms and Therapeutic Implications.International journal of medical sciences · 2025Review
- Magnolol Inhibits High Fructose-Induced Podocyte Inflammation via Downregulation of TKFC/Sp1/HDAC4/Notch1 Activation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Exosomal circSIPA1L3-mediated intercellular communication contributes to glucose metabolic reprogramming and progression of triple negative breast cancer.Molecular cancer · 2024Article
- Alternative splicing and related RNA binding proteins in human health and disease.Signal transduction and targeted therapy · 2024Review
- GLUT5: structure, functions, diseases and potential applications.Acta biochimica et biophysica Sinica · 2023Review
- Fructose drives de novo lipogenesis affecting metabolic health.The Journal of endocrinology · 2023Review
- Review
- Dietary Fructose and Fructose-Induced Pathologies.Annual review of nutrition · 2022Review
- Gene variants of the SLC2A5 gene encoding GLUT5, the major fructose transporter, do not contribute to clinical presentation of acquired fructose malabsorption.BMC gastroenterology · 2022Article
- Article
- Gut Microbiome Alterations and Hepatic Metabolic Flexibility in the Gansu Zokor,Frontiers in cardiovascular medicine · 2022Article
- Molecular aspects of fructose metabolism and metabolic disease.Cell metabolism · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Marked increases in fructose consumption have been tightly linked to metabolic diseases. One-third of ingested fructose is metabolized in the small intestine, but the underlying mechanisms regulating expression of fructose-metabolizing enzymes are not known. We used genetic mouse models to test the hypothesis that fructose absorption via glucose transporter protein, member 5 (GLUT5), metabolism via ketohexokinase (KHK), as well as GLUT5 trafficking to the apical membrane via the Ras-related protein in brain 11a (Rab11a)-dependent endosomes are required for the regulation of intestinal fructolytic and gluconeogenic enzymes. Fructose feeding increased the intestinal mRNA and protein expression of these enzymes in the small intestine of adult wild-type (WT) mice compared with those gavage fed with lysine or glucose. Fructose did not increase expression of these enzymes in the GLUT5 knockout (KO) mice. Blocking intracellular fructose metabolism by KHK ablation also prevented fructose-induced upregulation. Glycolytic hexokinase I expression was similar between WT and GLUT5- or KHK-KO mice and did not vary with feeding solution. Gavage feeding with the fructose-specific metabolite glyceraldehyde did not increase enzyme expression, suggesting that signaling occurs before the hydrolysis of fructose to three-carbon compounds. Impeding GLUT5 trafficking to the apical membrane using intestinal epithelial cell-specific Rab11a-KO mice impaired fructose-induced upregulation. KHK expression was uniformly distributed along the villus but was localized mainly in the basal region of the cytosol of enterocytes. The feedforward upregulation of fructolytic and gluconeogenic enzymes specifically requires GLUT5 and KHK and may proactively enhance the intestine's ability to process anticipated increases in dietary fructose concentrations.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.