Disease relevance of fructose

• When more stringent restriction of dietary fructose was instituted (approximately 40 mg per kilogram of body weight per day), growth velocity increased from the 25th to the 97th percentile in one child and from well below the 3d to above the 75th percentile in the other [1].
• When restriction of dietary fructose was experimentally relaxed (from 10 to 250 mg per kilogram per day), neither boy had symptoms, hypoglycemia, or evidence of hepatic or renal dysfunction, but both had sustained hyperuricemia and hyperuricosuria and increases in the plasma concentration and urinary excretion of magnesium [1].
• Hereditary fructose intolerance (HFI) is a human autosomal recessive disease caused by a deficiency of aldolase B that results in an inability to metabolize fructose and related sugars [2].
• Nerve glucose, fructose, sorbitol, myo-inositol, and fiber degeneration and regeneration in diabetic neuropathy [3].
• Intravenous infusions of manose or B-hydroxybutyrate, metabolic fuels which can be oxidized by brain, abolished adrenal discharge of epinephrine in rats during insulin-induced hypoglycemia, whereas infusion of fructose, a sugar which does not cross the blood-brain barrier, did not [4].

Psychiatry related information on fructose

• The associations of glycemic load and fructose intakes with pancreatic cancer risk were most apparent among women with elevated body mass index (>or=25 kg/m(2)) or with low physical activity [5].
• Under the same conditions, mutant Q200E exhibits cooperative behavior only at much higher concentration of fructose 6-phosphate [6].
• A form of phosphofructokinase (PFK) from Ascaris suum desensitized to hysteresis in the reaction time course and ATP allosteric inhibition has been used to study the activation by fructose 2,6-bisphosphate (F26P2) at varied pH in both reaction directions [7].
• The present study examined the effect of chronic fluoxetine administration on the feeding behavior of fructose-fed rats [8].
• METHODS: The authors' aim was to study the possible association between malabsorption of sugars (lactose and fructose) and depressive symptoms in adolescent patients of Spanish origin [9].

High impact information on fructose

• On repeat biopsy, six diabetics, treated for a year with the aldose reductase inhibitor sorbinil, had decreased endoneurial levels of sorbitol (P less than 0.01) and fructose (0.05 less than P less than 0.1), but unchanged levels of myo-inositol [3].
• Catalytic deficiency of human aldolase B in hereditary fructose intolerance caused by a common missense mutation [2].
• Pseudodominant transmission of fructose intolerance in an adult and three offspring: Heterozygote detection by intestinal biopsy [10].
• In the reverse reaction, the kinetics of wild-type and the Ser 72 mutant with respect to fructose 1,6-bisphosphate are hyperbolic, whereas those of the Ser 162 and Ser 243 mutants are sigmoidal [11].
• Arginines 162 and 243 reach into the active site from an adjacent subunit and interact with the cooperative substrate fructose 6-phosphate [11].

Chemical compound and disease context of fructose

• In the acute bile fistula rat, biliary cholesterol output was 700% increased by diosgenin and 50% decreased by fructose [12].
• An animal model was used to determine the basis for the increase in purine biosynthesis that results from hepatic depletion of purine nucleotides, such as seen in patients with type I glycogen storage disease or following fructose administration [13].
• The causes of diarrhea in 11 patients consenting to this study were microscopic colitis, steatorrhea secondary to exocrine pancreatic insufficiency, dietary lactose or fructose malabsorption, anal sphincter dysfunction causing fecal incontinence, and the irritable bowel syndrome [14].
• First reported in 1956, hereditary fructose intolerance (HFI) illustrates vividly how interactions between genes and nutrients can influence taste preferences; the disease also reflects the ascendancy of sucrose and fructose as energy sources and as the world's principal sweeteners [15].
• The role of phosphoenolpyruvate in the simultaneous uptake of fructose and 2-deoxyglucose by Escherichia coli [16].

Biological context of fructose

• Metabolic effects of dietary fructose and sucrose in types I and II diabetic subjects [17].
• Metabolic depletion of ATP by fructose inversely controls CD95- and tumor necrosis factor receptor 1-mediated hepatic apoptosis [18].
• Addition of equimolar amounts of glucose or mannose, but not of fructose, galactose, fucose, or glucosamine, to medium containing 50 mM 2-dG results in substantial reversal of the inhibitory effect of 2-dG on Fc and C3 receptor mediated phagocytosis [19].
• It predisposes to insulin resistance induced by high fructose and partially protects from that induced by high-fat diets [20].
• The concentration requirements for glucose, mannose, and fructose by CM-injured L1210 cells correlated with the concentrations required to support maximal glycolysis of these sugars by other murine ascites cells [21].

Anatomical context of fructose

• ATP was depleted either in primary hepatocytes or in vivo by various phosphate-trapping carbohydrates such as fructose [18].
• Using a cDNA probe complementary to rat aldolase B mRNA, we determined the amount of cytoplasmic RNAs in the liver, kidney, and small intestine of normal, adrenalectomized, thyroidectomized, diabetic, and glucagon- or cAMP-treated animals refed either a fructose-rich or a maltose-rich diet [22].
• In the cecum, areas under the concentration curves decreased from day 1 to day 8 for lactulose, galactose, and fructose (P less than 0.01), while an increase was found for lactic acid (P less than 0.001), acetic acid (P less than 0.0001), and total VFA (P less than 0.001) [23].
• The addition of MIF to differentiated L6 rat myotubes increased synthesis of fructose 2,6-bisphosphate (F2,6BP), a positive allosteric regulator of glycolysis [24].
• BACKGROUND: The exact roles of disaccharidases and GLUT5 in the brush border membrane and GLUT2 in the basolateral membrane in the absorption of fructose across the intestine have not been fully determined [25].

Associations of fructose with other chemical compounds

• Among other natural sugars examined, only mannose competed effectively with 2-DG and reversed the inhibition of cytolysis, whereas sodium pyruvate, fructose, galactose, fucose, and glucosamine were without effect [26].
• Measurements were made during 2 h of: (a) insulin/glucose infusion (hyperinsulinemic [6 pmol/kg per min] euglycemic clamp), (b) exogenous glucose infusion at a rate matched to that attained during protocol a, and (c) exogenous fructose infusion at the same rate as for glucose infusion in protocol b [27].
• In vitro nonezymatic glycosylation of basic fibroblast growth factor (bFGF) by fructose, glucose-6-phosphate (G6P), or glyceraldehyde-3-phosphate (G3P) reduced high affinity heparin-binding activity of recombinant bFGF by 73, 77, and 89%, respectively [28].
• Lactate production rate and fructose 2,6-bisphosphate level increased in the order of the fed plus insulin, fed, fed plus glucagon, fasted, and fasted plus insulin groups [29].
• Sorbitol, which mimics ethanol in generating reducing equivalents in the hepatocyte, also inhibited glycosylation; however, fructose, the immediate oxidation product of sorbitol, similarly inhibited glycoprotein synthesis without altering the redox state [30].

Gene context of fructose

• Genetic analysis showed that only in strains lacking both hexokinases (hxk1 hxk2) was the low Km system for fructose absent [31].
• The rbcL-rbcS transcript is equally abundant in Anabaena azollae grown in the light or on fructose in the dark [32].
• The results indicate that hxk1 or hxk2 single null mutants can ferment fructose but that hxk1 hxk2 double mutants cannot [33].
• In addition, the growth properties of snf3 mutants suggested that they were defective in uptake of glucose and fructose [34].
• At higher glucose concentrations or in the presence of low concentrations of fructose, GK translocated to the cytoplasm [35].

Analytical, diagnostic and therapeutic context of fructose

• To learn more about the metabolic effects of dietary fructose and sucrose, 12 type I and 12 type II diabetic subjects were fed three isocaloric (or isoenergic) diets for eight days each according to a randomized, crossover design [17].
• Evaluation of University of Wisconsin cold-storage solution in warm hypoxic perfusion of rat liver: the addition of fructose reduces injury [36].
• RESULTS: Reperfusion with the glycolytic substrate fructose plus the cytoprotective amino acid glycine prevented necrotic cell killing [37].
• METHODS: Transport of fructose was measured using rapid filtration of vesicles [25].
• The interaction of fructose diphosphate aldolase with F-actin, F-actin-tropomyosin, and F-actin-tropomyosin-troponin has been studied by using negative staining [38].

References