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PubMed1972

The functional significance of variants of fructose 1,6-diphosphatase in the gill and hypodermis of a marine crustacean. A kinetic study.

1. In the hypodermis and gill of the Crustacea fructose 1,6-diphosphatase (EC 3.1.3.11) functions at a primary branch point between glycogen and chitin synthesis. In these tissues of the Arctic king-crab, Paralithodes camtchatica, fructose diphosphatase occurs in two electrophoretically distinguishable forms. 2. Fructose diphosphatase I (pI7.2-7.5) accounts for 70 and 10% of total fructose diphosphatase activity in the hypodermis and gill respectively, whereas fructose diphosphatase II (pI5.3) accounts for 30 and 90% of the total activity in the two tissues. Both forms display a neutral pH optimum, have an absolute requirement for a bivalent cation, and are potently inhibited by high concentrations of AMP and substrate. 3. Fructose 1,6-diphosphate saturation follows Michaelis-Menten kinetics for both fructose diphosphatases; the K(m) (fructose diphosphate) for fructose diphosphatase I is somewhat higher than for fructose diphosphatase II. In the presence of 50-200mm-K(+), the K(m) (fructose diphosphate) increases and at high concentrations of K(+) fructose diphosphate saturation follows sigmoidal kinetics. 4. UDP-N-acetylglucosamine and UDP-glucose at high concentrations specifically and potently inhibit fructose diphosphatase II, but do not significantly affect fructose diphosphatase I activity. 5. Low concentrations of UDP-N-acetylglucosamine activate fructose diphosphatase II by a decrease in the apparent K(m) (fructose diphosphate), but fructose diphosphatase I is again refractory to UDP-N-acetylglucosamine under these conditions. 6. In the presence of K(+) and UDP-N-acetylglucosamine, fructose diphosphatase II is able to compete for limiting fructose diphosphate about three times more effectively than is fructose diphosphatase I. 7. AMP inhibition of both forms of the enzyme is subject to three independent variables: (a) alkaline pH increases the K(i) (AMP), (b) K(+) decreases the K(i), increases the sigmoidicity of inhibition kinetics, increases the maximum inhibition attained, and abolishes the effect of pH on AMP inhibition, and (c) Mg(2+) strongly de-inhibits AMP-inhibited fructose diphosphatase. 8. It is postulated that the presence of two forms of fructose diphosphatase aids controlled channelling of carbon through the fructose diphosphatase ;bottleneck' either towards glycogen synthesis or chitin synthesis, but not towards both simultaneously.

Adenosine Monophosphate↗
PubMed1998

Fructose and mannose metabolism in Aeromonas hydrophila: identification of transport systems and catabolic pathways.

Aeromonas hydrophila was examined for fructose and mannose transport systems. A. hydrophila was shown to possess a phosphoenolpyruvate (PEP): fructose phosphotransferase system (fructose-PTS) and a mannose-specific PTS, both induced by fructose and mannose. The mannose-PTS of A. hydrophila exhibited cross-reactivity with Escherichia coli mannose-PTS proteins. The fructose-PTS proteins exhibited cross-reactivities with E. coli and Xanthomonas campestris fructose-PTS proteins. In A. hydrophila grown on mannose as well as on fructose, the phosphorylated derivative accumulated from fructose was fructose 1-phosphate. Identification of fructose 1-phosphate was confirmed by 13C-NMR spectroscopy. 1-Phosphofructokinase (1-PFK), which converts the product of the PTS reaction to fructose 1,6-diphosphate, was present in A. hydrophila grown with fructose but not on mannose. An inducible phosphofructomutase (PFM) activity, an unusual enzyme converting fructose 1-phosphate to fructose 6-phosphate, was detected in extracts induced by mannose or fructose. These results suggest that in cells grown on fructose, fructose 1-phosphate could be converted to fructose 1,6-diphosphate either directly by the 1-PFK activity or via fructose 6-phosphate by the PFM and 6-phosphofructokinase activities. In cells grown on mannose, the degradation of fructose 1-phosphate via PFM and the Embden-Meyerhof pathway appeared to be a unique route.

Aeromonas hydrophila↗
PubMed1989

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.

Adult↗
PubMed2006

Is fructose the optimal low glycemic index sweetener?

Fructose is a monosaccharide which is abundant in nature. It is the sweetest naturally occurring carbohydrate. The availability of fructose increased substantially when it became possible in the 1960s to economically produce high fructose syrups from corn starch and other starches. Such high fructose syrups are now used to sweeten soft drinks, fruit drinks, baked goods, jams, syrups and candies. The most recent data available suggest that fructose consumption is increasing worldwide. Fructose presently accounts for about 10% of average total energy intake in the United States. Studies in both healthy and diabetic subjects demonstrated that fructose produced a smaller postprandial rise in plasma glucose and serum insulin than other common carbohydrates. Substitution of dietary fructose for other carbohydrates produced a 13% reduction in mean plasma glucose in a study of type-1 and type-2 diabetic subjects. However, there is concern that fructose may aggravate lipemia, particularly in men. In one study, daylong plasma triglycerides (estimated by determining the area under response curves) in healthy men was 32% greater during a high fructose diet than during a high glucose diet. There is also concern that fructose may be a factor contributing to the growing worldwide prevalence of obesity. Increasing fructose consumption is temporally associated with the increase in obesity. Moreover, on theoretical grounds, dietary fructose might increase energy intake. Fructose stimulates insulin secretion less than does glucose and glucose-containing carbohydrates. Since insulin increases leptin release, lower circulating insulin and leptin after fructose ingestion might inhibit appetite less than consumption of other carbohydrates and lead to increased energy intake. However, there is not yet any convincing experimental evidence that dietary fructose does increase energy intake. Although evidence that fructose has adverse effects is limited, adding fructose in large amounts to the diet may be undesirable, particularly for men. Fructose that occurs naturally in fruits and vegetables is a modest component of energy intake and should not be of concern.

Area Under Curve↗
PubMed2004

Cyclic AMP stimulates fructose transport in neonatal rat small intestine.

Intestinal fructose transporter (GLUT5) expression normally increases significantly after completion of weaning in neonatal rats. Increases in GLUT5 mRNA, protein, and activity can be induced in early weaning pups by precocious consumption of dietary fructose or by perfusion of the small intestine with fructose solutions. Little is known about the signal transduction pathway of the dietary fructose-mediated increase in GLUT5 expression during early intestinal development. Recent microarray results indicate that key gluconeogenic enzymes modulated by cAMP are markedly upregulated by fructose perfusion; hence, we tested the hypothesis that cAMP plays an important role in regulating intestinal fructose absorption by simultaneously perfusing adenylyl cyclase, phosphodiesterase, or protein kinase A (PKA) inhibitors along with fructose. Intestinal fructose uptake rates increased by 100% in rat pups perfused with 8-bromo-cAMP. Simultaneous fructose and dideoxyadenosine (DDA; inhibitor of adenylyl cyclase) perfusion completely inhibited increases in fructose uptake rate induced by perfusion with fructose alone. Fructose perfusion increased intestinal mucosal cAMP concentrations by 27%, but simultaneous perfusion of fructose and DDA inhibited the fructose-induced increase in cAMP. However, GLUT5 and sodium-glucose cotransporter (SGLT1) mRNA abundance and glucose transport rates were each not significantly affected by 8-bromo-cAMP and DDA. Moreover, simultaneous perfusion of the small intestine with fructose and PKA inhibitor or N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamid. 2HCl, both inhibitors of PKA, did not prevent the fructose-induced increases in GLUT5 mRNA abundance and fructose uptake rate. Cyclic AMP appears to modulate fructose transport without affecting GLUT5 mRNA abundance, and without involving PKA.

Animals↗
PubMed1984

Absorption and metabolism of fructose by rat jejunum.

The absorption and metabolism of fructose was investigated in the vascularly perfused jejunum of fructose-fed rats. With 10 mM-glutamate and 10 mM-fructose in the lumen, the viability of the tissue is maintained and fructose is absorbed and utilized at high rates. With 28 mM-fructose in the lumen, glucose appears in the vascular bed. With 10 mM- or 28 mM-fructose in the presence of 10 mM- or mM-glucose in the lumen, the fructose absorption is decreased. From 10 mM- or 28 mM-sucrose in the lumen, fructose uptake is also less than from the equivalent concentration of free fructose. The rate of appearance of fructose in the vascular bed is independent of the source of fructose from which it is derived. In the presence of glucose, either free or as sucrose, there is a marked decrease in the utilization of fructose, defined as the difference between that absorbed by the jejunum and that transported unchanged into the vascular bed. In all cases about half of the carbohydrate absorbed from the lumen is converted into lactate, most of which is secreted into the blood. The absorption of glucose and the rate of vascular appearance of glucose from glucose in the lumen are about 1.5 times greater than those of fructose from fructose in the lumen. It is concluded: firstly, that fructose uptake from the lumen of rat jejunum is determined by its concentration and by the demand for it as a fuel for the intestine, a demand that is severely decreased in the presence of glucose; secondly, that in the vascularly perfused jejunum there is no evident kinetic advantage for uptake of fructose or glucose from sucrose rather than from free monosaccharide in the lumen; thirdly, that some fructose can be converted into glucose.

Animals↗
PubMed1995

Carrier-mediated fructose uptake significantly contributes to carbohydrate metabolism in human skeletal muscle.

To determine whether fructose can be utilized as a metabolic substrate for skeletal muscle in man, we investigated its incorporation into glycogen, its oxidation and lactate production in isolated human skeletal muscle. Rates of fructose oxidation and incorporation into glycogen increased in the presence of increasing fructose concentrations (0.1-1.0 mM). Lactate production increased 3-fold when extracellular fructose was increased from 0.1 to 0.5 mM. Cytochalasin B, a competitive inhibitor of hexose transport mediated by the GLUT1 and GLUT4 facilitative glucose transporters, completely inhibited insulin-stimulated glucose incorporation into glycogen and glucose oxidation (P < 0.01), but did not alter fructose incorporation into glycogen or fructose oxidation. Insulin (1000 mu-units/ml) increased glucose incorporation into glycogen 2.7-fold and glucose oxidation 2.3-fold, whereas no effect on fructose incorporation into glycogen or fructose oxidation was noted. A physiological concentration of glucose (5 mM) decreased the rate of 0.5 mM fructose incorporation into glycogen by 60% (P < 0.001), whereas fructose oxidation was not altered in the presence of 5 mM glucose. Irrespective of fructose concentration, the majority of fructose taken up underwent non-oxidative metabolism. Lactate production accounted for approx. 80% of the fructose metabolism in the basal state and approx. 70% in the insulin (1000 mu-units/ml)-stimulated state. In the presence of 5 mM glucose, physiological concentrations of fructose could account for approximately 10-30% of hexose (glucose + fructose) incorporation into glycogen under non-insulin-stimulated conditions. In conclusion, fructose appears to be transported into human skeletal muscle via a carrier-mediated system that does not involve GLUT4 or GLUT1. Furthermore, under physiological conditions, fructose can significantly contribute to carbohydrate metabolism in human skeletal muscle.

Adult↗
PubMed1967

Inhibition of glucose phosphate isomerase by metabolic intermediates of fructose.

1. Purified rabbit-muscle and -liver glucose phosphate isomerase, free of contaminating enzyme activities that could interfere with the assay procedures, were tested for inhibition by fructose, fructose 1-phosphate and fructose 1,6-diphosphate. 2. Fructose 1-phosphate and fructose 1,6-diphosphate are both competitive with fructose 6-phosphate in the enzymic reaction, the apparent K(i) values being 1.37x10(-3)-1.67x10(-3)m for fructose 1-phosphate and 7.2x10(-3)-7.9x10(-3)m for fructose 1,6-diphosphate; fructose and inorganic phosphate were without effect. 3. The apparent K(m) values for both liver and muscle enzymes at pH7.4 and 30 degrees were 1.11x10(-4)-1.29x10(-4)m for fructose 6-phosphate, determined under the conditions in this paper. 4. In the reverse reaction, fructose, fructose 1-phosphate and fructose 1,6-diphosphate did not significantly inhibit the conversion of glucose 6-phosphate into fructose 6-phosphate. 5. The apparent K(m) values for glucose 6-phosphate were in the range 5.6x10(-4)-8.5x10(-4)m. 6. The competitive inhibition of hepatic glucose phosphate isomerase by fructose 1-phosphate is discussed in relation to the mechanism of fructose-induced hypoglycaemia in hereditary fructose intolerance.

Journal Article↗
PubMed1982

Fructose-2,6-P2, chemistry and biological function.

A new activator of phosphofructokinase, which is bound to the enzyme and released during its purification, has been discovered. Its structure has been determined as beta-D Fructose-2,6-P2 by chemical synthesis, analysis of various degradation products and NMR. D-Fructose-2,6-P2 is the most potent activator of phosphofructokinase and relieves inhibition of the enzyme by ATP and citrate. It lowers the Km for fructose-6-P from 6 mM to 0.1 mM. Fructose-6-P,2-kinase catalyzes the synthesis of fructose-2,6-P2 from fructose-6-P and ATP, and the enzyme has been partially purified. The degradation of fructose-2,6-P2 is catalyzed by fructose-2,6-bisphosphatase. Thus a metabolic cycle could occur between fructose-6-P and fructose-2,6-P2, which are catalyzed by these two opposing enzymes. The activities of these enzymes can be controlled by phosphorylation. Fructose-6-P,2-kinase is inactivated by phosphorylation catalyzed by either cAMP dependent protein kinase or phosphorylase kinase. The inactive, phospho-fructose-6,P,2-kinase is activated by dephosphorylation catalyzed by phosphorylase phosphatase. On the other hand, fructose-2,6-bisphosphatase is activated by phosphorylation catalyzed by cAMP dependent protein kinase. Investigation into the hormonal regulation of phosphofructokinase reveals that glucagon stimulates phosphorylation of phosphofructokinase which results in decreased affinity for fructose-2,6-P2 appears to be due to the decreased synthesis by inactivation of fructose-2,6-P2,2-kinase and increased degradation as a result of activation of fructose-2,6-bisphosphatase. Such a reciprocal change in these two enzymes has been demonstrated in the hepatocytes treated by glucagon and epinephrine. The implications of these observations in respect to possible coordinated controls of glycolysis and glycogen metabolism are discussed.

Enzyme Activation↗
PubMed1995

[Fructose vs. glucose in total parenteral nutrition in critically ill patients].

UNLABELLED: Parenteral nutrition required following surgery or injury should not only meet post-aggression caloric requirements but also match the specific metabolic needs so as not to worsen the metabolic disruptions already present in this situation. The primary objective of parenteral nutrition is body protein maintenance or restoration by reduction of protein catabolism or promotion of protein synthesis or both. Whether all parenteral energy donors, ie., glucose, fructose, other polyols, and lipid emulsions, are equally capable of achieving this objective continues to be a controversial issue. The objective of the present study was to answer the following questions: (1) Do glucose and fructose differ in their effects on the metabolic changes seen following surgery or injury, the changes in glucose metabolism in particular? (2) Can the observation of poorer glucose utilization in the presence of lipids be confirmed in ICU patients? PATIENTS, MATERIALS AND METHODS: A prospective, randomized clinical trial has been conducted in 20 aseptic surgical ICU patients to generate an objective database along these lines by performing a detailed analysis of the metabolic responses to different parenteral nutrition protocols. The effects of a glucose solution+lipid emulsion regimen vs fructose solution+lipid emulsion regimen on a number of carbohydrate and lipid metabolism variables were evaluated for an isocaloric (carbohydrates: 0.25 g/kg body weight/h; lipids: 0.166g/kg body weight/h) and isonitrogenous (amino acids: 0.0625 g/kg body weight/h) total nutrient supply over a 10-h study period. RESULTS: A significantly smaller rise in blood glucose concentrations (increase from baseline: glucose+lipids P<0.001 vs fructose+lipids n.s.) suggested that fructose had a small effect, if any at all, on glucose metabolism. Serum insulin activity showed significant differences as a function of carbohydrate regimen, i.e. infusion of fructose instead of glucose produced a less pronounced increase in insulin activity (increase from baseline: glucose+lipids P<0.001 vs fructose+lipids P<0.01). Impairment of glucose utilization by concomitant administration of lipids was observed neither in patients who first received glucose nor in those who first received fructose. CONCLUSIONS: As demonstrated, parenteral fructose, unlike parenteral glucose, has a significantly less adverse impact than glucose on the glucose balance, which is disrupted initially in the post-aggression state. In addition, the less pronounced increase in insulin activity during fructose infusion than during glucose infusion can be assumed to facilitate mobilization of endogenous lipid stores and lipid oxidation. Earlier workers pointed out that any rise in free fatty acid and ketone body concentrations in the serum produces inhibition of muscular glucose uptake and oxidation, and of glycolysis. These findings were recorded in a rat model and could not be confirmed in our post-aggression state patients receiving lipid doses commensurate with the usual clinical infusion rates. The serious complications that can result from hereditary fructose intolerance are completely avoidable if a careful patient history is taken before the first parenteral use of fructose. If the patient or family members and close friends, are simply asked whether he/she can tolerate fruit and sweet dishes, hereditary fructose intolerance can be ruled out beyond all reasonable doubt. Only in the extremely rare situations in which it is not possible to question either the patient or any significant other, a test dose will have to be administered to exclude fructose intolerance. The benefits of fructose-specific metabolic effects reported in the literature and corroborated by the results of out own study suggest that fructose is an important nutrient that contributes to metabolic stabilization, especially in the post-aggression phase and in septic patients. Hyperglycaemic states are largely prevented and fewer patients require ex

Adolescent↗
PubMed2001

True corrected seminal fructose level: a better marker of the function of seminal vesicles in infertile men.

This study was designed to determine if the value obtained after multiplying motile sperm concentration by seminal fructose concentration, named "true corrected fructose", correlates with sperm motility in asthenozoospermic men. Forty-two male partners in infertile couples were studied. Men were treated with 100 mg daily of clomiphene citrate for 5 days. Blood and semen samples were collected before treatment and 24 h after the end of treatment. Serum testosterone, seminal fructose and sperm motility were measured in each subject. Corrected fructose (log. sperm concentration multiplied by seminal fructose), and true corrected fructose (log. motile sperm concentration multiplied by seminal fructose) values were calculated. Prevalence of asthenozoospermia was 42.85% (18 of 42). Prevalence of hypofunction of the seminal vesicles was 9.5% using seminal fructose as a marker; 40.5% using seminal corrected fructose as a marker and 47.6% using true corrected fructose as a marker of seminal vesicle function. Regression analysis showed a better coefficient of determination between true corrected fructose and motile sperm concentration (R2=0.20, p < 0.001) than with corrected fructose (R(2)=0.05, p < 0.1) or fructose concentration (R(2)=0.006, p < 0.5). Asthenozoospermia was observed in 22.7% of subjects with normal function of the seminal vesicles, and in 65% of men with low values of true corrected fructose (z=6.02, p < 0.0001). Multivariate analysis showed that sperm motility grade 3 improved after treatment with clomiphene if true corrected fructose increased (p < 0.002). In those men whose seminal vesicle function improved after clomiphene treatment, a reduction in the prevalence of asthenozoospermia from 50 to 28.6% (z=3.10, p < 0.002) was observed whereas in those whose seminal vesicles did not respond to clomiphene the prevalence of asthenozoospermia was not reduced (z=1.05; p: NS). In conclusion, true corrected fructose measurement relates with sperm motility in cases of asthenozoospermia. Asthenozoospermia improves with clomiphene treatment if seminal vesicle function improves after treatment.

Adult↗
PubMed2000

The interaction between dietary fructose and magnesium adversely affects macromineral homeostasis in men.

OBJECTIVE: Studies with rats have found that an interaction between fructose and magnesium affects macromineral metabolism; high dietary fructose significantly increased kidney calcification in both male and female rats, particularly when dietary magnesium was low. This study tests the hypothesis that an interaction between dietary fructose and magnesium adversely affects macromineral homeostasis in men. METHODS: Eleven men aged 22 to 40 years were fed a mixed, Western diet for four 42-day dietary periods in which dietary magnesium was either approximately 170 or 370 mg/day and dietary fructose was either 4% or 20% of energy. A decaffeinated beverage containing high fructose corn syrup replaced cornstarch, bread and rice in the low fructose diet to give the high fructose diet. RESULTS: High dietary fructose significantly (p<0.01) increased magnesium balance during both low and high dietary magnesium intakes. Ultrafilterable and ionized serum magnesium also apparently were related to magnesium and fructose intakes; they were higher when fructose was fed and when Mg intakes were high. High fructose depressed calcium balance: the effect tended to be more marked when dietary Mg was low. High dietary fructose also significantly (p<0.005) decreased phosphorous balance. Urinary phosphorous losses were significantly (p<0.001) higher when high dietary fructose was fed. High dietary fructose also increased the concentration of serum alkaline phosphatase (p<0.005). CONCLUSION: These findings indicate that dietary fructose adversely affects macromineral homeostasis in humans and suggest further studies to see if a high fructose diet coupled with low dietary magnesium and marginal calcium leads to bone loss.

Adult↗
PubMed1995

Agrobacterium radiobacter and related organisms take up fructose via a binding-protein-dependent active-transport system.

Washed cells of Agrobacterium radiobacter prepared from a fructose-limited continuous culture (D 0.045 h-1) transported D(-)[U-14C]fructose in a linear manner for up to 4 min at a rate several-fold higher than the rate of fructose utilization by the growing culture. D(-)[U-14C]Fructose transport exhibited a high affinity for fructose (KT < 1 microM) and was inhibited to varying extents by osmotic shock, by the uncoupling agent carbonyl cyanide p-trifluoromethoxyphenylhydrazone, and by unlabelled sugars (D-fructose/D-mannose > D-ribose > D-sorbose > D-glucose/D-galactose/D-xylose; no inhibition by D-arabinose). Prolonged growth of A. radiobacter in fructose-limited continuous culture led to the selection of a novel strain (AR100) which overproduced a fructose-binding protein (FBP) and showed an increased rate of fructose transport. FBP was purified from osmotic-shock fluid using anion-exchange fast protein liquid chromatography (FPLC). The monomeric protein (M(r) 34,200 by SDS-PAGE and 37,700 by gel-filtration FPLC) bound D-[U-14C]-fructose stoichiometrically (1.17 nmol nmol FBP-1) and with high affinity (KD 0.49 microM) as shown by equilibrium dialysis. Binding of D-[U-14C]fructose by FBP was variably inhibited by unlabelled sugars (D-fructose/D-mannose > D-ribose > D-sorbose; no inhibition by D-glucose, D-galactose or D-arabinose). The N-terminal amino acid sequence of FBP (ADTSVCLI-) was similar to that of several sugar-binding proteins from other species of bacteria. Fructose transport and FBP were variably induced in batch cultures of A. radiobacter by growth on different carbon sources (D-fructose > D-ribose/D-mannose > D-glucose; no induction by succinate). An immunologically similar protein to FBP was produced by Agrobacterium tumefaciens and various species of Rhizobium following growth on fructose. It is concluded that fructose is transported into A. radiobacter and related organisms via a periplasmic fructose/mannose-binding-protein-dependent active-transport system, in contrast to the phosphotransferase system used by many other species of bacteria.

Amino Acid Sequence↗