Academic literature on the topic 'Fructose utilization'

SUMMARYThe capacity of Acanthocheilonema viteae to metabolize fructose was investigated in vitro. In common with other filarial species A. viteae oxidized fructose to lactate but its rate of consumption was only 40% of the glucose-containing control value. Fructose was not incorporated into glycogen. Release of 14CO2 from [U-14C]fructose was not detected in the presence of glucose and was about 40% of the glucose-containing value under conditions where fructose was the sole hexose substrate. Fructose consumption and lactate excretion increased in proportion to the external concentration of fructose. However, worm viability was not maintained in fructose over a 120 h in vitro incubation. In the presence of fructose, protein synthesis (measured incorporation of [35S]methionine into acid-insoluble material) was reduced compared to the glucose-containing control group; but was significantly greater than the value obtained under glucose-free conditions.

Spiroplasma citri is a plant-pathogenic mollicute. Recently, the so-called nonphytopathogenic S. citri mutant GMT 553 was obtained by insertion of transposon Tn4001 into the first gene of the fructose operon. Additional fructose operon mutants were produced either by gene disruption or selection of spontaneous xylitol-resistant strains. The behavior of these spiroplasma mutants in the periwinkle plants has been studied. Plants infected via leafhoppers with the wild-type strain GII-3 began to show symptoms during the first week following the insect-transmission period, and the symptoms rapidly became severe. With the fructose operon mutants, symptoms appeared only during the fourth week and remained mild, except when reversion to a fructose+ phenotype occurred. In this case, the fructose+ revertants quickly overtook the fructose¯ mutants and the symptoms soon became severe. When mutant GMT 553 was complemented with the fructose operon genes that restore fructose utilization, severe pathogenicity, similar to that of the wild-type strain, was also restored. Finally, plants infected with the wild-type strain and grown at 23°C instead of 30°C showed late symptoms, but these rapidly became severe. These results are discussed in light of the role of fructose in plants. Fructose utilization by the spiroplasmas could impair sucrose loading into the sieve tubes by the companion cells and result in accumulation of carbohydrates in source leaves and depletion of carbon sources in sink tissues.

ABSTRACT Fructose utilization by wine yeasts is critically important for the maintenance of a high fermentation rate at the end of alcoholic fermentation. A Saccharomyces cerevisiae wine yeast able to ferment grape must sugars to dryness was found to have a high fructose utilization capacity. We investigated the molecular basis of this enhanced fructose utilization capacity by studying the properties of several hexose transporter (HXT) genes. We found that this wine yeast harbored a mutated HXT3 allele. A functional analysis of this mutated allele was performed by examining expression in an hxt1-7Δ strain. Expression of the mutated allele alone was found to be sufficient for producing an increase in fructose utilization during fermentation similar to that observed in the commercial wine yeast. This work provides the first demonstration that the pattern of fructose utilization during wine fermentation can be altered by expression of a mutated hexose transporter in a wine yeast. We also found that the glycolytic flux could be increased by overexpression of the mutant transporter gene, with no effect on fructose utilization. Our data demonstrate that the Hxt3 hexose transporter plays a key role in determining the glucose/fructose utilization ratio during fermentation.

Enterocyte fructose absorption is a tightly regulated process that precedes the deleterious effects of excess dietary fructose in mammals. Glucose transporter (GLUT)8 is a glucose/fructose transporter previously shown to be expressed in murine intestine. The in vivo function of GLUT8, however, remains unclear. Here, we demonstrate enhanced fructose-induced fructose transport in both in vitro and in vivo models of enterocyte GLUT8 deficiency. Fructose exposure stimulated [14C]-fructose uptake and decreased GLUT8 protein abundance in Caco2 colonocytes, whereas direct short hairpin RNA-mediated GLUT8 knockdown also stimulated fructose uptake. To assess GLUT8 function in vivo, we generated GLUT8-deficient (GLUT8KO) mice. GLUT8KO mice exhibited significantly greater jejunal fructose uptake at baseline and after high-fructose diet (HFrD) feeding vs. wild-type mice. Strikingly, long-term HFrD feeding in GLUT8KO mice exacerbated fructose-induced increases in blood pressure, serum insulin, low-density lipoprotein and total cholesterol vs. wild-type controls. Enhanced fructose uptake paralleled with increased abundance of the fructose and glucose transporter, GLUT12, in HFrD-fed GLUT8KO mouse enterocytes and in Caco2 cultures exposed to high-fructose medium. We conclude that GLUT8 regulates enterocyte fructose transport by regulating GLUT12, and that disrupted GLUT8 function has deleterious long-term metabolic sequelae. GLUT8 may thus represent a modifiable target in the prevention and treatment of malnutrition or the metabolic syndrome.

Rapid proliferation and Warburg effect make cancer cells consume plenty of glucose, which induces a low glucose micro-environment within the tumor. Up to date, how cancer cells keep proliferating in the condition of glucose insufficiency still remains to be explored. Recent studies have revealed a close correlation between excessive fructose consumption and breast cancer genesis and progression, but there is no convincing evidence showing that fructose could directly promote breast cancer development. Herein, we found that fructose, not amino acids, could functionally replace glucose to support proliferation of breast cancer cells. Fructose endowed breast cancer cells with the colony formation ability and migratory capacity as effective as glucose. Interestingly, although fructose was readily used by breast cancer cells, it failed to restore proliferation of non-tumor cells in the absence of glucose. These results suggest that fructose could be relatively selectively employed by breast cancer cells. Indeed, we observed that a main transporter of fructose, GLUT5, was highly expressed in breast cancer cells and tumor tissues but not in their normal counterparts. Furthermore, we demonstrated that the fructose diet promoted metastasis of 4T1 cells in the mouse models. Taken together, our data show that fructose can be used by breast cancer cells specifically in glucose-deficiency, and suggest that the high-fructose diet could accelerate the progress of breast cancerin vivo.

Saccharomyces cerevisiae is the most important micro organism involved in the production of fermented alcoholic beverages such as wine. Despite its fermentative capacity and production of desirable metabolites, grape juice represents a hostile environment for yeasts. Sometimes, adverse conditions reduce yeast biomass formation or catabolic capacity, which may lead to stuck or sluggish fermentation. These phenomena represent one of the most common problems during the wine production process and mean that winery throughput is reduced and residual sugar adds unwanted sweetness in dry wine styles while offering substrates for microbial spoilage. The scientific community has always been alert to the problems linked with fermentation, considering the vital role of this organism during the production process. For this reason research has focussed on developing a range of techniques for strain improvement. With the emergence of modern molecular genetics, the new methodologies of hybridization and genetic engineering have been used to isolate and create new yeast strains. However, their application in wine microbiology is not without complications, as genetically modified yeasts are not universally favoured for commercial use in the food industry. A recent development is the notion of using the natural capacity of a population of single celled organisms to adapt themselves to an environment imposing a specific stress. The technique is termed “adaptive evolution” or “directed evolution”. In principle the process is simple: when a species is constricted to live and replicate under stressful conditions for many generations, some cells will present adaptive characteristics: i.e. “adaptive mutations” and outgrow the starting population. A key benefit of this technique is that it does not rely on direct manipulation at the level of DNA, and can be used to reproduce the stress conditions found in nature or in fermentation tanks. However, adaptive evolution is a technology that needs to be more fully explored and developed for its possible use in improving wine yeast strains. A possible improvement for wine yeasts targets their sugar catabolic capacity. The different affinity of S. cerevisiae for glucose and fructose is thought to be a cause of stuck or sluggish fermentations in the winemaking process. The possibility of obtaining a strain with improved fructose utilization using adaptive evolution is therefore the topic of this investigation. This thesis describes work that can be divided into four sections. The first part is the identification of a candidate strain from a selection of commercially available wine yeasts. The second part is aimed at evolving the candidate strain under a selective pressure. The third validates new methods for assessing the populations of candidate evolved yeast in order to isolate clones that can metabolize fructose more efficiently compared to the parental strain. The last part is focussed on a deeper investigation and comparison of a number of potentially evolved candidates with the parent. To identify a candidate strain for use in the adaptive evolution process, it was necessary to compare fermentative performances of commercially available strains. Fermentations for 20 strains were conducted in synthetic media, containing fructose as sole sugar or else an equivalent concentration of glucose and fructose. Particular attention was focussed on the rate of fructose consumption relative to glucose, and thus it was necessary to identify a methodology that was independent of sugar concentration, overall fermentation rate or duration. As such the value of the area under the fermentation curves determined by the composite trapezoid rule was utilised to compare glucose and fructose utilisation and hence define the fructophilicity of each strain screened. This approach allowed the most suitable candidate strain to be chosen for the application of adaptive evolution. Accordingly, strain AWRI 796 was cultured under fermentative conditions that elicited an appropriate selective pressure over some 350 generations. Samples of the population were collected every 50 generations for characterization of individual clones. The next stage of the project focussed on the identification of clones which showed improved fructose utilization compared to the parental strain. To define fermentative performance of a high number of isolates from the adaptive evolution experiment, it was necessary to develop screening methodologies. For this purpose fermentations in microtiter plates and automated colorimetric assays for determination of residual sugar were adopted. From 378 clones examined, four were identified to be faster consumers of fructose relative to the parent. Patterns of glucose utilisation in these clones were unchanged. The last stage of the study validated the improved fermentation ability of these novel phenotypes under winemaking related conditions in fermentations of 20 kg of red grapes. In these experiments two isolates again showed a significant reduction in the time required for completion of the fermentation. The results validate the approach used and the selective pressures applied as a means introducing specific improvements into wine yeast strains.
Thesis (Ph.D.) -- University of Adelaide, School of Agriculture, Food and Wine 2011

Sun, Fenghua.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2011.
Includes bibliographical references (leaves 177-204).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.

Many disorders of carbohydrate metabolism are characterized by hypoglycaemia and attacks of neuroglycopenia. Hypoglycaemia can also be caused by disorders affecting the use of other fuels, such as those producing fatty acids and ketone bodies which are important alternative sources of energy. Thus when investigating a patient with hypoglycaemia it is necessary to investigate not only pathways that provide glucose directly, but also those which spare glucose utilization and thus provide defence mechanisms when carbohydrate energy sources become depleted. The defence mechanisms that are activated during fasting to preserve blood glucose are: ◆ glycogenolysis—glucose liberation from glycogen degradation ◆ gluconeogenesis—glucose production from pyruvate/lactate and from noncarbohydrate sources such as glucogenic amino acids and glycerol ◆ fatty acid β‎-oxidation—catabolism of triglycerides to acetyl-CoA and ketone bodies The interrelation between these glucose generating pathways is shown in Fig. 12.3.1.1. Although there is much overlap, the activation of these defence mechanisms during fasting is sequential. The first defence mechanism, glycogenolysis, is exhausted within 8–12 h of fasting. The second and third defence mechanisms provide glucose once glycogen stores have been depleted. In a patient with glycogen storage disease (GSD) where glycogenolysis is blocked, gluconeogenesis and fatty acid oxidation are activated immediately on fasting and can only maintain normoglycaemia for a few hours. In patients with defects affecting gluconeogenesis or fatty acid oxidation, hypoglycaemia does not occur until glycogen stores have been depleted. When more than one pathway is affected, as in GSD I, where neither glycogenolysis nor gluconeogenesis can release glucose into the circulation, patients can be entirely dependent on oral carbohydrate intake to maintain normoglycaemia. These pathways are also susceptible to hormonal influences. Insulin in particular inhibits all three pathways and stimulates some enzymes of the reverse pathways: glycogen synthesis, glycolysis, and fatty acid synthesis. Therefore hyperinsulinaemia of whatever cause leads to severe hypoglycaemia which is resistant to treatment. Other hormones, such as glucagon, adrenaline, and growth hormone, also activate some enzymes of glucose homoeostasis, though less markedly. This is discussed elsewhere. The metabolism of the other monosaccharides, galactose and fructose, is connected with that of glucose. As well as causing hypoglycaemia, inherited defects that affect the metabolism of these sugars lead to the accumulation of toxic metabolites which also contribute to pathology (see below).