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KHK encodes ketohexokinase that catalyzes conversion of fructose to fructose-1-phosphate.
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This studies provided the first evidence that fructokinase modulates vasopressin (show AVP Proteins) synthesis in the SON and secretion from the posterior pituitary into circulation.
Fructokinase knockout mice were protected from renal injury both at baseline and after high salt intake (3 wk) compared with wild-type mice. This was associated with higher levels of active (phosphorylated serine 1177) endothelial nitric oxide synthase (show NOS3 Proteins) in their kidneys.
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.
Significant levels of blood fructose are maintained independent of dietary fructose, KHK, and GLUT5, probably by endogenous synthesis of fructose.
myocardial hypoxia actuates fructose metabolism in human and mouse models of pathological cardiac hypertrophy through hypoxia-inducible factor 1alpha (HIF1alpha (show HIF1A Proteins)) activation of SF3B1 (show SF3B1 Proteins) and SF3B1 (show SF3B1 Proteins)-mediated splice switching of KHK-A to KHK-C
Fructokinase-knockout mice with delayed hydration were protected from renal injury. Thus, recurrent dehydration can induce renal injury via a fructokinase-dependent mechanism, likely from the generation of endogenous fructose via the polyol pathway.
This study demonstrates that blocking KHK and redirecting fructose metabolism to alternative pathways is an effective way to prevent visceral obesity and insulin (show INS Proteins) resistance induced by high fructose, a widespread component of Western diets.
These studies identify fructokinase as a novel mediator of diabetic nephropathy and document a novel role for endogenous fructose production, or fructoneogenesis, in driving renal disease.
High-fat and high-sucrose (western) diet induces steatohepatitis that is dependent on fructokinase.
Fructose-induced metabolic syndrome is prevented in mice lacking both fructokinase B and A but is exacerbated in mice lacking fructokinase A.
Data indicate metabolic enzymes NAD kinase (show NADK Proteins) and ketohexokinase as candidate metabolic gene targets, and the chromatin remodeling protein INO80C (show INO80C Proteins) as a tumor suppressor in KRAS(MUT (show MUT Proteins)) colorectal tumor xenograft.
Angelica archangelica, Garcinia mangostana, Petroselinum crispum, and Scutellaria baicalensis were the top four botanical candidiates identified with inhibitory activity against ketohexokinase-C.
compared with normal hepatocytes, hepatocellular carcinoma (HCC (show FAM126A Proteins)) cells markedly reduce the rate of fructose metabolism and the level of reactive oxygen species, as a result of a c-Myc (show MYC Proteins)-dependent and heterogeneous nuclear ribonucleoprotein (show PCBP2 Proteins) (hnRNP (show HNRNPC Proteins)) H1- and H2-mediated switch from expression of the high-activity fructokinase (KHK)-C to the low-activity KHK-A isoform.
myocardial hypoxia actuates fructose metabolism in human and mouse models of pathological cardiac hypertrophy through hypoxia-inducible factor 1alpha (HIF1alpha (show HIF1A Proteins)) activation of SF3B1 (show SF3B2 Proteins) and SF3B1 (show SF3B2 Proteins)-mediated splice switching of KHK-A to KHK-C
This study determined if single nucleotide polymorphisms in genes involved in fructose transport,SLC2A2 and SLC2A5 and metabolism, etohexokinase affect inter-individual variability in metabolic phenotypes.
In human hepatocytes uric acid up-regulates KHK expression thus leading to the amplification of the lipogenic effects of fructose.
ketohexokinase-A serves an unknown physiologic function that remains intact in essential fructosuria.
The expression of ketohexokinase is diminished in human clear cell type of renal cell carcinoma (show MOK Proteins)
Ketohexokinase-dependent metabolism of fructose induces proinflammatory mediators in proximal tubular cells.
This gene encodes ketohexokinase that catalyzes conversion of fructose to fructose-1-phosphate. The product of this gene is the first enzyme with a specialized pathway that catabolizes dietary fructose. Alternatively spliced transcript variants encoding different isoforms have been identified.
, hepatic fructokinase