ArticleThe Journal of clinical investigation2018
Ketohexokinase C blockade ameliorates fructose-induced metabolic dysfunction in fructose-sensitive mice.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 119 citations in OpenAlex.
- Development landscape of ketohexokinase-C (KHK-C) inhibitors for fructose-driven metabolic disorders: from hit discovery to clinical trials.RSC medicinal chemistry · 2026Review
- Glyoxalase 1 loss reduces fatty liver but impairs glucose handling in male mice.Physiological reports · 2026Article
- Fructose induces PERK-dependent ER stress and mitochondrial dysfunction via nucleotide depletion in clear cell renal cell carcinoma.Cell death & disease · 2026Article
- Fructose 1-phosphate inhibits mannose phosphate isomerase to suppress hepatocellular carcinogenesis.Signal transduction and targeted therapy · 2026Article
- Fructose: metabolic signal and modern hazard.Nature metabolism · 2026Review
- Altered hepatic metabolism in Down syndrome.Cell reports · 2026Article
- The effect of liver-specific ketohexokinase deletion on the intestinal-liver-kidney axis in high-fructose-induced metabolic syndrome mice.Acta biochimica et biophysica Sinica · 2026Article
- New Insight Into Male Infertility: Deviation From Basic Tenets of Life.Oxidative medicine and cellular longevity · 2026Review
- Progress in Understanding the Regulation of Glucose and Fructose Metabolism.Annual review of nutrition · 2025Review
- LY3522348, A New Ketohexokinase Inhibitor: A First-in-Human Study in Healthy Adults.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025Article
- Do microglia metabolize fructose in Alzheimer's disease?Journal of neuroinflammation · 2025Review
- Safety and efficacy of pharmacological inhibition of ketohexokinase in hereditary fructose intolerance.The Journal of clinical investigation · 2025Article
- Pharmacophore-based virtual screening andFrontiers in pharmacology · 2025Article
- Fructose Metabolism in Cancer: Molecular Mechanisms and Therapeutic Implications.International journal of medical sciences · 2025Review
- Aldolase B Deficient Mice Are Characterized by Hepatic Nucleotide Sugar Abnormalities.Journal of inherited metabolic disease · 2025Article
- Knockdown of ketohexokinase versus inhibition of its kinase activity exert divergent effects on fructose metabolism.JCI insight · 2024Article
- CYP2E1 in 1,4-dioxane metabolism and liver toxicity: insights from CYP2E1 knockout mice study.Archives of toxicology · 2024Article
- Hepatic glucokinase regulatory protein and carbohydrate response element binding protein attenuation reduce de novo lipogenesis but do not mitigate intrahepatic triglyceride accumulation in Aldob deficiency.Molecular metabolism · 2024Article
- Activation of AMPD2 drives metabolic dysregulation and liver disease in mice with hereditary fructose intolerance.Communications biology · 2024Article
- Disruption in glutathione metabolism and altered energy production in the liver and kidney after ischemic acute kidney injury in mice.Scientific reports · 2024Article
21 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Increasing evidence suggests a role for excessive intake of fructose in the Western diet as a contributor to the current epidemics of metabolic syndrome and obesity. Hereditary fructose intolerance (HFI) is a difficult and potentially lethal orphan disease associated with impaired fructose metabolism. In HFI, the deficiency of aldolase B results in the accumulation of intracellular phosphorylated fructose, leading to phosphate sequestration and depletion, increased adenosine triphosphate (ATP) turnover, and a plethora of conditions that lead to clinical manifestations such as fatty liver, hyperuricemia, Fanconi syndrome, and severe hypoglycemia. Unfortunately, there is currently no treatment for HFI, and avoiding sugar and fructose has become challenging in our society. In this report, through use of genetically modified mice and pharmacological inhibitors, we demonstrate that the absence or inhibition of ketohexokinase (Khk), an enzyme upstream of aldolase B, is sufficient to prevent hypoglycemia and liver and intestinal injury associated with HFI. Herein we provide evidence for the first time to our knowledge of a potential therapeutic approach for HFI. Mechanistically, our studies suggest that it is the inhibition of the Khk C isoform, not the A isoform, that protects animals from HFI.
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Registered trials
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.