Effect Of Glucose Feeding Research Articles

Metabolic Flux Analysis of Simultaneous Production of Vitamin B12 and Propionic Acid in a Coupled Fermentation Process by Propionibacterium freudenreichii.

The metabolic processes involved in simultaneous production of vitamin B12 and propionic acid by Propionibacterium freudenreichii are very complicated. To further investigate the regulatory mechanism of this metabolism, a simplified metabolic network was established. The effects of glucose feeding, propionic acid removal, and 5,6-dimethylbenzimidazole (DMB) addition on the metabolic flux distribution were investigated. The results showed that synthesis of propionic acid can be increased by increasing the metabolic flux through the oxaloacetate and methylmalonyl-CoA branches in the early and middle stages of the coupled fermentation. After DMB addition, the synthesis of vitamin B12 was significantly enhanced via increased metabolic flux through the δ-aminolevulinate branch, which promoted the synthesis of uroporphyrinogen III, a precursor of vitamin B12. Therefore, the analysis of metabolic flux at key nodes can provide theoretical guidance for the optimization of P. freudenreichii fermentation processes. In an experimental coupled fermentation process, the concentrations of vitamin B12 and propionic acid reached 21.6 and 50.12 g/L respectively, increased by 105.71% and 73.91% compared with batch fermentation, which provides a new strategy for industrial production.

Effect of glucose feeding on the glycosylation quality of antibody produced by a human cell line, F2N78, in fed-batch culture

The human cell line rF2N78 produces an antibody with a high galactosylation ratio which resembles human IgG. However, it has been observed that the aglycosylated antibody starts to appear when glucose is depleted. To determine whether glucose depletion is a main cause for aglycosylation of the antibody, fed-batch cultures of rF2N78 cells were performed using different feeding cocktails (glucose only, nutrient feeding cocktail without glucose, and nutrient feeding cocktail with glucose). In the fed-batch culture with nutrient feeding cocktail without glucose, aglycosylated antibody was produced in a later phase of culture, when glucose was depleted. Approximately 44% of antibodies produced were aglycosylated at the end of culture. In contrast, aglycosylated antibody was not produced in cultures with glucose feeding. The expression levels of oligosaccharyl transferases determined by Western blot analysis were similar among the cultures, suggesting that aglycosylation of the antibody was not due to altered expression of oligosaccharyl transferases under glucose-deficient conditions. Thus, it is likely that glucose deficiency led to insufficiency of the precursor for glycosylation and induced aglycosylation of the antibody. Taken together, glucose feeding in fed-batch cultures successfully prevented occurrence of aglycosylated antibody during the cultures, confirming that glucose depletion is a main cause for aglycosylation of antibody.

GLUCOSE FEEDING EXACERBATES PARATHION-INDUCED NEUROTOXICITY

Excessive dietary intake of sugars could alter various biotransformation processes and the pharmacological and toxicological properties of numerous xenobiotics. In the present study, the effects of glucose supplementation were examined on the neurotoxicity of the organophosphorus (OP) pesticide parathion (PS) and its active metabolite, paraoxon (PO), a potent inhibitor of acetylcholinesterase (AChE). Rats (n = 6-12/treatment group) were given free access to tap water or 15% glucose (w/v) in tap water beginning 7 d prior to OP toxicant exposure. Food, caloric intake, and body weight were measured daily. Animals were challenged with either PS (4.5, 9, or 18 mg/kg, sc) or PO (0.3, 0.5, or 0.7 mg/kg, sc) and clinical signs of neurotoxicity (i.e., autonomic dysfunction, involuntary movements) were recorded daily for the following 13 d. Glucose feeding was associated with a dramatic drop (~50%) in feed intake and an increase (~20%) in total caloric consumption over the 7 d prior to OP exposure. Functional toxicity associated with PS exposure was increased in glucose-fed (GF) rats, but the glucose diet had no apparent effect on clinical signs of toxicity following PO treatment. Glucose feeding increased the magnitude of AChE inhibition in the frontal cortex and plasma at lower dosages (i.e., 4.5 and 9 mg/kg) 3 d following PS treatment. Time-course studies (3, 7, and 11 d after PS exposure, 18 mg/kg, sc) indicated significantly greater brain and plasma AChE inhibition in glucosefed animals at later time points. In contrast, glucose feeding had no effect on the degree of AChE inhibition following PO exposure. Neither liver microsomal oxidative desulfuration of PS, nor liver or plasma paraoxonase, nor liver or plasma carboxylesterase activities were measurably affected by glucose feeding. Downregulation of muscarinic receptors 7 d after PS exposure (18 mg/kg, sc) was more extensive in GF rats. It is postulated that excessive glucose consumption decreases the intake of other dietary components, in particular amino acids, limiting the de novo synthesis of AChE and consequent recovery of synaptic transmission. Due to the shorter duration of inhibition following PO exposure, spontaneous reactivation of AChE may be more important than de novo protein synthesis in recovery of function, and thus with the effects of glucose feeding on its toxicity. Individuals that derive a large proportion of their calories from sugars may be at higher risk of acute toxicity from organophosphorus pesticides such as PS.

Modelling the effects of glucose feeding on a recombinant E. coli fermentation

A simple unstructured model is described and compared with experimental data for fed-batch fermentations. The process studied is typical of the most common industrial recombinant fermentation in which temperature induced E. coli produces high yields of a heterologous protein (4 g met-asp-Bovine Somatotropin/l) using a complex peptone feed and a glucose feed. The model accurately predicts the effect of glucose feeding and shows that there is an optimal glucose feedrate to maximize productivity. At higher glucose feedrates, acetate levels become inhibitory and at lower levels glucose starvation occurs. The model is novel since it combines terms for acetate production and inhibition, effect of peptone feeding and temperature induction into a single relatively simple unstructured model. However the present model is unable to predict the effect of induction at different cell densities and reasons for this are suggested.

Modelling the effects of glucose feeding on a recombinant

Modelling the effects of glucose feeding on a recombinant

Glutamate dehydrogenase regulation in callus cultures of Nicotiana plumbaginifolia: effect of glucose feeding and carbon source starvation on the isoenzymatic pattern

Abstract. In callus cultures of Nicotiana plumbaginifolia, the activity of glutamate dehydrogenase was repressed by glucose, whereas, on the contrary, carbon and energy source deprivation induced a remarkable increase in specific activity. Definition of these two opposite types of response was made possible by the use of glycerol as a non‐repressing carbon source: in this condition, glutamate dehydrogenase activity reached an intermediate level, which was similar to the derepressed values of activity obtainable when cultures were allowed to exhaust the glucose supply in the medium. Isoelectric focusing analysis revealed the existence of three different isoenzymatic patterns which could be correlated to the three different levels of specific activity: repressed (glucose), induced (carbon starvation) and intermediate (glycerol). Repression affected mainly the four more cathodic bands which were predominant in non‐repressed conditions. The possible catabolic role of these isoenzymes is discussed.

Effect and control of glucose feeding on bacitracin production by fed-batch culture of Bacillus licheniformis

The effect of glucose feeding on bacitracin production was investigated by fed-batch culture of Bacillus licheniformis. In batch culture, bacitracin secretion was induced after the glucose initially contained in the medium was completely consumed. The concentration of bacitracin, however, increased to no more than 340 units·ml −1 in the batch cultivations. Therefore, additional glucose was supplied after exhaustion of the initial glucose. The effect of glucose feeding on bacitracin biosynthesss was investigated in two ways, the pH-stat modal feeding method and the CO 2-dependent feeding method. A kinetic study of bacitracin production found that some glucose was necessary, even during the bacitracin production phase. Excessive feeding of glucose, however, caused a reduction in bacitracin biosynthetic activity. When 50 g· l −1 of defatted soy bean meal (SBM) was used, the bacitracin concentration reached 670 units·ml −1 with the pH-stat modal feeding method and 610 units·ml −1 with the CO 2-dependent feeding method, respectively. The yield of bacitracin from consumed glucose was better for the pH-stat method. Using this control strategy, the highest concentration of bacitracin (940 units·ml −1) was obtained with 150 g· l −1 of SBM.

Effects of glucose feeding on renal electrolyte and H + transport

1. 1. Changes of urinary pH, titratable acidity, ammonium, bicarbonate and PCO 2, as well as plasma insulin and various plasma and urine electrolytes were studied in 15 normal individuals during a 5-hr glucose tolerance test. 2. 2. After glucose ingestion, urine pH and bicarbonate excretion rose while urine titratable and total acidity, ammonium, Na, K, Cl, phosphorus and PCO 2 fell significantly. 3. 3. Serum bicarbonate rose while serum potassium, phosphorus, and anion gap decreased following oral glucose administration. 4. 4. Glucose feeding and the resultant rise in insulin are, therefore, associated with a considerable reduction in urine acidity and Na, K, Cl, and phosphorus excretion. 5. 5. While a significant fall in urinary Na, K and phosphorus has been shown to occur following glucose and insulin administration, their effect on renal H + excretion in man has not been investigated previously. 6. 6. The mechanism of the observed fall in urine acidity is not clear and requires further investigation.

Interactions between insulin and thyroid hormone in the control of lipogenesis.

1. The effects of intragastric glucose feeding and L-tri-iodothyronine (T3) administration on rates of hepatic and brown-fat lipogenesis in vivo were examined in fed and 48 h-starved rats. 2. T3 treatment increased hepatic lipogenesis in the fed but not the starved animals. Brown-fat lipogenesis was unaffected or slightly decreased by T3 treatment of fed or starved rats. 3. Intragastric glucose feeding increased hepatic lipogenesis in control or T3-treated fed rats, but did not increase hepatic lipogenesis in starved control rats. Glucose feeding increased hepatic lipogenesis if the starved rats were treated with T3. Glucose feeding increased rates of brown-fat lipogenesis in all experimental groups. The effects of glucose feeding on liver and brown-fat lipogenesis were mimicked by insulin injection. 4. The increase in hepatic lipogenesis in T3-treated 48 h-starved rats after intragastric glucose feeding was prevented by short-term insulin deficiency, but not by (-)-hydroxycitrate, an inhibitor of ATP citrate lyase. The increase in lipogenesis in brown adipose tissue in response to glucose feeding was inhibited by both short-term insulin deficiency and (-)-hydroxycitrate. 5. The results tend to preclude pyruvate kinase and acetyl-CoA carboxylase as the sites of interaction of insulin and T3 in the regulation of hepatic lipogenesis in 48 h-starved rats. Other potential sites of interaction are discussed.

Plasma insulin response in pregnant and non-pregnant rats: effects of different dietary carbohydrates.

The effects of prolonged feeding of diets containing various carbohydrates on the plasma insulin response to glucose (given intravenously) have been investigated in 20-day pregnant rats and compared with the effects in non-pregnant rats. In pregnant animals the insulin response was similar for all diets; the insulin concentration was approximately 120 μU/ml for at least 10 min after injecting glucose. In non-pregnant rats, except those fed glucose, the insulin response was lower than in pregnant rats. The mean insulin concentrations were80, 70 and 50 μU/ml at 2.5, 5 and 10 min after intravenous glucose. The effect of glucose feeding was to increase the response in non-pregnant animals so that it approached the values found in pregnant animals. The maximum concentrations of plasma insulin for glucose-fed pregnant and non-pregnant rats were 141±23 and 134±15 (SEM) μU/ml respectively. It was concluded that the increased availability of glucose in the diet during pregnancy plays a role in regulating the insulin secretory response.

Effects of glucose feeding on insulin and glucagon secretion and hepatic gluconeogenesis in the rat.

ARTICLESEffects of glucose feeding on insulin and glucagon secretion and hepatic gluconeogenesis in the ratRP Eaton, DM Kipnis, I Karl, and AB EisensteinRP Eaton, DM Kipnis, I Karl, and AB EisensteinPublished Online:01 Jul 1974https://doi.org/10.1152/ajplegacy.1974.227.1.101MoreSectionsPDF (983 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByGlucagon and HyperlipoproteinemiasEffects of intravenously administered fructose and glucose on splanchnic secretion of plasma triglycerides in hypertriglyceridemic menMetabolism, Vol. 26, No. 9Glucagon and lipoproteinsMetabolism, Vol. 25, No. 11Effect of contraceptive steroids on arginine-stimulated glucagon and insulin secretion in women: I-lipid physiologyMetabolism, Vol. 24, No. 9DECREASED GLUCAGON ACTIVITY: A MECHANISM FOR GENETIC AND ACQUIRED ENDOGENOUS HYPERLIPÆMIAThe Lancet, Vol. 304, No. 7896 More from this issue > Volume 227Issue 1July 1974Pages 101-104 Copyright & PermissionsCopyright © 1974 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1974.227.1.101PubMed4843362History Published online 1 July 1974 Published in print 1 July 1974 Metrics

The effect of glucose feeding on fatty acid synthesis in human platelets.

Abstract Platelets were isolated from volunteers who had fasted for 15 hours and again 1 hour after these subjects had ingested glucose. After feeding, incorporation of (C 14 ) acetate into fatty acids of washed platelets was increased 68 per cent. Ingestion of fructose produced a comparable stimulation of fatty acid synthesis, but ingestion of galactose had no effect. Pre-incubation of the whole blood from fasting donors with glucose prior to incubation of the platelets did not increase the subsequent incorporation of (C 14 ) acetate by washed cells. Ingestion of glucose did not alter the level of glycogen or of lactate in platelets, nor did it alter their rate of glycogenolysis or of lactate production. Similarly, evolution of 14 CO 2 from [1- 14 C] or [6- 14 C] glucose or from [1- 14 C] acetate was unchanged by feeding. The results suggest that the stimulatory effect of feeding glucose or fructose on fatty acid synthesis in platelets is not due to increased availability of these sugars to the cell. It is conceivable that a humoral factor is released by ingestion of glucose or fructose which stimulates lipogenesis in platelets.

Effect of glucose feeding on lipoprotein synthesis in the rat.

ARTICLESEffect of glucose feeding on lipoprotein synthesis in the ratRP Eaton, and DM KipnisRP Eaton, and DM KipnisPublished Online:01 Oct 1969https://doi.org/10.1152/ajplegacy.1969.217.4.1153MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByProinflammatory Cytokines Are Soluble Mediators Linked with Ventricular Arrhythmias and Contractile Dysfunction in a Rat Model of Metabolic SyndromeOxidative Medicine and Cellular Longevity, Vol. 2017Effect of the apolipoprotein C-IIC-III1 ratio on the capacity of purified milk lipoprotein lipase to hydrolyse triglycerides in monolayer vesiclesAtherosclerosis, Vol. 127, No. 2Einbau von15N-Glyzin in VLDL und LDL: In-vivo-Synthese von Apolipoprotein B beim Menschen postabsorptiv und im FastenzustandKlinische Wochenschrift, Vol. 67, No. 5Increasing dextrose concentrations in total parenteral nutrition (TPN) causes alterations in hepatic morphology and plasma levels of insulin and glucagon in ratsJournal of Surgical Research, Vol. 44, No. 6Stimulation by acetoacetate of hepatic triacylglycerol synthesisDiabetes Research and Clinical Practice, Vol. 3, No. 1Dietary carbohydrate decreases 3-hydroxy-3-methylglutaryl coenzyme a reductase activity and cholesterol synthesis in rat liverBiochemical and Biophysical Research Communications, Vol. 113, No. 3Glucagon and HyperlipoproteinemiasMechanism of carbohydrate-induced hypertriglyceridemia: Plasma lipid metabolism in miceMetabolism, Vol. 29, No. 10Effects of ethanol on lipid metabolism.Journal of Lipid Research, Vol. 20, No. 3Sex-dependence in triglyceride metabolism in response to dietary carbohydratesExperientia, Vol. 35, No. 2Some mechanisms of the different effects of sucrose on the blood and liver lipid levels in experimental animalsBulletin of Experimental Biology and Medicine, Vol. 84, No. 6Effects of intravenously administered fructose and glucose on splanchnic secretion of plasma triglycerides in hypertriglyceridemic menMetabolism, Vol. 26, No. 9Serum cholinesterase: Function in lipoprotein metabolismExperientia, Vol. 33, No. 4Effects of clofibrate on ethanol-induced modifications in liver and adipose tissue metabolism: Role of hepatic redox state and hormonal mechanismsBiochemical Pharmacology, Vol. 26, No. 5Altered insulin and glucagon secretion in treated genetic hyperlipemia: A mechanism of therapy?Metabolism, Vol. 25, No. 3Mammalian Low Density LipoproteinsSUBSTRATE INCORPORATION INTO HEPATIC LIPIDS AND PROTEINS IN VITRO IN PATIENTS WITH PRE-β HYPERLIPOPROTEINEMIA24 April 2009 | Acta Medica Scandinavica, Vol. 197, No. 1-6Effect of intravenously administered glucose on glucagon and insulin secretion during fat absorptionMetabolism, Vol. 24, No. 1DECREASED GLUCAGON ACTIVITY: A MECHANISM FOR GENETIC AND ACQUIRED ENDOGENOUS HYPERLIPÆMIAThe Lancet, Vol. 304, No. 7896Incorporation Rate of Leucine into Proteins in Human Liver Slices2 March 2011 | European Journal of Clinical Investigation, Vol. 4, No. 6Polypeptide composition of rat high density lipoprotein: Characterization by SDS-gel electrophoresisBiochemical and Biophysical Research Communications, Vol. 59, No. 2Alpha- and beta-cell interrelationships in health and diseaseMetabolism, Vol. 23, No. 6Effect of clofibrate on arginine-stimulated glucagon and insulin secretion in manMetabolism, Vol. 23, No. 5Incorporation Rate of Leucine into Proteins in Human Liver SlicesEuropean Journal of Clinical Investigation, Vol. 4, No. 1REFERENCES24 April 2009 | Acta Medica Scandinavica, Vol. 195, No. S561Effect of ethanol on plasma triglycerides in male and female ratsLipids, Vol. 8, No. 9Effect of clofibrate on arginine-induced insulin and glucagon secretionMetabolism, Vol. 22, No. 6Studies of the mechanisms of carbohydrate-induced lipaemia in normal manAtherosclerosis, Vol. 17, No. 3Hypolipemic action of glucagon in experimental endogenous lipemia in the ratJournal of Lipid Research, Vol. 14, No. 3GLUCAGON RESISTANCE AS A HORMONAL BASIS FOR ENDOGENOUS HYPERLIPÆMIAThe Lancet, Vol. 301, No. 7810Type IV hyperlipoproteinaemiaClinics in Endocrinology and Metabolism, Vol. 2, No. 1CARBOHYDRATE-STIMULATED FATTY ACID SYNTHESIS DE NOVO IN HUMAN ADIPOSE TISSUE OF DIFFERENT CELLULAR TYPES24 April 2009 | Acta Medica Scandinavica, Vol. 194, No. 1-6Eine mögliche Rolle der Pankreashormone Insulin und Glucagon und des Enteroglucagons im postprandialen FettstoffwechselPlasma triglyceride transport kinetics in diabetes mellitusMetabolism, Vol. 22, No. 1Effects of high sucrose diets and 4-aminopyrazolopyrimidine on serum lipids and lipoproteins in the ratJournal of Lipid Research, Vol. 12, No. 5The effect of prolonged fasting and of glucose refeeding on rat serum and liver lipid levelsLipids, Vol. 6, No. 5 More from this issue > Volume 217Issue 4October 1969Pages 1153-1159 Copyright & PermissionsCopyright © 1969 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1969.217.4.1153PubMed4980948History Published online 1 October 1969 Published in print 1 October 1969 Metrics

Effect of glucose feeding on net transport of plasma free fatty acids

The effect of a single glucose feeding upon the net inflow and outflow transport of plasma free fatty acids (FFA) has been studied in 75 unanesthetized rats. The animals were fasted for 22 +/- 2 hr; then 50 rats were refed 2 ml of 50% glucose by gastric intubation. At 0, 10-15, and 30-35 min after glucose refeeding, the rats were injected with palmitate-1-(14)C complexed to rat serum. The tracer dose included (131)I-labeled albumin. Plasma FFA concentration, (131)I concentration, and FFA-(14)C were measured at five time intervals after injection of the tracer dose. From these data the irreversible disposal rate, or net outflow transport, and the net inflow transport of plasma FFA were calculated. Estimations were based upon a special case of a general solution for measuring net inflow and outflow transport of a circulating metabolite. The general solution is independent of the number of compartments, how they are interconnected, the number of nonradioactive inflows, and where the inflows enter the system. Net inflow = net outflow transport = 7.6 micro eq/min in the fasted state and 3.5 micro eq/min in the new steady state that is reached 30-40 min after glucose refeeding. A very slight imbalance between the rates of net inflow and outflow transport could account for the rapid fall in plasma FFA concentration that results from a single glucose feeding. Theoretical and practical problems associated with studying inflow and outflow transport by means of the technique using a single injection of racer are discussed.

Effects of glucose feeding on tumour development in vivo.

Effects of glucose feeding on tumour development in vivo.

Effects of glucose feeding, cortisol, and insulin on liver glycogen synthesis in the rat.

To determine maximal rates of liver glycogen synthesis in vivo, normal, diabetic and adrenalectomized rats were fasted 48 hr, then were given repeated, heavy oral doses of glucose during a 16-hr period, then fasted 24–32 hr. Liver glycogen was assayed at regular intervals throughout these periods of glucose foeding and subsequent fasting. Normal rats synthesized liver glycogen at an extremely rapid rate of about 1% of fresh liver weight/hr to reach a peak of 16–18 % in 16 hr. Similar rates were observed in similarly fed 3-day cortisol-treated rats. Adrenalectomized rats displayed initially a slow rate of liver glycogen synthesis, but after a 2-hr lag period synthesized liver glycogen almost as rapidly as normal rats. However, the level “plateaued” at about 8–9 % after 8–10 hr. Similarly fed adrenalectomized rats treated with cortisol for 3 days responded exactly like normal rats. Similarly fed alloxan-diabetic rats, whose liver glycogen was depleted by prior glucagon injection, synthesized glycogen initia...

EFFECTS OF GLUCOSE FEEDING UPON THE KETONEMIA IN HEALTHY MAN

EFFECTS OF GLUCOSE FEEDING UPON THE KETONEMIA IN HEALTHY MAN