A Role for Fructose Metabolism in Development of Sheep and Pig Conceptuses

2021 ◽  
pp. 49-62 ◽  
Author(s):  
Robyn M. Moses ◽  
Avery C. Kramer ◽  
Heewon Seo ◽  
Guoyao Wu ◽  
Gregory A. Johnson ◽  
...  
Keyword(s):  
Fructose Metabolism

Fructose metabolism in hepatocytes: primary cells or cell lines?

2007 ◽  
Vol 45 (01) ◽  
Author(s):  
T Speicher ◽  
G Künstle ◽  
A Wendel
Keyword(s):  
Cell Lines ◽  
Primary Cells ◽  
Fructose Metabolism

scholarly journals D-Glyceric Acidemia: An Inborn Error Associated with Fructose Metabolism

1987 ◽  
Vol 21 (5) ◽  
pp. 502-506 ◽  
Author(s):  
M Duran ◽  
F A Beemer ◽  
L Bruinvis ◽  
D Ketting ◽  
S K Wadman
Keyword(s):  
Inborn Error ◽  
Fructose Metabolism

Fructose Metabolism

1954 ◽  
Vol 30 (9) ◽  
pp. 902
Author(s):  
Kopilovich Shai
Keyword(s):  
Fructose Metabolism

scholarly journals Dietary Fructose Metabolism By Splanchnic Organs: Size Matters

2018 ◽  
Vol 27 (3) ◽  
pp. 483-485 ◽  
Author(s):  
Javier T. Gonzalez ◽  
James A. Betts
Keyword(s):  
Fructose Metabolism ◽  
Dietary Fructose

scholarly journals Co‐immunolocalizing proteins involved in fructose metabolism and calcitriol regulation in the rat kidney

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Marline Dorcinvil ◽  
Veronique Douard ◽  
Luke Fritzky ◽  
David Lagunoff ◽  
Yves Sabbagh ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Fructose Metabolism

scholarly journals Endogenous Fructose Metabolism Could Explain the Warburg Effect and the Protection of SGLT2 Inhibitors in Chronic Kidney Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Takahiko Nakagawa ◽  
Laura G. Sanchez-Lozada ◽  
Ana Andres-Hernando ◽  
Hideto Kojima ◽  
Masato Kasahara ◽  
...  
Keyword(s):  
Uric Acid ◽  
Kidney Disease ◽  
Warburg Effect ◽  
Communicable Diseases ◽  
Sglt2 Inhibitors ◽  
Biologically Active ◽  
Low Grade ◽  
Non Communicable Diseases ◽  
Fructose Metabolism ◽  
The Warburg Effect

Chronic low-grade inflammation underlies the pathogenesis of non-communicable diseases, including chronic kidney diseases (CKD). Inflammation is a biologically active process accompanied with biochemical changes involving energy, amino acid, lipid and nucleotides. Recently, glycolysis has been observed to be increased in several inflammatory disorders, including several types of kidney disease. However, the factors initiating glycolysis remains unclear. Added sugars containing fructose are present in nearly 70 percent of processed foods and have been implicated in the etiology of many non-communicable diseases. In the kidney, fructose is transported into the proximal tubules via several transporters to mediate pathophysiological processes. Fructose can be generated in the kidney during glucose reabsorption (such as in diabetes) as well as from intra-renal hypoxia that occurs in CKD. Fructose metabolism also provides biosynthetic precursors for inflammation by switching the intracellular metabolic profile from mitochondrial oxidative phosphorylation to glycolysis despite the availability of oxygen, which is similar to the Warburg effect in cancer. Importantly, uric acid, a byproduct of fructose metabolism, likely plays a key role in favoring glycolysis by stimulating inflammation and suppressing aconitase in the tricarboxylic acid cycle. A consequent accumulation of glycolytic intermediates connects to the production of biosynthetic precursors, proteins, lipids, and nucleic acids, to meet the increased energy demand for the local inflammation. Here, we discuss the possibility of fructose and uric acid may mediate a metabolic switch toward glycolysis in CKD. We also suggest that sodium-glucose cotransporter 2 (SGLT2) inhibitors may slow the progression of CKD by reducing intrarenal glucose, and subsequently fructose levels.

scholarly journals Ketohexokinase knockout mice, a model for essential fructosuria, exhibit altered fructose metabolism and are protected from diet-induced metabolic defects

2018 ◽  
Vol 315 (3) ◽  
pp. E386-E393 ◽  
Author(s):  
Corin O. Miller ◽  
Xiaodong Yang ◽  
Ku Lu ◽  
Jin Cao ◽  
Kithsiri Herath ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
De Novo ◽  
Liver Weight ◽  
De Novo Lipogenesis ◽  
Chow Diet ◽  
Fructose Metabolism ◽  
Metabolic Defects ◽  
Glucose And Lipid Metabolism ◽  
High Fructose ◽  
Altered Glucose

Fructose consumption in humans and animals has been linked to enhanced de novo lipogenesis, dyslipidemia, and insulin resistance. Hereditary deficiency of ketohexokinase (KHK), the first enzymatic step in fructose metabolism, leads to essential fructosuria in humans, characterized by elevated levels of blood and urinary fructose following fructose ingestion but is otherwise clinically benign. To address whether KHK deficiency is associated with altered glucose and lipid metabolism, a Khk knockout (KO) mouse line was generated and characterized. NMR spectroscopic analysis of plasma following ingestion of [6-13C] fructose revealed striking differences in biomarkers of fructose metabolism. Significantly elevated urine and plasma 13C-fructose levels were observed in Khk KO vs. wild-type (WT) control mice, as was reduced conversion of 13C-fructose into plasma 13C-glucose and 13C-lactate. In addition, the observation of significant levels of fructose-6-phosphate in skeletal muscle tissue of Khk KO, but not WT, mice suggests a potential mechanism, whereby fructose is metabolized via muscle hexokinase in the absence of KHK. Khk KO mice on a standard chow diet displayed no metabolic abnormalities with respect to ambient glucose, glucose tolerance, body weight, food intake, and circulating trigylcerides, β-hydroxybutyrate, and lactate. When placed on a high-fat and high-fructose (HF/HFruc) diet, Khk KO mice had markedly reduced liver weight, triglyceride levels, and insulin levels. Together, these results suggest that Khk KO mice may serve as a good model for essential fructosuria in humans and that inhibition of KHK offers the potential to protect from diet-induced hepatic steatosis and insulin resistance.

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