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PubMed1996

Regulation of skeletal muscle metabolism in the lizard Dipsosaurus dorsalis by fructose-2,6-bisphosphate.

Changes in liver and skeletal muscle fructose-2,6-bisphosphate (Fru-2,6-P2) concentrations were compared during fasting, exercise, and recovery in the lizard Dipsosaurus dorsalis and in outbred mice (Mus musculus). We present the first correlative evidence that suggests that a decrease in the content of Fru-2,6-P2 may mediate elevated gluconeogenesis in lizard skeletal muscle. Contents of Fru-2,6-P2 in lizard gastrocnemius and red and white iliofibularis (IF) were significantly lower (as much as 55% in white IF) during recovery from exhaustive exercise than at rest. Recovery from exhaustive exercise had no significant effect on Fru-2,6-P2 concentrations in any mouse muscle examined. Fasting significantly depressed lizard and mouse liver Fru-2,6-P2 contents and decreased lizard red IF by over 84% from the fed condition. Lizard red and white muscle fiber bundles incubated in 20 mM lactate had significantly lower Fru-2,6-P2 (94 and 61% depression, respectively) than those incubated in 8.5 mM glucose. These results are consistent with the hypothesis that Fru-2,6-P2 acts as a signal for controlling gluconeogenesis in lizard skeletal muscle.

Animals↗
PubMed1991

Fructose 1,6-diphosphate augments paraquat injury in isolated dog lungs.

Paraquat (PQ; 1,1'-dimethyl-4,4'-bipyridylium dichloride), a widely used herbicide, causes pulmonary edema by a cyclic oxidation and reduction reaction with oxygen molecules with the production of oxygen free radicals. Because fructose 1,6-diphosphate (FDP) has recently been shown to inhibit the generation of oxygen free radicals by activated neutrophils, we determined the effects of FDP on PQ-induced increase in microvascular permeability in isolated blood-perfused dog lungs. Vascular permeability was assessed using the capillary filtration coefficient (Kf,c) and isogravimetric capillary pressure (Pc,i). There was no change in these variables over 5 h in the control lungs treated with saline (n = 5). A significant increase in Kf,c and a decrease in Pc,i, both of which indicated increased vascular permeability, were observed at 5 h of perfusion with 4 x 10(-3) M PQ (n = 5). Unexpectedly, an increase in microvascular permeability occurred within 4 h after administration of PQ in the lungs that were pretreated with FDP (2.7-14.2 mM, n = 6). Moreover the increases of Kf,c in the FDP-pretreated lungs were significantly greater than those in the lungs treated with PQ alone. Also, the final-to-initial lung weight ratio of the FDP-pretreated group was greater than those of the other groups. Thus the FDP dose used in the present study accentuated rather than prevented the PQ lung injury.

Animals↗
PubMed1992

Effect of prior exercise and insulin on potential thermogenic systems in rat skeletal muscle.

We previously reported that insulin stimulates oxygen consumption by the perfused rat hindquarter after high-intensity exercise. The purpose of the present study was to examine whether fructose 6-phosphate-fructose 1,6-bisphosphate cycling or an uncoupling of mitochondrial respiration contributes to this phenomenon. Hindquarter skeletal muscle was analyzed after perfusion in the absence or presence of insulin (150-200 microU/ml) for high-energy phosphate content, fructose 6-phosphate-fructose 1,6-bisphosphate cycling of glucose before incorporation into glycogen, and mitochondrial respiratory control. Muscle from exercised rats perfused with insulin did not display greater rates of glucose cycling or mitochondrial uncoupling; in fact, insulin decreased the rate of fructose 6-phosphate cycling and tended to increase respiratory control in skeletal muscle mitochondria. In addition, the concentrations of ATP and creatine phosphate and the calculated free ADP level in muscle of previously exercised rats perfused with insulin were similar to those of control rats. The results do not exclude the possibility that localized subcellular changes in ADP occurred, however. In conclusion, the results suggest that insulin-induced increases in other substrate cycles, ion transport systems, and/or as yet unidentified energy-requiring processes account for the 25-30% increase in hindquarter oxygen consumption after intense exercise.

Animals↗
PubMed1994

Effect of endurance training on activators of glycolysis in muscle during exercise.

Endurance training attenuates exercise-induced increases in blood lactate at the same submaximal work rate. Three intramuscular compounds that influence muscle lactate production were measured in fasted non-trained (NT) and endurance-trained (T) rats. The T rats were subjected to a progressive endurance-training program. At the end of the program (11 wk), they were running 2 h/day at 31 m/min up a 15% grade 5 days/wk. NT and T rats were fasted for 24 h and then anesthetized (pentobarbital, iv) at rest or after running for 30 min at 21 m/min (15% grade). Blood lactate levels were significantly lower in the T rats than in the NT rats after 30 min of running (2.3 +/- 0.2 vs. 3.9 +/- 0.2 mM). The lower blood lactate concentration was accompanied by lower plasma epinephrine (2.8 +/- 0.4 vs. 6.0 +/- 0.8 nM), adenosine 3', 3',5'-cyclic monophosphate (0.36 +/- 0.02 vs. 0.50 +/- 0.03 pmol/mg), mg), glucose 1,6-diphosphate (26 +/- 2 vs. 40 +/- 5 pmol/mg), and fructose 2,6-diphosphate (3.2 +/- 0.2 vs. 4.3 +/- 0.3 pmol/mg) in white quadriceps muscle in T than in NT rats. Red quadriceps muscle glucose 1,6-diphosphate and adenosine 3',5'-cyclic monophosphate were also lower in T than in NT rats. These adaptations may be responsible in part for the lower exercise-induced blood lactate in fasted rats as a consequence of endurance training.

Animals↗
PubMed1994

Muscle fructose-2,6-bisphosphate and glucose-1,6-bisphosphate during insulin-induced hypoglycemia.

Glucose production during insulin-induced hypoglycemia in the fasted state is heavily dependent on the process of hepatic gluconeogenesis. Skeletal muscle glycogen is one possible source of lactate for hepatic gluconeogenesis. Fructose 2,6-bisphosphate (F-2,6-P2) and glucose 1,6-bisphosphate (G-1,6-P2) are two allosteric activators of muscle glycolysis. To investigate their putative role in the control of muscle lactate production during hypoglycemia, fasted rats were infused via jugular catheters with insulin in 0.9% NaCl or with 0.9% NaCl alone for 60 or 120 min. Muscles were removed and clamp frozen in liquid nitrogen. The insulin infusion produced plasma insulin values of 97 +/- 13 microU/ml after 1 h and 100 +/- 9 microU/ml after 2 h. Blood glucose in the saline-infused rats was 4.6 +/- 0.2 mM after 1 h and 5.1 +/- 0.1 mM after 2 h compared with 1.5 +/- 0.01 and 1.0 +/- 0.1 mM after 1 and 2 h, respectively, in the insulin-infused rats. The hypoglycemic rats had significantly elevated plasma epinephrine and blood lactate levels compared with the saline-infused rats. F-2,6-P2 and G-1,6-P2 were increased two- to five-fold in white quadriceps of hypoglycemic rats compared with that of saline-infused rats. The results are consistent with F-2,6-P2 and G-1,6-P2 playing a role in stimulating muscle lactate production as a source of gluconeogenic substrate during insulin-induced hypoglycemia.

Animals↗
PubMed1994

Correlation between fructose 2,6-bisphosphate and lactate production in skeletal muscle.

The epinephrine-induced production of lactate in nonexercising muscles may be due in part to allosteric activation of 6-phosphofructo-1-kinase by fructose 2,6-bisphosphate (F-2,6-P2). To determine if a correlation exists between F-2,6-P2 and lactate production in skeletal muscle, isolated rat hindlimbs were perfused for 30 min with a medium containing epinephrine at concentrations varying between 1.7 +/- 0.5 and 72.4 +/- 4.2 nM. In comparison to control values, hindlimbs perfused with 72.4 +/- 4.2 nM epinephrine had a two- to threefold increase in F-2,6-P2 and a fourfold increase in muscle lactate production. Hindlimb lactate production was highly correlated to gastrocnemius adenosine 3',5'-cyclic monophosphate (r = 0.80), fructose 6-phosphate (r = 0.87), and F-2,6-P2 (r = 0.81). The adenosine 3',5'-cyclic monophosphate-mediated increase in glycogenolysis with consequent increase in fructose 6-phosphate (substrate for 6-phosphofructo-1-kinase and 6-phosphofructo-2-kinase) is likely important for induction of lactate production by inactive muscle. The high correlation between muscle F-2,6-P2 and muscle lactate production at varying concentrations of epinephrine supports the hypothesis that the epinephrine-induced activation of glycolysis and lactate production in nonexercising muscle is mediated in part by increases in F-2,6-P2 levels.

Animals↗
PubMed2000

Effect of intravenous fructose 1,6-diphosphate administration in malnourished chronic obstructive pulmonary disease patients with chronic respiratory failure.

BACKGROUND: Weight loss and skeletal muscle wasting are common in patients with chronic obstructive pulmonary disease (COPD) and can influence the course and the prognosis of COPD. Hypophosphatemia is a pathologic status often characterized by muscle weakness and is a frequent laboratory finding in these patients. OBJECTIVE: The aim of the present study was to evaluate the effect of an organic phosphate (fructose 1,6-diphosphate, FDP) administration on respiratory performance in 45 malnourished COPD patients in stable clinical conditions. METHODS: Physiologic evaluation including spirometry, maximal voluntary ventilation (MMV), elevated arm test, maximal mouth pressures (PImax and PEmax), respiratory response to CO(2), oxygen (PaO(2)) and carbon dioxide (PaCO(2)) arterial tension, a visual analogic scale (VAS) to measure dyspnea, and complete blood tests were done at the beginning and again at the end of the study. RESULTS: After FDP administration, there was a significant increase in PImax (43.0 +/- 18.3 cm H(2)O before treatment vs. 49.8 +/- 14.9 cm H(2)O after treatment; p < 0.005). This did not occur in the placebo group (40.3 +/- 17.4 cm H(2)O before treatment vs. 42.6 +/- 20.1 cm H(2)O after treatment, nonsignificant). There was also a trend of VAS to decrease and of MVV to increase. CONCLUSIONS: These results show that FDP administration may be useful in the management of malnourished COPD patients, especially in increasing their respiratory muscle strength.

Aged↗
PubMed1991

Prevention of galactosamine-induced hepatotoxicity in rats with fructose-1,6-diphosphate.

Galactosamine (GalN) administration produces hepatitis-like liver injury in animals. The hepatotoxicity of GalN is attenuated by several interventions, including activation of the reticuloendothelial system (RES). Fructose-1,6-diphosphate (FDP) administration significantly increases the phagocytic activity of the RES in animals. Thus, investigations were designed to determine whether FDP affords protection against GalN toxicity. Rats were injected with GalN (375 mg/kg) and treated with 0.9% NaCl (n = 8) or FDP (n = 9). Eight rats were sham-operated. Serum glutamic oxaloacetic transaminase was 40 times higher in the saline group as compared to the FDP-treated rats (p less than 0.0001). Glutamic pyruvic transaminase, gamma-glutamyltranspeptidase and bilirubin were similarly elevated (saline vs. FDP, p less than 0.005, p less than 0.01 and p less than 0.05, respectively). These values were not different between FDP-treated and sham-operated rats. Extensive hepatic necrosis was observed in all saline-treated rats, whereas in the FDP group only isolated foci of hepatocellular necrosis were noted. The hepatoprotective effect of FDP in this model is attributed to its ability to enhance the phagocytic activity of RES and to suppress release of oxyradicals by the leukocytes during the inflammatory phase.

Alanine Transaminase↗
PubMed1997

Effects of fructose-1,6-diphosphate on the activity of rat liver nitric oxide synthase in vitro.

Fructose-1,6-diphosphate (FDP) was found to cause significant stimulation of nitric oxide synthase (NOS) in rat liver homogenates in vitro. This effect was more pronounced for the inducible isoform than its constitutive counterpart. Furthermore, FDP restored rat liver inducible NOS levels following their depletion by carbon tetrachloride (CCl4). This finding may have further practical implications in hepatoprotection from various noxious chemical and biological agents.

Animals↗
PubMed1996

Fructose-1,6-diphosphate: potential protection in cyclosporine-induced renal impairment.

There is evidence that fructose-1,6-diphosphate (FDP) provides protection from hepatic and cardiac toxic-induced damage and ischemic renal insult. To determine if FDP also protects against cyclosporine (CsA)-induced nephrotoxicity, two groups of adult male Wistar rats were studied for whole kidney clearance rates. After two initial control periods, group 1 received only CsA (CsA, n = 8). Group 2 received FDP 350 mg/kg, followed by CsA 50 mg/kg (FDP-CsA, n = 6). In both groups, after a 30-min equilibration period, two additional clearance rates were measured (Post 1 and Post 2). A significant reduction in clearance rates was observed after drug infusion in both groups (approximately 58 and 64% in CsA and FDP-CsA groups, respectively, p < 0.05) with a recovery to control values in the Post 2 period in the FDP-CsA group. These data suggest a protective effect of FDP on CsA-induced renal impairment.

Animals↗
PubMed1987

Phosphoglycolate synthesis by human erythrocyte pyruvate kinase.

R2-type pyruvate kinase purified monogeneously from human red cells catalyzes the phosphorylation of glycolate (glycolate kinase). Maximum activation of glycolate kinase was observed at 100 microM fructose-1,6-bisphosphate (Fru-1,6-P2) and at 2 mM glucose-1,6-bisphosphate (Glc-1,6-P2). The Km for ATP was 1.1 mM in the absence of Fru-1,6-P2 and 1.5 mM in the presence of 1 mM Fru-1,6-P2. The Km for glycolate was 20 mM in the absence of Fru-1,6-P2 and 5 mM in the presence of 1.0 mM Fru-1,6-P2. The optimum pH was over 10.5. At the physiological concentrations of Fru-1,6-P2, Glc-1,6-P2 and ATP, the glycolate kinase activity is too low to maintain the reported level of phosphoglycolate (approx. 2-5 microM). It is demonstrated that phosphorylation of glycolate by R2-type pyruvate kinase which is predominant in mature red cells plays no physiological role. The questions whether an unknown pathway for phosphoglycolate synthesis exists or whether there is actually phosphoglycolate in red cells are raised.

2,3-Diphosphoglycerate↗
PubMed1987

Action of acetaldehyde on glucose metabolism of newborn and adult erythrocytes.

This paper reports the effect of acetaldehyde on erythrocytes (RBC) of human adults and newborns. Acetaldehyde increases glucose consumption in adult RBC, but has no effect on that of newborn RBC. The compound stimulates the hexose monophosphate shunt and decreases the pyruvate production of the two RBC suspensions. In newborn RBC, acetaldehyde slightly modifies triose-P and fructose-1,6-bisphosphate but has no effect on the ATP/ADP ratio and glucose-1,6-bisphosphate content, which change markedly in adult RBC. Analysis of aldehyde dehydrogenase reveals nearly one half of enzyme activity in newborn RBC. The data indicate that in both adult and newborn RBC, acetaldehyde causes an intracellular reduced state, but the newborn cells take advantage of their greater pyruvate production for complete removal of the exceeding NADH equivalents.

2,3-Diphosphoglycerate↗
PubMed1991

Fructose-1,6-diphosphate, when given five minutes after injury, does not ameliorate hypoxic ischemic injury to the central nervous system in the newborn pig.

Hypoxic ischemic injury to the brain was induced in 12 0- to 3-day-old piglets. At time 0, the carotid arteries were ligated, and the blood pressure was reduced by one third by hemorrhage. At 15 min, inspired FIO2 was reduced from 50 to 6%. After 10 min of flat EEG, the FIO2 was changes to 100%, the carotid ligations were released, and the withdrawn blood was reinfused. Five minutes after reoxygenation, the piglets were randomly assigned to either receive 350 mg of fructose-1,6-diphosphate over 5 min, followed by 6 mg/kg/min for the ensuing 50 min, or an equivalent volume of normal saline. 3 days after the experiment, the animals received a neurologic examination by a blinded observer, were then sacrificed, and the brains examined by a blinded observer. There were no significant differences in the degree of damage between the two groups.

Animals↗
PubMed1993

An enzymological profile of the production of lactic acid in caries-associated plaque and in plaque formed on sound surfaces of deciduous teeth.

Specific activities of lactate dehydrogenase (LDH) and its fructose 1,6-bisphosphate (FBP) dependency in the small amount of plaque formed on deciduous teeth were determined and compared between those from carious lesions and from sound surfaces. Although the caries-associated plaque showed a higher production of lactic acid than the plaque formed on sound surfaces, it occurred only when sufficient FBP was present. The proportion of activity of FBP-dependent LDH relative to that of total LDH varied much more in the caries-associated plaque than in the plaque formed on sound surfaces. Hence, the varying activity of FBP-dependent LDH might be a distinguishing feature of caries-associated plaque compared with plaque formed on sound surfaces.

Child↗
PubMed1983

Enhancement of the stimulating effect of fructose-1.6-diphosphate on the metabolic energy balance of carbohydrate-deficient bovine lenses by additional supply with ADP.

The energy supply in carbohydrate-deficient bovine lenses was disturbed, as could be demonstrated by measuring the content of free adenine nucleotides. It could be regenerated in part by a 3-hour-incubation in TCM 199 in the presence of fructose-1.6-diphosphate (FDP). Additional supply of ADP enhanced the stimulating effect of FDP towards formation of ATP, providing sufficient receptor molecules for the activated rate of glycolysis and probably also for the citric acid cycle.

Adenosine Diphosphate↗
PubMed1979

Long-term effect of glucagon administration on rat liver L-type pyruvate kinase.

After 5 h of treatment with glucagon, liver L-type pyruvate kinase (ATP: pyruvate 2-0-phosphotransferase; EC 2.7.1.40) showed a significant decrease of K0.5 and the Hill coefficient (nH) in the absence of fructose 1,6-diphosphate. However, in the presence of fructose 1,6-diphosphate, liver enzymes from treated rats showed a slight decrease of K0.5 but nH remained unchanged. In both circumstances, no changes of Vmax were observed after treatment. These changes in the kinetic properties of liver L-type pyruvate kinase are consistent with the dephosphorylation of the enzyme caused by insulin release in response to treatment with glucagon.

Animals↗
PubMed1991

Presence of a truncated M-type subunit and altered kinetic properties of 6-phosphofructo-1-kinase isozymes in the brain of a dog affected by glycogen storage disease type VII.

6-Phosphofructo-1-kinase (PFK) activity in the brain of a dog affected by glycogen storage disease type VII was only 31% of the PFK activity in the normal dog brain. PFK in the normal dog brain was composed of L-type, M-type and C-type subunits with apparent molecular weights of 78,000, 86,000, and 88,000, respectively, and subunit proportions (L:M:C) of 27:49:24. PFK in the affected dog brain was composed of nearly equal levels of the normal L-type and C-type subunits, but a normal M-type subunit was not detected. Using antidog muscle PFK IgG, immunoblots of gels containing partially purified PFK from the affected dog brain revealed a small amount of immunoreactive protein with an apparent molecular weight of 84,000, suggesting the presence of a truncated M-type subunit. Kinetic studies indicated that the PFK isozymes in the affected dog brain exhibited significantly different kinetic regulatory properties when compared to the PFK isozyme pool in the normal dog brain.

Adenosine Triphosphate↗
PubMed1991

Mechanism of the effect of exogenous fructose 1,6-bisphosphate on myocardial energy metabolism.

The effects of fructose 1,6-bisphosphate (F-1,6-P2) on the isolated Langendorff-perfused heart were studied by monitoring flavoprotein fluorescence, oxygen consumption (MVO2), coronary flow (Fc), systolic intraventricular pressure (Psys), diastolic intraventricular pressure, and contraction frequency. The cellular energy state and cytosolic pH were determined by means of 31P nuclear magnetic resonance. Infusion of 5 mM F-1,6-P2 caused a rapid shift toward reduction in the flavoprotein redox state and initial 50% and 44% decreases in Psys and MVO2, respectively. After a partial recovery, these measures remained 11% and 25% below the basal value. Concomitantly, after an initial transient increase of 13%, Fc remained 17% lower than in the basal state. When the F-1,6-P2 concentration was subsequently increased to 10 mM, psys and MVO2 dropped temporarily to 31% and 29% of the basal value and then remained at 50% and 53%, respectively. Simultaneously, a brief increase was observed in Fc, which then fell 34% below the basal value. Rapid reoxidation of the flavoproteins and increases in MVO2, Psys, and Fc occurred on discontinuation of the F-1,6-P2 infusion. 31P nuclear magnetic resonance during infusions of both 5 and 10 mM F-1,6-P2 revealed a decrease in cytosolic inorganic phosphate and a tendency to increase creatine phosphate, suggesting elevation in the cellular energy state. No changes in intracellular pH occurred as estimated from the chemical shift of the nuclear magnetic resonance of inorganic phosphate. F-1,6-P2 (5 mM and 10 mM) lowered the free Ca2+ concentration in the Krebs-Henseleit bicarbonate buffer (by 32% and 47%, respectively). This probably explains the effects of F-1,6-P2 on mechanical work performance and cellular respiration. A direct metabolic effect also exists, however, because flavoprotein reduction by F-1,6-P2 could be observed in the K(+)-arrested heart, where its effects on MVO2 were minimal. This redox effect may not be caused by changes in free Ca2+ concentration because it could not be reproduced by infusion of EGTA.

Animals↗