Intravenous Infusion Of Fructose Research Articles

Dietary intake of fructose increases purine de novo synthesis: A crucial mechanism for hyperuricemia.

Fructose consumption is a potential risk factor for hyperuricemia because uric acid (UA) is a byproduct of fructose metabolism caused by the rapid consumption of adenosine triphosphate and accumulation of adenosine monophosphate (AMP) and other purine nucleotides. Additionally, a clinical experiment with four gout patients demonstrated that intravenous infusion of fructose increased the purine de novo synthesis rate, which implied fructose-induced hyperuricemia might be related to purine nucleotide synthesis. Moreover, the mechanistic (mammalian) target of rapamycin (mTOR) is a key protein both involved in fructose metabolism and purine de novo synthesis. The present study was conducted to elucidate how fructose influences mTOR and purine de novo synthesis in a hepatic cell line and livers of mice. RNA-sequencing in NCTC 1469 cells treated with 0- and 25-mM fructose for 24 h and metabolomics analysis on the livers of mice fed with 0- and 30-g/kg fructose for 2 weeks were assessed. Gene and protein expression of phosphoribosyl pyrophosphate synthase (PRPSAP1), Glutamine PRPP aminotransferase (PPAT), adenyl succinate lyase (ADSL), adenyl succinate synthetase isozyme-1 (Adss1), inosine-5'-monophosphate dehydrogenase (IMPDH), and guanine monophosphate synthetase (GMPS) was measured. The location of PRPSAP1 and PPAT in the liver was assessed by an immunofluorescence assay. Metabolite profiling showed that the level of AMP, adenine, adenosine, hypoxanthine, and guanine was increased significantly. RNA-sequencing showed that gene expression of phosphoribosyl pyrophosphate synthase (PRPS2), phosphoribosyl glycinamide formyl transferase (GART), AICAR transformylase (ATIC), ADSL, Adss1, and IMPDH were raised, and gene expression of adenosine monophosphate deaminase 3 (AMPD3), adenosine deaminase (ADA), 5',3'-nucleotidase, cytosolic (NT5C), and xanthine oxidoreductase (XOR) was also increased significantly. Fructose increased the gene expression, protein expression, and fluorescence intensity of PRPSAP1 and PPAT in mice livers by increasing mTOR expression. Fructose increased the expression and activity of XOR, decreased the expression of uricase, and increased the serum level of UA. This study demonstrated that the increased purine de novo synthesis may be a crucial mechanism for fructose-induced hyperuricemia.

Investigating the effects of an oral fructose challenge on hepatic ATP reserves in healthy volunteers: A 31P MRS study

Impaired homeostasis of hepatic ATP has been associated with NAFLD. An intravenous fructose infusion has been shown to be an effective challenge to monitor the depletion and subsequent recovery of hepatic ATP reserves using (31)P MRS. The purpose of this study was to evaluate the effects of an oral rather than intravenous fructose challenge on hepatic ATP reserves in healthy subjects. Self-reported healthy males were recruited. Following an overnight fast, baseline liver glycogen and lipid levels were measured using Magnetic Resonance Spectroscopy (MRS). Immediately after consuming a 500ml 75g fructose drink (1275kJ) subjects were scanned continuously for 90min to acquire dynamic (31)P MRS measurements of liver ATP reserves. A significant effect on ATP reserves was observed across the time course (P<0.05). Mean ATP levels reached a minimum at 50min which was markedly lower than baseline (80±17% baseline, P<0.05). Subsequently, mean values tended to rise but did not reach statistical significance above minimum. The time to minimum ATP levels across subjects was negatively correlated with BMI (R(2)=0.74, P<0.005). Rates of ATP recovery were not significantly correlated with BMI or liver fat levels, but were negatively correlated with baseline glycogen levels (R(2)=0.7, P<0.05). Depletion of ATP reserves can be measured non-invasively following an oral fructose challenge using (31)P MRS. BMI is the best predictor of postprandial ATP homeostasis following fructose consumption.

Fructose Administration Increases Intraoperative Core Temperature by Augmenting Both Metabolic Rate and the Vasoconstriction Threshold

The authors tested the hypothesis that intravenous fructose ameliorates intraoperative hypothermia both by increasing metabolic rate and the vasoconstriction threshold (triggering core temperature). Forty patients scheduled to undergo open abdominal surgery were divided into two equal groups and randomly assigned to intravenous fructose infusion (0.5 g . kg(-1) . h(-1) for 4 h, starting 3 h before induction of anesthesia and continuing for 4 h) or an equal volume of saline. Each treatment group was subdivided: Esophageal core temperature, thermoregulatory vasoconstriction, and plasma concentrations were determined in half, and oxygen consumption was determined in the remainder. Patients were monitored for 3 h after induction of anesthesia. Patient characteristics, anesthetic management, and circulatory data were similar in the four groups. Mean final core temperature (3 h after induction of anesthesia) was 35.7 degrees +/- 0.4 degrees C (mean +/- SD) in the fructose group and 35.1 degrees +/- 0.4 degrees C in the saline group (P = 0.001). The vasoconstriction threshold was greater in the fructose group (36.2 degrees +/- 0.3 degrees C) than in the saline group (35.6 degrees +/- 0.3 degrees C; P < 0.001). Oxygen consumption immediately before anesthesia induction in the fructose group (214 +/- 18 ml/min) was significantly greater than in the saline group (181 +/- 8 ml/min; P < 0.001). Oxygen consumption was 4.0 l greater in the fructose patients during 3 h of anesthesia; the predicted difference in mean body temperature based only on the difference in metabolic rates was thus only 0.4 degrees C. Epinephrine, norepinephrine, and angiotensin II concentrations and plasma renin activity were similar in each treatment group. Preoperative fructose infusion helped to maintain normothermia by augmenting both metabolic heat production and increasing the vasoconstriction threshold.

First-pass metabolism of ethanol in human beings: effect of intravenous infusion of fructose

Intravenous infusion of fructose has been shown to enhance reduced form of nicotinamide adenine dinucleotide reoxidation and, thereby, to enhance the metabolism of ethanol. In the current study, the effect of fructose infusion on first-pass metabolism of ethanol was studied in human volunteers. A significantly higher first-pass metabolism of ethanol was obtained after administration of fructose in comparison with findings for control experiments with an equimolar dose of glucose. Because fructose is metabolized predominantly in the liver and can be presumed to have virtually no effects in the stomach, results of the current study support the assumption that only a negligible part of first-pass metabolism of ethanol occurs in the stomach.

Effects of Intravenous Fructose Infusion on Sodium Handling and Peripheral Vascular Tone in Pre-Hypertensive Subjects.

The hemodynamic and humoral effects of i.v. fructose infusion and a control infusion were studied in 12 borderline hypertensive patients according to a single-blind, cross-over, randomized protocol. Fructose infusion decreased urinary sodium excretion and significantly increased plasma insulin, plasma Na+/K+ ATPase inhibitory activity, and forearm arterial and venous tone (+13%), the last of which was not observed during the control infusion (-2.5%). Levels of ANF and PRA in plasma were not altered by either infusion. We conclude that the sodium retention caused by acute i.v. fructose loading could be related to the increase in plasma insulin levels, which may directly affect individual susceptibility to sodium by enhancing sodium reabsorption at renal tubules. This sodium retention could contribute to the release of a plasma Na+-pump inhibitor apparently unrelated to extracellular volume expansion and potentially responsible for the early peripheral vascular involvement found in hypertension-prone men. (Hypertens Res 1994; 17: 239-242)

Splanchnic and muscle fructose metabolism during and after exercise

Regional substrate exchange was studied in 12 healthy males during 90 min of bicycle exercise at 30% of maximal O2 consumption with a 20-min recovery. Six subjects received an intravenous fructose infusion (8.5 mmol/min) from 40 min of exercise to the end of recovery. Splanchnic glucose output, muscle glucose uptake, arterial glucose, and insulin were uninfluenced by the infusion. The respiratory exchange ratio rose to 0.93 +/- 0.04, and arterial free fatty acids fell by 50% (P less than 0.05). Fructose was taken up by splanchnic tissues (45% of administered load), leg muscle (28%), and resting muscle (28%). During infusion, arterial lactate and pyruvate rose two- to threefold, and these substrates were released from splanchnic tissues and taken up by exercising and resting muscle. Splanchnic release of lactate, pyruvate, and glucose accounted for 78% of fructose uptake at 90 min of exercise. Uptake of fructose, lactate, and pyruvate accounted for 55% and together with glucose for 103% of the total oxidative metabolism by exercising muscle. The regional fructose uptakes and lactate exchanges persisted throughout recovery. The present results indicate that fructose infusion during leg exercise 1) results in increased carbohydrate oxidation from fructose, lactate, and pyruvate in exercising muscle, 2) exerts a glycogenic effect in resting muscle and liver during exercise and in liver and muscle recovering from exercise, and 3) does not interfere with glucose metabolism, and that fructose transport into muscle differs from that of glucose.

Splanchnic and renal exchange of infused fructose in insulin-deficient type 1 diabetic patients and healthy controls.

Fructose raises blood glucose and lactate levels in normal as well as diabetic man, but the tissue origin (liver and/or kidney) of these responses and the role of insulin in determining the end products of fructose metabolism have not been fully established. Splanchnic and renal substrate exchange was therefore examined during intravenous infusion of fructose or saline in six insulin-deficient type I diabetics who fasted overnight and in five healthy controls. Fructose infusion resulted in similar arterial concentrations and regional uptake of fructose in the two groups. Splanchnic glucose output increased threefold in the diabetics but remained unchanged in controls in response to fructose infusion, and the arterial glucose concentration rose more in diabetics (+5.5 mmol/liter) than in controls (+0.5 mmol/liter). Splanchnic uptake of both lactate and pyruvate increased twofold in response to fructose infusion in the diabetics. In contrast, a consistent splanchnic release of both lactate and pyruvate was seen during fructose infusion in controls. In diabetics fructose-induced hyperglycemia was associated with no net renal glucose exchange, while there was a significant renal glucose production during fructose infusion in the controls. In both groups fructose infusion resulted in renal output of lactate and pyruvate. In the diabetics this release corresponded to the augmented uptake by splanchnic tissues. In two diabetic patients given insulin infusion, all responses to fructose infusion were normalized. Fructose infusion in diabetics did not influence either splanchnic ketone body production or its relationship to splanchnic FFA inflow. We conclude that in insulin-deficient, mildly ketotic type I diabetes, (a) both the liver, by virtue of lactate, pyruvate, and fructose-derived gluconeogenesis, and the kidneys , by virtue of fructose-derived lactate and pyruvate production, contribute to fructose-induced hyperglycemia; (b) outcome of hepatic fructose metabolism; and (c) fructose does not exert an antiketogenic effect. These data suggest that while total fructose metabolism is not altered in diabetics, intermediary hepatic fructose metabolism is dependent on the presence of insulin.

Gastric emptying of glucose loads in rats: effects of insulin-induced hypoglycemia.

Previous work has established that the increased food intake of rats in response to insulin-induced hypoglycemia can be inhibited by the intravenous infusion of fructose, a sugar that cannot cross the blood-brain barrier and nourish cerebral chemoreceptors, and that this effect of fructose is abolished by hepatic vagotomy. The present series of experiments examined the effects of these treatments on gastric emptying of various glucose solutions in rats. Gastric emptying of the administered loads decreased in proportion to increasing concentration of glucose solution but not by enough for caloric delivery to be regulated precisely. Insulin-induced hypoglycemia increased the rate at which the glucose solutions emptied from the stomach. This enhanced emptying was suppressed by infusion of fructose, and that suppression was eliminated by hepatic vagotomy. These and other findings support previous proposals that food intake is controlled in part by satiety signals reflecting the nutrient content of the stomach and in part by satiety signals related to the delivery of utilizable calories to the liver.

Visceral factors in the control of food intake

Some years ago, we reported that the increased food intake of hypoglycemic rats was inhibited by the intravenous infusion of fructose, a sugar that cannot cross the blood-brain barrier and nourish cerebral chemoreceptors. More recent experiments therefore have focused on visceral factors in the control of food intake. Three observations have been emphasized in this review. First, we found that gastric emptying was increased during insulin-induced hypoglycemia, and that this effect also was eliminated by administration of fructose. Hepatic vagotomy abolished both this effect of fructose on gastric emptying and its effect on food intake. Second, we found that in rats with severe diabetes, the rate of gastric emptying did decrease in proportion to increasing concentration of an administered glucose load, as it does in intact rats, but calories emptied more rapidly than normal regardless of the concentration of the load. Third, we found that rats with varying degrees of streptozotocin-induced damage to the pancreas ate more food than intact rats did after an overnight fast, and that individual intakes were proportional to the induced glucose intolerance.The increased eating took the form of shorter intermeal intervals, as if the initial postfast meal did not remain satiating for a normal amount of time. These and other findings suggest that food intake is controlled in part by satiety signals apparently related to the delivery of utilizable calories plus insulin to the liver. These signals also seem to affect gastric emptying and thereby might influence other satiety signals related to gastric distention.

Mechanism of sympathetic activation during prolonged physical exercise in dogs. The role of hepatic glucoreceptors.

It seems likely that depletion of body carbohydrates may account for the rise in the sympathetic activity during prolonged exercise, since glucose given during or before exercise reduces the increase in plasma catecholamines. The aim of the present study was to find out whether the increase in plasma noradrenaline (NA) in response to exercise can be reduced by 1. increasing of the amount of carbohydrate available for metabolism without producing hyperinsulinemia and 2. by inhibition of afferent activity from hepatic glucoreceptors. The study was performed on dogs which exercised whilst receiving either the intravenous fructose infusion (2.2 mmol/min) or a slow glucose infusion (0.25 mmol/min) which was given either via the portal or a peripheral vein. Fructose infusion reduced the muscle glycogen depletion during exercise and reduced the increase in plasma NA and glycerol concentrations without altering the blood glucose or insulin levels. The exercise-induced increases in plasma NA and glycerol concentrations were significantly smaller with intraportal than with peripheral glucose infusion but there were no differences between these two cases in the concentration of glucose in the systemic circulation. These findings indicate that the reduction of the plasma NA response to physical effort under conditions of increased carbohydrate availability cannot be attributed to the inhibitory effect of insulin on sympathetic activity and provide evidence for the participation of hepatic glucoreceptors in the control of the sympathetic activity during exercise.

Role of the kidney in the metabolism of fructose in 60-hour fasted humans.

Arterial (A) and renal venous (RV) concentrations and net splanchnic exchange of glucose, fructose, lactate, pyruvate, glycerol, and alanine were studied in the basal state and during a 135-min intravenous infusion of fructose at 2 mmol/min in healthy subjects after a 60-h fast. After 45 min of the fructose infusion, somatostatin (9 microgram/min) was infused for 60 min to induce hypoglucagonemia. Fructose infusion resulted in a net uptake of this hexose by the kidney as well as the splanchnic bed. Estimated renal uptake of fructose could account for the disposal of 20% of the administered fructose load while splanchnic uptake accounted for 38%. The fructose infusion resulted in a rise in blood glucose of 0.9 mmol/L, a 35% increase in net glucose output from the splanchnic bed, and a consistent net output of glucose from the kidney (A-RV = -0.17 +/- 0.05 mmol/L as compared with 0 +/- 0.03 in the basal state, P less than 0.02). Net glucose release from the kidney could account for 55% of the net renal uptake of fructose. The fructose infusion also resulted in a marked change in renal lactate balance from a net uptake in the basal state (A - RV = 0.05 +/- 0.01 mmol/L) to a net output during fructose administration (A - RV = -0.10 +/- 0.04). Administration of somatostatin resulted in a fall in arterial glucagon levels and a 35% decrease in splanchnic glucose output but failed to alter the arterial-renal venous difference for glucose observed during the fructose infusion. We conclude that in 60-h fasted man: (a) intravenous infusion of fructose results in a net uptake of this hexose by the kidney as well as the liver, (b) this uptake is accompanied by stimulation of renal as well as hepatic glucose production and renal production of lactate, and (c) hypoglucagonemia inhibits splanchnic but not renal glucose output during fructose infusion. These data indicate that the kidney is an important site of fructose disposal and that glucose and lactate are end products of renal fructose metabolism.

Plasma lactate and urate concentrations following oral fructose in patients with liver disease.

Plasma lactate and urate concentrations, following 50 g oral fructose, were compared in 12 control subjects and 13 patients with liver disease. No serious adverse effects occurred following fructose ingestion, and in neither group did the plasma lactate concentration exceed 5.2 mmol/l. There were no significant differences in plasma lactate and urate concentration between the patients or controls in either the fasting state or following fructose ingestion. It is concluded that oral fructose, in contrast to intravenous fructose infusion, is unlikely to produce lactic acidosis in patients with liver disease. Also an oral fructose tolerance test based on the measurement of post-fructose plasma lactate or urate concentrations is of no value as a test of liver function.

Impaired insulin secretion after oral sucrose and fructose in rats.

The effects of sucrose and fructose on responses in plasma glucose and insulin to glucose given orally and/or iv were examined in unanesthetized, unrestrained rats. The plasma insulin response to oral administration of sucrose or a mixture of glucose and fructose was much lower than that to oral glucose despite the fact that plasma glucose responses to these administrations were similar. Oral administration fructose had no effect on the insulin response to iv infusion of glucose. Intravenous infusion of fructose also did not affect the plasma glucose and insulin responses to oral administration of glucose. The inhibitory effect of oral fructose on the insulin response to oral glucose was reversed by oral administration of soybean oil, which is known to stimulate insulin secretion induced by iv glucose. We conclude that the inhibitory effect of fructose on insulin secretion is mediated by some signals generated in the gastrointestinal tract.

Glucoregulatory response to intravenous fructose administration in the dog.

This study was designed to evaluate the influence of fructose administration on glucose kinetics and the role of fructose conversion to glucose in the maintenance of glucose homeostasis. Intravenous fructose infusion (4.5 mg/kg min-1) produced a stable plasma fructose concentration of about 20 mg/dl and a small but sustained decrease (10 mg/dl) of plasma glucose levels. The latter effect was entirely attributable to a rapid 30-35% fall in hepatic glucose output which later returned slowly to pre-infusion levels. No significant change in the rate of glucose utilization was observed. The rate of fructose conversion to glucose rose progressively during fructose infusion reaching a plateau of 1.4 mg/kg min-1 which corresponded to about 40% of total glucose production. Furthermore, as much as one third of the infused fructose was converted to circulating glucose. No appreciable changes in plasma insulin and glucagon levels occurred during fructose infusion while plasma alanine concentration increased remarkably. These data indicate that 1) fructose administration induces a transient fall in endogenous glucose production not accompanied by significant changes in glucose utilization; 2) the rapid conversion of the infused fructose to circulating glucose provides for the restoration of normal rates of glucose production; and 3) the glucoregulatory response to the administration of fructose occurs in the absence of detectable changes in plasma pancreatic hormone concentration.

Alcohol metabolism in man: Effect of intravenous fructose infusion on blood ethanol elimination rate following stimulation by phenobarbital treatment or chronic alcohol consumption

The effect of phenobarbital (PB) pretreatment and of chronic alcoholism on blood ethanol elimination rate (BEER) was investigated in man. In order to gain additional information concerning the mechanism of possible changes BEER was determined before and during intravenous infusion of fructose, a compound known to increase the NADH-oxidizing capacity of the liver and thereby stimulating alcohol oxidation rate. Following PB-treatment (300 mg/day for 5-6 days, n = 8) a marked increase in unstimulated (U-) BEER was obtained. But the fructose stimulated (FS-) BEER was not significantly changed by PB-treatment. In chronic alcoholics (n = 15) U-BEER values above the upper limit (chi + 2 S D) obtained in healthy controls, were observed only when the time of sobriety was less than one week (n = 6). Values of FS-BEER in chronic alcoholics with increased basal alcohol oxidation rates were in the same range as those of healthy controls. In 5 out of the 6 alcoholics in whom the values were elevated on admission, BEER decreased significantly after withdrawal of alcohol for 2-4 weeks. Since FS-BEER was nearly identical in all conditions tested, the distinct changes in U-BEER are probably independent of changes in the activity of enzymes involved in alcohol oxidation. It is assumed that alcohol metabolism in man is mainly controlled by the rate of NADH reoxidation in the liver.

Effects of intravenously administered fructose and glucose on splanchnic secretion of plasma triglycerides in hypertriglyceridemic men

Studies were undertaken in man to test the hypothesis that fructose produces higher rates of triglyceride secretion from the liver than equimolar amounts of glucose. Splanchnic metabolism of triglycerides and other substrates was studied during prolonged intravenous administration of 9,10- 3H-palmitate and either fructose or glucose (30 g/hr) to hypertriglyceridemic men maintained on a highcarbohydrate diet for 2 wk. The secretion of plasma triglycerides from the splanchnic region was quantified from splanchnic flow and chemical (and radio-chemical) measurements of the transsplanchnic gradients of 3H-labeled free fatty acids and triglycerides. Very high rates of release of triglycerides from the splanchnic region (average 84 g triglyceride/day) were observed during the infusion of hypercaloric amounts of either hexose. Mean values for splanchnic secretion of plasma triglyceride fatty acids were not significantly different during administration of fructose versus glucose [values for chemical production: 108 ± 28 (SE) and 96 ± 20 μmole/min/sq m, respectively] and were more than one-half the rate of transport of plasma free fatty acids. In contrast to the postabsorptive state, labeled plasma free fatty acids did not comprise a major source of the secreted plasma triglyceride fatty acids. During intravenous infusion of fructose versus glucose, the mean fraction of triglyceride fatty acids of plasma very low-density lipoproteins derived from plasma free fatty acids was 14.8% versus 8.9%, respectively; after a 12-hr infusion of either labeled hexose, that derived from fructose or glucose, though it increased with time, it reached only 5.1% and 3.6%, respectively. Elevated rates of secretion of plasma triglycerides, evidently derived from stored liver fat or glycogen, contribute to the accentuation of lipemia by either fructose or glucose. Considering the high capacity for triglyceride release of the human liver during hypercaloric carbohydrate administration, the results imply that impaired peripheral removal mechanisms may underlie the elevation of serum triglyceride levels in many patients with endogenous hyperlipemia.

Leiomyosarcoma developing in a child during remission of leukemia

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Serum Free Fatty Acid and Triglyceride Levels Before and After Intravenous Fructose Infusion in Obese Subjects with Fatty Liver

Serum Free Fatty Acid and Triglyceride Levels Before and After Intravenous Fructose Infusion in Obese Subjects with Fatty Liver

Fructose induced hyperuricemia. Effects of fructose on the de novo synthesis of adenine nucleotides in the liver and skeletal muscles of rats.

The intravenous infusion of fructose (0.7 and 2.4 g/kg/30 min) increases the incorporation of14C-glycine into rat liver adenine nucleotides significantly as compared to controls treated with 0.9% NaCl. A decrease of the total adenine nucleotide content of the livers occurs concomitantly. In contrast to its effect upon liver tissue fructose neither effects the content of adenine nucleotides nor the incorporation of glycine into these nucleotides in skeletal muscle of rats. — The results support the hypothesis that large quantities of fructose cause an increasedde novo synthesis of purine nucleotides in the liver. However, they do not as yet present clear cut evidence as to whether this is a direct effect of fructose or is secondary to the depletion of adenine nucleotides.

Utilization and turnover rate of fructose during continuous intravenous infusion in pre-term and term newborns in dependence on age.

Fructose turnover and utilization in dependence on age were examined in 55 pre-term and term newborns appropriate for gestational age during continuous intravenous infusion of fructose (0.25–1.0 g . kg&lt;sup&gt;––&lt;/sup&gt;&lt;sup&gt;1&lt;/sup&gt; · h&lt;sup&gt;––1&lt;/sup&gt;). (1) The linear turnover range of fructose is exceeded during the first 3 days of life independently of gestational age with infusions of 1.0 g · kg&lt;sup&gt;––1&lt;/sup&gt; · h&lt;sup&gt;––1&lt;/sup&gt;. This, however, is not the case in pre-term and term infants 10–12 days old. For the postnatal development of the fructose metabolism, the age of life is important, but not the gestational age. (2) During the first 3 days of life in pre-term and term infants, less than 10% of the fructose infused are eliminated. Thus, the fructose utilization is high even in the neonatal period, amounting to more than 90%. (3) The influence of fructose on the blood glucose concentration is not uniform and depends on fructose intake rate, gestational age, and age of life. Hypoglycemias were not observed.