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 Fructose-responsive genes in the small intestine of neonatal rats

2004 ◽  
Vol 18 (2) ◽  
pp. 206-217 ◽  
Author(s):  
Xue-Lin Cui ◽  
Patricia Soteropoulos ◽  
Peter Tolias ◽  
Ronaldo P. Ferraris
Keyword(s):  
Small Intestine ◽  
De Novo ◽  
Mrna Abundance ◽  
Metabolic Intermediate ◽  
Gluconeogenic Enzymes ◽  
Fructose Metabolism ◽  
High Fructose ◽  
Fructose 1,6 Bisphosphatase ◽  
Dietary Fructose

The intestinal brush border fructose transporter GLUT5 (SLC2A5) typically appears in rats after weaning is completed. However, precocious consumption of dietary fructose or in vivo perfusion for 4 h of the small intestine with high fructose (HF) specifically stimulates de novo synthesis of GLUT5 mRNA and protein before weaning is completed. Intermediary signals linking the substrate, fructose, to GLUT5 transcription are not known but should also respond to fructose perfusion. Hence, we used microarray hybridization and RT-PCR to identify genes whose expression levels change during HF relative to high-glucose (HG) perfusion. Expression of GLUT5 and NaPi2b, the intestinal Na+-dependent phosphate transporter, dramatically increased and decreased, respectively, with HF perfusion for 4 h. Expression of >20 genes, including two key gluconeogenic enzymes, glucose-6-phosphatase (G6P) and fructose-1,6-bisphosphatase, also increased markedly, along with fructose-2,6-bisphosphatase, an enzyme unique to fructose metabolism and regulating fructose-1,6-bisphosphatase activity. GLUT5 and G6P mRNA abundance, which increased dramatically with HF relative to HG, α-methylglucose, and normal Ringer perfusion, may be tightly and specifically linked to changes in intestinal luminal fructose but not glucose concentrations. G6P but not GLUT5 mRNA abundance increased after just 20 min of HF perfusion. This cluster of gluconeogenic enzymes and their common metabolic intermediate fructose-6-phosphate may regulate fructose metabolism and GLUT5 expression in the small intestine.

Non-dietary Fructose Metabolism Contributes to the Warburg effect in Cancers

2020 ◽  
Author(s):  
Bing Han ◽  
Lu Wang ◽  
Meilin Wei ◽  
Cynthia Rajani ◽  
Runming Wei ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Warburg Effect ◽  
Glucose Transporter ◽  
Self Control ◽  
Metabolic Reprogramming ◽  
Atp Production ◽  
Fructose Metabolism ◽  
Energy Needs ◽  
Dietary Fructose ◽  
The Warburg Effect

AbstractFructose metabolism is increasingly recognized as a preferred energy source for cancer cell proliferation. However, dietary fructose rarely enters the bloodstream. Therefore, it remains unclear how cancer cells acquire a sufficient amount of fructose to supplement their energy needs. Here we report that the cancer cells can convert glucose into fructose through intra- and extracellular polyol pathways. The fructose metabolism bypasses normal aerobic respiration’s self-control to supply excessive metabolites to glycolysis and causes the Warburg effect. Inhibition of fructose production drastically suppressed glycolysis and ATP production in cancers. Furthermore, we determined that a glucose transporter, SLC2A8/GLUT8, exports intracellular fructose to other cells in the tumor microenvironment. Taken together, our study identified overlooked fructose resources for cancer cells as an essential part of their metabolic reprogramming and caused the Warburg effect.Statement of SignificanceOur findings in this study suggest that the Warburg effect is actually achieved by means of fructose metabolism, instead of glucose metabolism alone. Fructose metabolism results in accelerated glycolysis and an increased amount of ATP and key intermediates for anabolic metabolism.

scholarly journals The Contribution of Dietary Fructose to Non-alcoholic Fatty Liver Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Siyu Yu ◽  
Chunlin Li ◽  
Guang Ji ◽  
Li Zhang
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
De Novo ◽  
Close Association ◽  
Metabolic Phenotype ◽  
Alcoholic Fatty Liver ◽  
Fructose Metabolism ◽  
Dietary Fructose ◽  
Alcoholic Fatty Liver Disease

Fructose, especially industrial fructose (sucrose and high fructose corn syrup) is commonly used in all kinds of beverages and processed foods. Liver is the primary organ for fructose metabolism, recent studies suggest that excessive fructose intake is a driving force in non-alcoholic fatty liver disease (NAFLD). Dietary fructose metabolism begins at the intestine, along with its metabolites, may influence gut barrier and microbiota community, and contribute to increased nutrient absorption and lipogenic substrates overflow to the liver. Overwhelming fructose and the gut microbiota-derived fructose metabolites (e.g., acetate, butyric acid, butyrate and propionate) trigger the de novo lipogenesis in the liver, and result in lipid accumulation and hepatic steatosis. Fructose also reprograms the metabolic phenotype of liver cells (hepatocytes, macrophages, NK cells, etc.), and induces the occurrence of inflammation in the liver. Besides, there is endogenous fructose production that expands the fructose pool. Considering the close association of fructose metabolism and NAFLD, the drug development that focuses on blocking the absorption and metabolism of fructose might be promising strategies for NAFLD. Here we provide a systematic discussion of the underlying mechanisms of dietary fructose in contributing to the development and progression of NAFLD, and suggest the possible targets to prevent the pathogenetic process.

scholarly journals Fructose Metabolism in Cancer

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2635
Author(s):  
Nils Krause ◽  
Andre Wegner
Keyword(s):  
Metabolic Pathways ◽  
Polyol Pathway ◽  
Cancer Cell Proliferation ◽  
Nucleotide Synthesis ◽  
Metabolic Intermediates ◽  
Fructose Metabolism ◽  
Fructose Intake ◽  
Endogenous Production ◽  
Increased Risk ◽  
Dietary Fructose

The interest in fructose metabolism is based on the observation that an increased dietary fructose consumption leads to an increased risk of obesity and metabolic syndrome. In particular, obesity is a known risk factor to develop many types of cancer and there is clinical and experimental evidence that an increased fructose intake promotes cancer growth. The precise mechanism, however, in which fructose induces tumor growth is still not fully understood. In this article, we present an overview of the metabolic pathways that utilize fructose and how fructose metabolism can sustain cancer cell proliferation. Although the degradation of fructose shares many of the enzymes and metabolic intermediates with glucose metabolism through glycolysis, glucose and fructose are metabolized differently. We describe the different metabolic fates of fructose carbons and how they are connected to lipogenesis and nucleotide synthesis. In addition, we discuss how the endogenous production of fructose from glucose via the polyol pathway can be beneficial for cancer cells.

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 Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nicholas Jones ◽  
Julianna Blagih ◽  
Fabio Zani ◽  
April Rees ◽  
David G. Hill ◽  
...  
Keyword(s):  
Oxidative Metabolism ◽  
Mononuclear Phagocytes ◽  
Alcoholic Fatty Liver ◽  
Lps Challenge ◽  
Fructose Intake ◽  
Mouse Macrophages ◽  
Dietary Fructose ◽  
Monocytes And Macrophages ◽  
Developed World

AbstractFructose intake has increased substantially throughout the developed world and is associated with obesity, type 2 diabetes and non-alcoholic fatty liver disease. Currently, our understanding of the metabolic and mechanistic implications for immune cells, such as monocytes and macrophages, exposed to elevated levels of dietary fructose is limited. Here, we show that fructose reprograms cellular metabolic pathways to favour glutaminolysis and oxidative metabolism, which are required to support increased inflammatory cytokine production in both LPS-treated human monocytes and mouse macrophages. A fructose-dependent increase in mTORC1 activity drives translation of pro-inflammatory cytokines in response to LPS. LPS-stimulated monocytes treated with fructose rely heavily on oxidative metabolism and have reduced flexibility in response to both glycolytic and mitochondrial inhibition, suggesting glycolysis and oxidative metabolism are inextricably coupled in these cells. The physiological implications of fructose exposure are demonstrated in a model of LPS-induced systemic inflammation, with mice exposed to fructose having increased levels of circulating IL-1β after LPS challenge. Taken together, our work underpins a pro-inflammatory role for dietary fructose in LPS-stimulated mononuclear phagocytes which occurs at the expense of metabolic flexibility.

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