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At least 775 records · Page 43Linked to original sources
PubMed1983

Plasmid linkage of the D-tagatose 6-phosphate pathway in Streptococcus lactis: effect on lactose and galactose metabolism.

The three enzymes of the D-tagatose 6-phosphate pathway (galactose 6-phosphate isomerase, D-tagatose 6-phosphate kinase, and tagatose 1,6-diphosphate aldolase) were absent in lactose-negative (Lac-) derivatives of Streptococcus lactis C10, H1, and 133 grown on galactose. The lactose phosphoenolpyruvate-dependent phosphotransferase system and phospho-beta-galactosidase activities were also absent in Lac- derivatives of strains H1 and 133 and were low (possibly absent) in C10 Lac-. In all three Lac- derivatives, low galactose phosphotransferase system activity was found. On galactose, Lac- derivatives grew more slowly (presumably using the Leloir pathway) than the wild-type strains and accumulated high intracellular concentrations of galactose 6-phosphate (up to 49 mM); no intracellular tagatose 1,6-diphosphate was detected. The data suggest that the Lac phenotype is plasmid linked in the three strains studied, with the evidence being more substantial for strain H1. A Lac- derivative of H1 contained a single plasmid (33 megadaltons) which was absent from the Lac- mutant. We suggest that the genes linked to the lactose plasmid in S. lactis are more numerous than previously envisaged, coding for all of the enzymes involved in lactose metabolism from initial transport to the formation of triose phosphates via the D-tagatose 6-phosphate pathway.

Aldehyde-Lyases↗
PubMed1986

Biosynthesis of a galactose-and galacturonic acid-containing polysaccharide in Rhizobium meliloti.

Previous work showed that two different strains derived from a culture of Rhizobium meliloti 102F51 differed with respect to phage specificity, agglutinability by alfalfa seed lectin, and synthesis of a galactose-containing polysaccharide (R. A. Ugalde, H. Handelsman, and W. J. Brill, J. Bacteriol. 166:148-154, 1986). Inner membranes from the more competitive strain incorporated galactose from UDP-galactose when a thermostable factor was present. This factor has now been identified as UDP-galacturonic acid. UDP-glucuronic acid was also active as a donor; however, this activity may be due to the presence of a 4-epimerase. Galacturonic acid, together with galactose, is incorporated into the reaction product, which appears to be a polysaccharide formed by several repeating units of these two monosaccharides. Partial acid hydrolysis liberates the disaccharide with galactose at the reducing end.

Galactose↗
PubMed2001

Genes involved in control of galactose uptake in Lactobacillus brevis and reconstitution of the regulatory system in Bacillus subtilis.

The heterofermentative lactic acid bacterium Lactobacillus brevis transports galactose and the nonmetabolizable galactose analogue thiomethyl-beta-galactoside (TMG) by a permease-catalyzed sugar:H(+) symport mechanism. Addition of glucose to L. brevis cells loaded with [(14)C]TMG promotes efflux and prevents accumulation of the galactoside, probably by converting the proton symporter into a uniporter. Such a process manifests itself physiologically in phenomena termed inducer expulsion and exclusion. Previous evidence suggested a direct allosteric mechanism whereby the phosphocarrier protein, HPr, phosphorylated at serine-46 [HPr(Ser-P)], binds to the galactose:H(+) symporter to uncouple sugar transport from proton symport. To elucidate the molecular mechanism of inducer control in L. brevis, we have cloned the genes encoding the HPr(Ser) kinase, HPr, enzyme I, and the galactose:H(+) symporter. The sequences of these genes were determined, and the relevant phylogenetic trees are presented. Mutant HPr derivatives in which the regulatory serine was changed to either alanine or aspartate were constructed. The cloned galP gene was integrated into the chromosome of Bacillus subtilis, and synthesis of the mutant HPr proteins in this organism was shown to promote regulation of GalP, as expected for a direct allosteric mechanism. We have thus reconstituted inducer control in an organism that does not otherwise exhibit this phenomenon. These results are consistent with the conclusion that inducer exclusion and expulsion in L. brevis operates via a multicomponent signal transduction mechanism wherein the presence of glycolytic intermediates such as fructose 1,6-bisphosphate (the intracellular effector), derived from exogenous glucose (the extracellular effector), activates HPr(Ser) kinase (the sensor) to phosphorylate HPr on Ser-46 (the messenger), which binds to the galactose:H(+) symporter (the target), resulting in uncoupling of sugar transport from proton symport (the response). This cascade allows bacteria to quickly respond to changes in external sugar concentrations. Understanding the molecular mechanism of inducer control advances our knowledge of the link between metabolic and transport processes in bacteria.

Amino Acid Sequence↗
PubMed1961

Enzymatic expression of genetic units of function concerned with galactose metabolism in Escherichia coli.

Soffer, Richard L. (Stanford University, Palo Alto, Calif.). Enzymatic expression of genetic units of function concerned with galactose metabolism in Escherichia coli. J. Bacteriol. 82:471-478. 1961.-A series of genetically characterized galactose-negative mutants of Escherichia coli strain K12 were studied with respect to the enzymes of the Leloir pathway for utilization of this sugar. The functions pertaining to the three genetically defined cistrons were found to relate, respectively, to the expression of galactokinase, galactose 1-phosphate uridyl transferase, and uridine diphosphate galactose 4-epimerase. Mutants defective in the latter enzyme represent a new biochemical class in this strain of E. coli. Most of the mutants defective in galactokinase were found to exhibit significantly elevated levels of galactose 1-phosphate uridyl transferase as compared with the wild type when grown under conditions of induction. A suppressed transferase-deficient mutant was found to have regained this enzymatic activity.

Carbohydrate Metabolism↗
PubMed1996

Phosphorylation of Ga14p at a single C-terminal residue is necessary for galactose-inducible transcription.

Gal4p regulates expression of genes necessary for galactose catabolism in Saccharomyces cerevisiae. We have previously shown that phosphorylation of Gal4p requires both its DNA binding and transcriptional-activation functions and have suggested that phosphorylation occurs as a consequence of interaction with general transcription factors. In this study, we show that phosphorylation occurs rapidly on a limited fraction of overexpressed Gal4p present in a sodium dodecyl sulfate-extractable subcellular fraction while a significant fraction remains stably unphosphorylated. Taken together with our previous observations, we conclude that Gal4p is phosphorylated only if it becomes localized to the nucleus and is capable of both DNA binding and transcriptional activation. We demonstrate that Gal4p is multiply phosphorylated at both the C and N termini, and we identify the precise locations of three sites of phosphorylation at serines 691, 696, and 699. Of these sites, only serine 699 must be phosphorylated for galactose-inducible transcription to occur. Mutation of S-699 to alanine significantly impairs GAL induction by galactose in GAL80+ cells but does not affect transcriptional activation by Gal4p in gal80- cells. In gal80- cells, Gal4p phosphorylation, including that of serine 699, is stimulated by the presence of both galactose and glucose, indicating that phosphorylation at this site is not specifically activated by galactose. Serine 699 phosphorylation requires Gal4p's DNA binding function and is influenced by the function of the RNA polymerase II holoenzyme component Gal11p. These results suggest that a phosphorylation on Gal4p, likely resulting from interaction with the holoenzyme, modulates the induction process by regulating interaction between Gal4p and Gal80p.

Base Sequence↗
PubMed1987

GAL4 of Saccharomyces cerevisiae activates the lactose-galactose regulon of Kluyveromyces lactis and creates a new phenotype: glucose repression of the regulon.

A Kluyveromyces lactis mutant defective in lac9 cannot induce beta-galactosidase or galactokinase activity and is unable to grow on lactose or galactose. When this strain was transformed with the GAL4 positive regulatory gene of Saccharomyces cerevisiae it was able to grow on lactose or galactose as the sole carbon source. Transformants bearing GAL4 exhibited a 4.5-h generation time on galactose or lactose, versus 24 h for the nontransformed lac9 strain. A K. lactis lac9 strain bearing two integrated copies of GAL4 showed 3.5-fold induction of beta-galactosidase activity and 1.8-fold induction of galactokinase activity compared with 15.6-fold and 4.4-fold induction, respectively, for the LAC9 wild-type strain. In transformants bearing 10 integrated copies of GAL4, the induced level of beta-galactosidase was nearly as high as in the LAC9 wild-type strain. In addition to restoring lactose and galactose gene expression, GAL4 in K. lactis lac9 mutant cells conferred a new phenotype, severe glucose repression of lactose and galactose-inducible enzymes. Glucose repressed beta-galactosidase activity 35- to 74-fold and galactokinase activity 14- to 31-fold in GAL4 transformants, compared with the 2-fold glucose repression exhibited in the LAC9 wild-type strain. The S. cerevisiae MEL1 gene was repressed fourfold by glucose in LAC9 cells. In contrast, the MEL1 gene in a GAL4 lac9 strain was repressed 20-fold by glucose. These results indicate that the GAL4 and LAC9 proteins activate transcription in a similar manner. However, either the LAC9 or GAL4 gene or a product of these genes responds differently to glucose in K. lactis.

Enzyme Induction↗
PubMed1981

Galactosaemia: a new severe variant due to uridine diphosphate galactose-4-epimerase deficiency.

A baby presented on day 5 with symptoms of classical galactosaemia which are believed to be owing to a lack of uridine diphosphate-4-epimerase, rather than to the usual galactose-1-phosphate uridyl transferase defect. Apart from galactosaemia the condition was characterised biochemically by a red cell accumulation of galactose-1-phosphate and uridine diphosphate galactose. Galactose restriction modified the acute clinical and biochemical abnormality, but it appears essential to include some galactose in the diet in this condition to allow synthesis of galactosides, including the brain gangliosides.

Carbohydrate Epimerases↗
PubMed1976

Galactose elimination capacity as a prognostic index in patients with fulminant liver failure.

In 25 patients with fulminant hepatic failure the prognostic value of a quantitative liver function test, the galactose elimination capacity, was assessed and comapred with routine liver function tests and clinical features. The galactose elimination capacity was significantly higher (P less than 0-05) in the five patients who survived than in the 20 patients who died. None of the other liver function tests, was significantly different. The values of the galactose elimination capacity overlapped considerably between survivors and non-survivors, but all patients with a galactose elimination capacity below 12-8 mumol galactose/min and kg body weight died. The disease among most patients who died having a galactose elimination capacity greater than 13 mumol ran a subacute course. It is suggested that quantitative liver function tests be included when new treatments of fulminant hepatic failure are investigated.

Adolescent↗
PubMed1996

Galactose induces in Saccharomyces cerevisiae sensitivity of the utilization of hexoses to inhibition by D-glucosamine.

Inhibition by glucosamine of the utilization of hexoses by Saccharomyces cerevisiae is induced by growing the cells in media with galactose as carbon source. The intensity of inhibition parallels the induction of the galactose pathway. These findings contrast with the fact that glucosamine is a substrate of the constitutive glucose but not of the inducible. galactose transport and phosphorylation systems. The inhibition by glucosamine is pH dependent; the extent seems to be related with phosphorylation of the hexosamine, as shown by its greater effect with substrates or with conditions that less interfere with the phosphorylation of the inhibitor. Inhibition is not a consequence of ATP depletion of the cell. Intracellular accumulated glucosamine derivatives impair the transport of glucose and mannose in yeast cells grown in galactose-supplemented media but not those grown with glucose or ethanol supplements (i.e., under conditions in which the utilization of these sugars is inhibited). However, impairment of the transport is not enough to explain the characteristics of the observed inhibition. The changes induced by growing the yeast in galactose that render the cells sensitive to glucosamine are under the control of the gal80 and gal4 genes.

Culture Media↗
PubMed1989

Fish oil prevents effect of high cholesterol diet on active intestinal transport of galactose.

We tested the hypothesis that diets containing fish oils prevent the effects of a high cholesterol diet on the morphology and nutrient uptake of the intestine. Isocaloric semisynthetic diets were supplemented with beef tallow or fish oil containing low or high amounts of cholesterol and were fed to growing female Wistar rats for 14 days, after which the in vitro jejunal and ileal uptake of glucose, galactose, long-chain fatty acids, and cholesterol was determined. Feeding cholesterol with beef tallow was associated with a 12% decrease in the jejunal mucosal surface area. Feeding fish oil decreased jejunal mucosal surface area by 24%, as compared with the beef tallow diet, but the reduction was increased to 42% when fish oil and cholesterol were fed together. Ileal surface area was unaffected by varying the major source of dietary lipid, or by adding cholesterol. Despite the effect of fish oil on the mucosal surface area, the jejunal and ileal uptake of saturated as well as unsaturated long-chain fatty acids and cholesterol was similar in the four diet groups. Cholesterol supplementation enhanced the jejunal uptake of high concentrations of galactose only when fed with beef tallow, i.e., feeding fish oil prevented the enhancing effect of cholesterol on galactose uptake observed when beef tallow was fed. Thus, (i) a fish oil diet prevents the enhancing effect of cholesterol on jejunal active transport of galactose, an effect not explained by the reduction in jejunal mucosal surface area observed with the fish oil diet; (ii) these dietary manipulations result in a clear dissociation of the morphological from the transport adaptation of the intestine; and (iii) substitution of fish oil for beef tallow as the major source of lipid in the diet prevents the influence of cholesterol on the active intestinal transport of galactose.

Animals↗
PubMed1992

Hepatic metabolism of glucose, galactose, and lactate after milk feeding in newborn lambs.

The purpose of this study was to test the ability of the liver to efficiently clear substrates absorbed from the gastrointestinal tract after a feeding before entry into the systemic circulation. We placed a hepatic vein (HV) catheter in utero at 135-140 days gestation. The lamb was then allowed to deliver spontaneously, and additional catheters were placed in the portal vein (PV) and femoral artery (FA) at 1-3 days postnatal age. After at least 2 days recovery, lambs were fasted overnight at 4-10 days of age and then allowed to nurse ad libitum. There was significant hepatic glucose release during fasting and after 80 min postprandially. No net hepatic uptake of glucose was observed before or after feeding. PV galactose was significantly greater than FA and HV from 40 to 160 min after feeding (P less than 0.005). Hepatic glucose extraction was negligible in the fasted state (1 +/- 3%) and increased after feeding to 75 +/- 2% when PV galactose was less than 1.0 mM. There was a significant hepatic arteriovenous concentration difference of lactate (0.23 +/- 0.03 mM) and of oxygen (0.27 +/- 0.01 mM), which did not change significantly after feeding. The metabolic quotient for galactose increased significantly after feeding, such that galactose was the largest carbon contributor for postprandial hepatic carbon accretion. After a milk feeding, the newborn liver efficiently extracts galactose, lactate, and oxygen, but not glucose.

Animals↗
PubMed2000

[1-(13)C]Galactose breath test for quantitative measurement of liver function in a short period.

BACKGROUND: Using a rat model of hepatectomy, we investigated whether the severity of hepatopathy could be quantitatively measured from changes in expiratory (13)CO(2) levels after intravenous administration of [1-(13)C]galactose. MATERIALS AND METHODS: Under nembutal anesthesia, 100 mg/kg [1-(13)C]galactose was administered to rats via the femoral vein, and expiratory (13)CO(2) levels were measured for 60 min. Then, 30, 70 or 90% hepatectomy was performed. In the control group, simple laparotomy was performed. Breath test was conducted 20 min after laparotomy. We examined the correlation of total (13)CO(2) output (S) or single point (13)CO(2) level (SP) every 5 min until 30 min, and at 45 and 60 min with liver weight/body weight (LW/BW) (%). RESULTS: In the control group, the breath test graph reached a plateau level, but in all groups undergoing hepatectomy a plateau level was not reached during measurement. The correlation coefficient between S(30) after [1-(13)C]galactose administration and LW/BW was 0.889 (p< 0.0001). The correlation coefficient between SP(25) after [1-(13)C]galactose administration and LW/BW was highest, 0.923 (p< 0.0001). CONCLUSION: In the breath test with intravenously administered [1-(13)C]galactose, hepatopathy could be evaluated by measuring S(30) and hepatopathy could be more accurately quantitatively evaluated by measuring SP(25) over a short period.

Animals↗
PubMed1986

[Influence of glucose on the conversion of galactose into galactitol in the young adult].

The levels of galactose and galactitol in the sera of 6 young adults after ingestion of 0.25 g/kg of galactose alone or with the same quantity of glucose were studied. The results showed that: glucose decreased significantly the galactosemia and galactitolemia observed after ingestion of galactose alone; repeated consumption on 4 consecutive days of galactose alone induced an increase in galactosemia, and more significantly in galactitolemia. The addition of glucose to galactose in the same conditions abolished these effects.

Adult↗
PubMed1988

Effect of sodium iodate injection on the development of galactose cataract in the rat.

The effect of sodium iodate injection on the development of galactose cataract in the rat was investigated clinically and biochemically. Galactose cataracts were induced in animals which had been injected with a single dose of sodium iodate and compared with those given a saline injection. The degeneration of retinal pigment epithelium was observed electron microscopically after sodium iodate injection. A slit lamp examination of the lens showed that, in animals injected with sodium iodate, galactose-associated lens alterations progressed faster, and mature cataract development was achieved earlier than in the saline-injected animals. Biochemical data which indicated a significantly higher concentration of Na+ and lower concentration of K+ in lenses of sodium iodate-injected animals confirmed the above clinical data. The level of galactitol was higher in lenses of sodium iodate-injected than those of saline-injected animals. Acceleration of the development of galactose cataract following sodium iodate injection is apparently due to the higher level of galactose entering the aqueous humor because of breakdown of blood-ocular barriers.

Animals↗
PubMed2004

Ultrastructural aging of the RPE-Bruch's membrane-choriocapillaris complex in the D-galactose-treated mouse.

PURPOSE: Low-dose D-galactose treatment in mice induces accelerated aging due to advanced glycation endproduct (AGEs) formation. The purpose of this study was to identify ultrastructural aging in the retinal pigment epithelium (RPE)-Bruch's membrane-choriocapillaris. METHODS: Five-month-old C57Bl6 mice were injected daily with D-galactose or control buffer for 8 weeks. Eighteen-month-old mice were also treated with control buffer for 8 weeks. Eyes were prepared for electron microscopy and AGE-specific fluorescence at ex = 370 nm/em = 440 nm and ex = 330 nm/ex = 390 nm. RESULTS: D-Galactose treatment induced AGE-specific fluorescence in lens and RPE/choroid compared to buffer-treated controls. In D-galactose-treated animals, the RPE had dilated and fewer basolateral infoldings. Bruch's membrane had alterations that included significant thickening, sub-RPE and prominent outer collagenous layer deposits, and choriocapillaris basement membrane duplication/splitting and thickening. The choriocapillaris endothelium displayed fenestration loss. CONCLUSIONS: Ultrastructural aging to the RPE-Bruch's membrane-choriocapillaris developed in mice treated with low-dose D-galactose. These changes could contribute to age-related changes that promote early age-related disease.

Aging, Premature↗
PubMed1987

Galactose ingestion increases vascular permeability and collagen solubility in normal male rats.

In view of the similarity of cataracts and neuropathy in galactose-fed and diabetic rats, the present experiments were undertaken to determine whether consumption of galactose-enriched diets (10, 25, or 50% by weight) also increases collagen crosslinking and permeation of vessels by 125I-albumin analogous to that observed in diabetic rats. The observations in these experiments: demonstrate that consumption of galactose-enriched diets for 3 wk selectively increases 125I-albumin permeation of the same vascular beds affected in diabetic rats and by diabetic vascular disease in humans (i.e., the aorta and vessels in the eye, kidney, sciatic nerve, and new tissue formed in the diabetic milieu); demonstrate that the susceptibility of the vasculature to aldose reductase-linked injury (increased permeability) varies greatly in different tissues; indicate that collagen solubility (crosslinking) changes in galactose-fed rats differ sharply from those in diabetic rats; and provide new evidence that consumption of galactose-enriched diets induces a hypogonadal state in male rats.

Aldehyde Reductase↗
PubMed2005

D-galactose injured neurogenesis in the hippocampus of adult mice.

OBJECTIVES: We studied the effects of the reactive oxygen species (ROS) on neural progenitor cell proliferation and survival in the dentate gyrus (DG). METHODS: The adult mice were treated with D-galactose for 7 weeks to mimic natural aging in mice. The level of malondialdehyde (MDA) and the activities of antioxidant enzymes in the serum were detected. Neurodegeneration and neurogenesis in the hippocampus were explored using terminal deoxynucleotidyltransferase-mediated UTP nick-end labeling (TUNEL) to detect the dying cells and bromodeoxyuridine (BrdU) was used to label the newly born cells. RESULTS: After the treatment of D-galactose, the level of MDA increased and the activities of the antioxidant enzyme decreased in the serum. TUNEL-positive cells significantly increased in the DG, CA1 and CA3 subfields. The BrdU-labeled proliferating cells and surviving cells in the DG decreased significantly in number after D-galactose treatment. DISCUSSION: D-Galactose induced the impairment of neurogenesis in the DG, which is similar to natural aging in mice. ROS accumulation as a result of D-galactose may be related to the decrease of neurogenesis in the DG.

Animals↗
PubMed1979

Metabolic effects of glucose, mannose, galactose, and fructose in man.

The effects of various hexoses upon immunoreactive insulin (IRI) secretion, glucose disposal, and gastric inhibitory polypeptide (GIP) release have been compared in 10 normal nonobese men. Rapid iv infusion (0.5 g/kg in 3 min) of D-mannose resulted in significant ITI release, the peak levels approaching those after D-glucose infusion. D-Galactose, however, was ineffective. The 60-min urine excretions of mannose, galactose, and glucose were 35 +/- 7%, 16 +/- 4%, and 5.5 +/- 0.7% (mean +/- SEM) of the administered dose, respectively. All subjects also received 50 g oral glucose, mannose, galactose, and fructose on different days, each followed by an iv glucose infusion 30 min later. The ingestion of glucose or galactose resulted in a similar increment of GIP (P less than 0.01), followed by a similar increment in the IRI response to iv glucose. Furthermore, the glucose disposal rate increased 2.5-fold compared to that after iv glucose alone (P less than 0.001). However, oral msnnose or oral fructose caused no significant GIP release, yet the IRI response to a subsequent iv glucose load was moderately augmented after oral mannose or oral fructose when compared to iv glucose alone. In addition, there was a similar enhancement of glucose disposal of the iv glucose load after both oral mannose and oral fructose (P less than 0.01). From these studies we conclude that 1) galactose does not elicit IRI secretion per se, yet, like glucose, potentiates GIP and IRI secretion; 2) mannose, despite weak transport across gut or kidney, evokes significant betacytotropic effects; and 3) mannose- and fructose-induced enhancement of glucose disposal might be mediated by a factor(s) other than GIP.

Adolescent↗