Yamashita H., Takenoshita M., Sakurai M., Bruick R.K., Henzel W.J., Shillinglaw W., Arnot D., Uyeda K. A glucose-responsive transcription factor that regulates carbohydrate metabolism in the liver. and A.W. The fructose metabolism pathway is elegant for making the most of that short term situation with a variety of mechanisms. De novo Lipogenesis Protects Cancer Cells from Free Radicals and Chemotherapeutics by Promoting Membrane Lipid Saturation. High-fructose intake in healthy men is associated with characteristics of metabolic syndrome. 2022 Jul 19. doi: 10.1007/s10974-022-09623-3. The advantage of fructose degradation via KHK is to bypass PFK. Kawasaki T., Akanuma H., Yamanouchi T. Increased Fructose Concentrations in Blood and Urine in Patients With Diabetes. government site. Disclaimer, National Library of Medicine Monit. Arthritis Fructose consumption, as the combined intake of sucrose and HFCS, increased from 64 g/day in 1970 to 81 g/day in 1997 in the US. This fairly complex diagram is a reasonable summary of what happens in the liver to Fructose. Increased fructose consumption results in insulin resistance, which in turn increases insulin secretion in a compensatory manner. Differential subcellular distribution of glucose transporters GLUT16 and GLUT9 in human cancer: Ultrastructural localization of GLUT1 and GLUT5 in breast tumor tissues. Ketohexokinase: Expression and Localization of the Principal Fructose-metabolizing Enzyme. Feedback mechanism to create tissue Insulin resistance via IRS-1 (insulin receptor substrate-1). Accessibility Epidemiological studies show growing evidence that consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose) is associated with a high energy intake, increased body weight, and the occurrence of metabolic and cardiovascular disorders. Redox imbalance stress in diabetes mellitus: Role of the polyol pathway. Here, KHK could become an interesting therapeutic target. ; visualization, N.K. Before The Pathway of Fructose Metabolism There are two pathways for the metabolism of fructose; one occurs in muscle and adipose tissue, the other in liver. Almost exclusive Liver absorption via GLUT 2 receptors. Over the last few years, there were several studies describing the link between fructose consumption and the development of obesity [3,24,25,26,27]. As such, the fructose carbon backbone can enter the non-oxidative branch as glyceraldehyd-3-phosphate or fructose-6-phosphate, catalyzed by the transketolase (TKT) enzyme (Figure 2). It was shown that the microbiome of mice converts fructose to acetate. ATP is a molecule involved in energy transfer within cells. Dietary fructose feeds hepatic lipogenesis via microbiota-derived acetate. [Research on the intestinal absorption of hexoses. Immune effect by inhibiting phagocyte (white cell) activity. II. Comp. Liu H., Heaney A.P. The metabolism of starch and sucrose begins with D-fructose interacting with a D-glucose in a reversible reaction through a maltodextrin glucosidase resulting in a water molecule and a sucrose. Kidney Disease The ePub format is best viewed in the iBooks reader. They all act as Endothelium-Derived Relaxing Factor (EDRF) and have a vasodilatory effect through their action in the production of Nitric Oxide. This genetic disorder is asymptotic and harmless. Liver Disease The green diagram above reveals that the VLDLs are then ultimately converted into LDLs in the transport around the body. Thus in liver, fructose is metabolized instead by the fructose 1-phosphate pathway: Fructose is converted to fructose 1-phosphate by fructokinase with the use of an ATP. The increased fructose uptake resulted in an increased proliferation rate, colony growth, and enhanced migration and invasion. National Library of Medicine. Fructose metabolism as a common evolutionary pathway of - PubMed Epub 2015 Jun 12. The green pathway is related to the phosphorylation of Fructose and the by-product of this is Uric Acid. Behavioural Recent studies show that fructose-induced uric acid generation causes mitochondrial oxidative stress that stimulates fat accumulation independent of excessive caloric intake. The latter, in contrast to the products of aldolase, must be phosphorylated to function. Fructose is a major component of added sugars and is distinct from other sugars in its ability to cause intracellular ATP depletion, nucleotide turnover, and the generation of uric acid. Biochemistry. FBPase deficiency is a rare, autosomal recessive disorder affecting one of the key enzymes of gluconeogenesis. In glycolysis, aldolase-B does a lysis step that is different from aldolase. While virtually absent in our diet a few hundred years ago, fructose has now become a major constituent of our modern diet. Dr. Catherine Ellis, MD is an Endocrinology, Diabetes & Metabolism Specialist in Arlington, VA. Dr. Ellis has extensive experience in Osteoporosis & Screening, Thyroid Disorders, and Diabetes & Glucose Monitoring. When SORD is upregulated, AKR1B1 was decreased and KHK was upregulated. Federal government websites often end in .gov or .mil. Obrosova I.G. Preliminary analysis of C. salexigens genome suggests that fructose metabolism could proceed through the Entner-Doudoroff and Embden-Meyerhof . Ricciardelli C., Lokman N.A., Cheruvu S., Tan I.A., Ween M.P., Pyragius C.E., Ruszkiewicz A., Hoffmann P., Oehler M.K. Fructose degradation via KHK to GA3P consumes two ATP just as glucose in glycolysis. Res. Gerrits P.M., Tsalikian E. Diabetes and fructose metabolism. I. 1968 Dec 15;46(24):1300-8. doi: 10.1007/BF01747120. Pereira R., Botezelli J., da Cruz Rodrigues K., Mekary R., Cintra D., Pauli J., da Silva A., Ropelle E., de Moura L. Fructose Consumption in the Development of Obesity and the Effects of Different Protocols of Physical Exercise on the Hepatic Metabolism. De novo lipogenesis driven by fructose and glucose carbon. HHS Vulnerability Disclosure. The return of metabolism: Biochemistry and physiology of the pentose phosphate pathway. Accessibility Fig: Metabolism of Fructose. You may notice problems with Transport, metabolism, and endosomal trafficking-dependent regulation of intestinal fructose absorption. Because insulin and leptin, and possibly ghrelin, function as key signals to the central nervous system in the long-term regulation of energy balance, decreases of circulating insulin and leptin and increased ghrelin concentrations, as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose. Potischman N., McCulloch C.E., Byers T., Houghton L., Nemoto T., Graham S., Campbell T.C. As Hunter Gatherers we have a primitive survival instinct for finding sweetness in foods. National Library of Medicine. Both of these options provide an interesting perspective on cancer cell metabolism. Snaebjornsson M.T., Janaki-Raman S., Schulze A. Greasing the Wheels of the Cancer Machine: The Role of Lipid Metabolism in Cancer. Metabolism | No Fructose Dr. Catherine Ellis, MD - Endocrinology, Diabetes & Metabolism Furthermore, fructose is also involved in SREBF-mediated DNL gene expression. Gallagher E.J., LeRoith D. Obesity and Diabetes: The Increased Risk of Cancer and Cancer-Related Mortality. 2010;121:295-305; discussion 305-8. Fan J., Ye J., Kamphorst J.J., Shlomi T., Thompson C.B., Rabinowitz J.D. The https:// ensures that you are connecting to the After absorption, nevertheless, the metabolism of the two monosaccharides follows different pathways, since glucose can be used directly by the cells to produce energy in a variety of organs, while fructose is primarily metabolized in the liver, which takes up at least 50% of the initial fructose flux . Mate A, Barfull A, Hermosa AM, Planas JM, Vzquez CM. Unable to load your collection due to an error, Unable to load your delegates due to an error. Unable to load your collection due to an error, Unable to load your delegates due to an error. 1975 Sep;14(3):184-216. doi: 10.1007/BF02021198. Philadelphia: USA. Consequently, high expression of GLUT5 and enhanced fructose utilization are associated with poor outcomes and exacerbate leukemic phenotypes [11]. While glucose is directly metabolized by virtually every cell type in the human body, fructolysis is assumed to be mainly restricted to the liver. The actions of fructose are driven in part by vasopressin and the generation of uric acid. . 3 talking about this. In the US, the sole HFCS intake increased from 0.4 g/day per capita in 1970 to a maximum of 46.6 g/day in 1998, and reduced to 26.8 g/day of HFCS in 2019 [4]. In the following, we will describe the metabolic fates of fructose in humans and the key enzymes involved in fructose metabolism. Formation of Polyols by the Lens of the Rat with Sugar Cataract. Subsequently, we will highlight the link between fructose metabolism and cancer cell proliferation, focusing on how fructose is metabolized in different types of cancer, which enzymes are involved, and how fructose metabolism is associated with cancer development and outcome. The polyol pathway is interesting for fructose metabolism because it provides the means to either convert fructose to glucose or to endogenously produce fructose from glucose. National Institutes of Health. In liver, the cells contain mainly glucokinase instead of hexokinase and this enzyme phosphorylates only glucose. ACC: acetyl-CoA carboxylase; ACSS2: acyl-coenzyme A synthetase short-chain family member 2; ACLY: ATP citrate lyase; AKG: -ketoglutarate; FASN: fatty acid synthase; G3P: glycerol 3-phosphate; TCA: tricarboxylic acid cycle; TAG: triacylglyceride. Over time this can result in fibrosis and the ultimate situation of cirrhosis and liver failure. Online ahead of print. Contact. Nakagawa T., Lanaspa M.A., Millan I.S., Fini M., Rivard C.J., Sanchez-Lozada L.G., Andres-Hernando A., Tolan D.R., Johnson R.J. Fructose contributes to the Warburg effect for cancer growth. I. Although we will focus on the link between fructose metabolism and cancer, we will briefly mention other diseases affected by fructose metabolism, as some of them are known risk factors for cancer development. The so-called polyol pathway consists of two reversible reactions, with sorbitol as an intermediate (Figure 1). The authors declare no conflict of interest. The results are in line with experiments showing that KHK knockout mice are protected from fructose-induced fatty liver [98,99]. 8600 Rockville Pike, Bethesda, MD, 20894 USA. At the same time other animals right through to insects would be in the same environment and competition for this food source would have been significant. Fructose Metabolism - Microbe Notes Fructose and mannose metabolism - Reference pathway [ Pathway menu | Organism menu | Pathway entry | Image file | Help] Option. Godoy A., Ulloa V., Rodrguez F., Reinicke K., Yaez A.J., de los Angeles Garca M., Medina R.A., Carrasco M., Barberis S., Castro T., et al. Acute myeloid leukemic cells upregulate the serine synthesis pathway to metabolize fructose-derived carbons, and targeting PHGDH, a rate-limiting enzyme in the serine synthesis pathway, significantly reduces the tumor burden in the presence of high . The intake of fructose as monosaccharide increased from less than 0.5 g/day to more than 40 g/day [3]. [On the utilization and renal excretion of fructose during the long-term intravenous administration]. Obesity Int. This will prove challenging, as standard metabolic flux techniques (e.g., stable-isotope assisted metabolomics) will have difficulties to distinguish the polyol pathway flux from the normal glycolytic flux. The evidence is less compelling in humans, but high fructose intake has indeed been shown to cause dyslipidemia and to impair hepatic insulin sensitivity. show an unexpected metabolism of fructose in cancer cells. Enhanced Fructose Utilization Mediated by SLC2A5 Is a Unique Metabolic Feature of Acute Myeloid Leukemia with Therapeutic Potential. 2022 Oct;30(10):1917-1926. doi: 10.1002/oby.23540. Biochem J. THIRSTY FOR FRUCTOSE: Arginine Vasopressin, Fructose, and the Pathogenesis of Metabolic and Renal Disease. This site needs JavaScript to work properly. Sweet taste receptor signaling in beta cells mediates fructose - PubMed Because of this, the metabolism of fructose is much faster and less tightly controlled than the metabolism of glucose. Small intestine absorption via GLUT 5 gut receptors. This bypassing effect was recently observed in naked mole-rats by Park et al. Zamora-Leon S.P., Golde D.W., Concha I.I., Rivas C.I., Delgado-Lopez F., Baselga J., Nualart F., Vera J.C. It is worth underlining the importance of the non-oxidative branch for cancer cells, and it was shown that a G6PD deficiency does not reduce the risk of getting cancer [71], showing that NADPH requirements can be fulfilled by other pathways (e.g., serine-driven one-carbon metabolism [72]) and that the non-oxidative branch is sufficient to sustain nucleotide synthesis. 8600 Rockville Pike, Bethesda, MD, 20894 USA. Andres-Hernando A., Johnson R.J., Lanaspa M.A. Perspective: A Historical and Scientific Perspective of Sugar and Its Relation with Obesity and Diabetes. Kador P.F., Kinoshita J.H. We demonstrate that fructose activates sweet taste receptors (TRs) on beta cells and synergizes with glucos 8600 Rockville Pike, Bethesda, MD, 20894 USA. MeSH terms . Fructose uptake is mediated by GLUT5 and can be metabolized via different pathways: (1) phosphorylation via KHK to F1P, which is then hydrolyzed by aldolase B to DHAP and GA. Sucrose (sugar) is rapidly cleaved in to Glucose and Fructose. Entering glycolysis, F6P is phosphorylated to fructose-1,6-bisphosphate (F1,6BP) via phosphofructokinase (PFK). Fructose was initially thought to be advisable for patients with diabetes due to its low glycemic index. Entry of fructose carbon atoms into the glycolytic pathway in hepatocytes, kidney, and small intestine is outlined. Excess goes to the liver and is involved in Glycogen replenishment, Any further excess goes to Fatty Acid production and this is processed in to Fat storage, The Glucose effect on the pancreas promotes secretion of Insulin which acts on the Hypothalamus as a satiety agent (makes you less hungry), Acts on white cells involved in immunity and tissue damage homeostasis. Crescenzo R., Bianco F., Falcone I., Coppola P., Liverini G., Iossa S. Increased hepatic de novo lipogenesis and mitochondrial efficiency in a model of obesity induced by diets rich in fructose. Although the degradation of fructose shares many of the enzymes and metabolic intermediates with glucose metabolism through glycolysis, glucose and fructose are metabolized differently. Neuropathy John W. Pelley, Edward F. Goljan (2011). Besides bypassing PFK regulation and entering glycolysis for ATP production, endogenously produced fructose could enter several other pathways important for cancer cell physiology such as the hexosamine pathway [59], the pentose phosphate pathway [60], or de novo lipogenesis [61]. Clipboard, Search History, and several other advanced features are temporarily unavailable. AKR1B1: aldo-keto reductase family 1, member B1; ALDO: aldolase; G3P: glycerol 3-phosphate; GA3P: glyceraldehyde 3-phosphate; GLUT1: glucose transporter 1; GLUT5: fructose transporter; GPDH: glycerol 3-phosphate dehydrogenase; GPI: glucose-6-phosphate isomerase; HK: hexokinase; KHK: keto hexokinase; PFK: phosphofructokinase; SORD: sorbitol dehydrogenase; TCA: tricarboxylic acid cycle; TK: triose kinase; TPI: triose-phosphate isomerase. Goncalves M.D., Lu C., Tutnauer J., Hartman T.E., Hwang S.K., Murphy C.J., Pauli C., Morris R., Taylor S., Bosch K., et al. The polyol pathway is well known for its pathological implications in diabetes [40,41,42,43]. Themetabolismoffructosefromdietarysources is referred to as. With the discovery of the enzymatic conversion of glucose to fructose in 1957 [1], fructose is used as a supplement in the food industry. AKR1B1: aldo-keto reductase family 1, member B1; ALDO: aldolase; E4P: erythrose 4-phosphate; F6P: fructose 6-phosphate; G3P: glycerol 3-phosphate; GA3P: glyceraldehyde 3-phosphate; GLUT1: glucose transporter 1; GLUT5: fructose transporter; GPI: glucose-6-phosphate isomerase; HK: hexokinase; KHK: keto hexokinase; PFK: phosphofructokinase; SORD: sorbitol dehydrogenase; TCA: tricarboxylic acid cycle; TPI: triose-phosphate isomerase. Do thrifty genes exist? Liu H., Huang D., McArthur D.L., Boros L.G., Nissen N., Heaney A.P. Fructose metabolism as a common evolutionary pathway of survival Made with by Sagar Aryal. The increase in fat and glycogen driven by fructose metabolism is much greater than that observed with glucose alone and is consistent with a relative reduction in mitochondrial energy (ATP) production with preferential storage of the energy as a fuel 22, 24. MeSH TKT: transketolase; TALDO: transaldolase; G6PDH: glucose-6-phosphate deyhdrogenase; GSH: glutathione; GSSG: glutathione disulfide; 6PGL: 6-phosphogluconolactonase; 6PGDH: 6-phosphogluconate dehydrogenase; RPE: ribulose 5-phosphate 3-epimerase; RPI: ribose-5-phosphate isomerase; X5P: xylulose 5-phosphate. Using the non-oxidative branch of the PPP for ribose synthesis has the advantage that it is uncoupled from the generation of NADPH. The .gov means its official. Circulating fat is transported by Lipoproteins which vary in size and density. Here, glucose transporter 2 (GLUT2) is the main fructose transporter. From an energetic point of view, the degradation pathways from fructose and glucose to pyruvate do not differ. TNF then induced SREBF1 signaling in hepatocytes [100]. Recently, it was observed that fructose, even at a moderate dose, induces fatty acid synthesis and can enhance tumorigenesis in mice [92]. It has been suggested that hexose-phosphate metabolites are important for ChREBP activation [96,97], highlighting the importance of KHK in the fructose dependent activation of ChREBP. Smith, C. M., Marks, A. D., Lieberman, M. A., Marks, D. B., & Marks, D. B. Based on 13C-tracer experiments, it was shown in vitro that around 80% of ribonucleotides are derived from the non-oxidative PPP [66]. Hence, fructose metabolism is less tightly regulated and occurs at a much faster rate than glucose. Fructose and mannose metabolism [ Pathway menu | Organism menu | Pathway entry | Download KGML | Image file | Help] Option. already built in. Besides an increased demand of ribonucleotides, proliferating cancer cells require a constant supply of fatty acids for the biogenesis of more complex lipids (e.g., membrane lipids) [73]. Ras B., Comin B., Puigjaner J., Brandes J.L., Creppy E., Saboureau D., Ennamany R., Lee W.N.P., Boros L.G., Cascante M. Oxythiamine and dehydroepiandrosterone induce a G1 phase cycle arrest in Ehrlichs tumor cells through inhibition of the pentose cycle. In fructose-fed rats, it was observed that the expression levels of FASN and SCD1 were significantly increased compared to controls [91]. Furthermore, restoration of the FGF21 signaling pathway also led to increased expression of ATGL and HSL in WAT, which promotes lipolysis. Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism. Elegant Fructose (1/2 of Sugar) metabolism to support that primitive addiction. KHK phosphorylates fructose to fructose-1-phosphate (F1P), which is then hydrolyzed via aldolase B to dihydroxyacetone phosphate (DHAP) and glyceraldehyde (GA) (Figure 1). While there is mounting experimental evidence showing the connection of aldo reductases and cancer, little is known about the connection between SORD and cancer. 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