Galactose
Galactose Oxidase
Galactose Dehydrogenases
Galactosemias
Uridine Diphosphate Galactose
UDPglucose 4-Epimerase
Galactokinase
UTP-Hexose-1-Phosphate Uridylyltransferase
Galactitol
Carbohydrates
Lactose
Monosaccharides
Galactosyltransferases
Lectins
Mannose
Carbohydrate Sequence
UDPglucose-Hexose-1-Phosphate Uridylyltransferase
Oligosaccharides
Glucose
Galactosidases
Carbohydrate Epimerases
Carbohydrate Metabolism
Phosphoglucomutase
Chromatography, Paper
Molecular Sequence Data
Glycopeptides
Amino Sugars
Sialic Acids
Glycolipids
Glycoproteins
Galactosides
Plant Lectins
Asialoglycoproteins
Glycosides
Rhamnose
Fetuins
Glycosphingolipids
Chromatography, Thin Layer
Melibiose
Glycosylation
N-Acetylneuraminic Acid
Uronic Acids
Saccharomyces cerevisiae
Ricin
alpha-Galactosidase
Escherichia coli
Actinomycetales
Fructose
Neuraminidase
beta-Galactosidase
Fermentation
Cell Wall
Uridine Diphosphate Glucose
Mutation
UTP-Glucose-1-Phosphate Uridylyltransferase
Monosaccharide Transport Proteins
Lactococcus lactis
Amino Acids
Globosides
Chromatography, Gas
Chromatography, Gel
Asialoglycoprotein Receptor
Sodium-Glucose Transport Proteins
Galactans
Erythrina
Culture Media
Kluyveromyces
Phosphotransferases
Glycoconjugates
Magnetic Resonance Spectroscopy
Cerebrosides
Carbon Isotopes
Substrate Specificity
Gene Expression Regulation, Fungal
Gangliosides
N-Acetyllactosamine Synthase
Amino Acid Sequence
Hydrogen-Ion Concentration
Electrophoresis, Polyacrylamide Gel
Sialyltransferases
Gangliosides of human kidney. (1/3083)
Five gangliosides isolated from human kidney have been characterized. The two main fractions were shown to be typical extraneural gangliosides in having lactose as their neutral carbohydrate moiety. Their structures were identified as: AcNeu(alpha2-3)Gal(beta1-4)Glc(beta1-1)Cer and AcNeu(alpha2-8)AcNeu(alpha2-3)Gal(beta1-4)Glc(beta1-1)Cer. The two main hexosamine-containing gangliosides are structurally related to human blood group substances of glycosphingolipid nature. The following structures are postulated: AcNeu(alpha2-3)Gal(beta1-4)GlcNAc(beta1-3)Gal(beta1-4)Glc(beta1-1)Cer and AcNeu(alpha2-3)Gal(beta1-4)[Fuc(alpha1-3)]GlcNAc(beta1-3)Gal(beta1-4)Glc(beta1-1) Cer. The third hexosamine-containing ganglioside belongs to a different series of glycolipids and was shown to have the structure of a major ganglioside of human brain: AcNeu(alpha2-3)Gal(beta1-3)GalNAc(beta1-4)[AcNeu(alpha2-3)]Gal(beta1-4)Glc(beta1- 1)Cer. The fatty acid structure of different gangliosides was shown to resemble that of neutral glycolipids of human kidney with the nonhydroxy acids C16:0, C22:0, and C24:0 as major components. (+info)Missense mutations in SGLT1 cause glucose-galactose malabsorption by trafficking defects. (2/3083)
Glucose-galactose malabsorption (GGM) is an autosomal recessive disorder caused by defects in the Na+/glucose cotransporter (SGLT1). Neonates present with severe diarrhea while on any diet containing glucose and/or galactose [1]. This study focuses on a patient of Swiss and Dominican descent. All 15 exons of SGLT1 were screened using single stranded conformational polymorphism analyses, and aberrant PCR products were sequenced. Two missense mutations, Gly318Arg and Ala468Val, were identified. SGLT1 mutants were expressed in Xenopus laevis oocytes for radiotracer uptake, electrophysiological experiments, and Western blotting. Uptakes of [14C]alpha-methyl-d-glucoside by the mutants were 5% or less than that of wild-type. Two-electrode voltage-clamp experiments confirmed the transport defects, as no noticeable sugar-induced current could be elicited from either mutant [2]. Western blots of cell protein showed levels of each SGLT1 mutant protein comparable to that of wild-type, and that both were core-glycosylated. Presteady-state current measurements indicated an absence of SGLT1 in the plasma membrane. We suggest that the compound heterozygote missense mutations G318R and A468V lead to GGM in this patient by defective trafficking of mutant proteins from the endoplasmic reticulum to the plasma membrane. (+info)Carbohydrate on human factor VIII/von Willebrand factor. Impairment of function by removal of specific galactose residues. (3/3083)
Human factor VIII/von Willebrand factor protein containing 120 +/- 12 nmol of sialic acid and 135 +/- 13 nmol of galactose/mg of protein was digested with neuraminidase. The affinity of native factor VIII/von Willebrand factor and its asialo form for the hepatic lectin that specifically binds asialoglycoproteins was assessed from in vitro binding experiments. Native factor VIII/von Willebrand factor exhibited negligible affinity while binding of the asialo derivative was comparable to that observed for asialo-alpha1-acid glycoprotein. Incubation of asialo-factor VIII/von Willebrand factor with Streptococcus pneumoniae beta-galactosidase removed only 62% of the galactose but abolished binding to the purified hepatic lectin. When the asialo derivative was incubated with purified beta-D-galactoside alpha2 leads to 6 sialyltransferase and CMP-[14C]NeuAc, only 61% of the galactose incorporated [14C]NeuAc. From the known specificites of these enzymes, it is concluded that galactose residues important in lectin binding are present in a terminal Gal/beta1 leads to 4GlcNAc sequence on asialo-factor VIII/von Willebrand factor. The relative ristocetin-induced platelet aggregating activity of native, asialo-, and agalacto-factor VIII/von Willebrand factor was 100:38:12, respectively, while procoagulant activity was 100:100:103. (+info)Stimulation of collagen galactosyltransferase and glucosyltransferase activities by lysophosphatidylcholine. (4/3083)
Lysophosphatidylcholine stimulated the activities of collagen galactosyl- and glucosyl-transferases in chick-embryo extract and its particulate fractions in vitro, whereas essentially no stimulation was noted in the high-speed supernatant, where the enzymes are soluble and membrane-free. The stimulatory effect of lysophosphatidylcholine was masked by 0.1% Triton X-100. In kinetic experiments lysophosphatidylcholine raised the maximum velocities with respect to the substrates and co-substrates, whereas no changes were observed in the apparant Km values. Phospholipase A preincubation of the chick-embryo extract resulted in stimulation of both transferase activities, probably gy generating lysophosphatides from endogenous phospholipids. No stimulation by lysophosphatidylcholine was found when tested with 500-fold-purified glycosyltransferase. The results suggest that collagen glycosyltransferases must be associated with the membrane structures of the cell in order to be stimulated by lysophosphatidylcholine. Lysophosphatidylcholine could have some regulatory significance in vivo, since its concentration in the cell is comparable with that which produced marked stimulation in vitro. (+info)Oligomycin induces a decrease in the cellular content of a pathogenic mutation in the human mitochondrial ATPase 6 gene. (5/3083)
A T --> G mutation at position 8993 in human mitochondrial DNA is associated with the syndrome neuropathy, ataxia, and retinitis pigmentosa and with a maternally inherited form of Leigh's syndrome. The mutation substitutes an arginine for a leucine at amino acid position 156 in ATPase 6, a component of the F0 portion of the mitochondrial ATP synthase complex. Fibroblasts harboring high levels of the T8993G mutation have decreased ATP synthesis activity, but do not display any growth defect under standard culture conditions. Combining the notions that cells with respiratory chain defects grow poorly in medium containing galactose as the major carbon source, and that resistance to oligomycin, a mitochondrial inhibitor, is associated with mutations in the ATPase 6 gene in the same transmembrane domain where the T8993G amino acid substitution is located, we created selective culture conditions using galactose and oligomycin that elicited a pathological phenotype in T8993G cells and that allowed for the rapid selection of wild-type over T8993G mutant cells. We then generated cytoplasmic hybrid clones containing heteroplasmic levels of the T8993G mutation, and showed that selection in galactose-oligomycin caused a significant increase in the fraction of wild-type molecules (from 16 to 28%) in these cells. (+info)Quantitative determination of N-acetylglucosamine residues at the non-reducing ends of peptidoglycan chains by enzymic attachment of [14C]-D-galactose. (6/3083)
The ability of human milk galactosyltransferase to attach D-galactose residues quantitatively to the C-4 of N-acetylglucosamine moieties at the ends of oligosaccharides has been utilized for the specific labeling and quantitative determination of the chain length of the glycan moiety of the bacterial cell wall. The average polysaccharide chain length of the soluble, uncrosslinked peptidoglycan secreted by Micrococcus luteus cells on incubation with penicillin G was studied with this technique and found to be approximately 70 hexosamines long. Furthermore, the peptidoglycan chain length of Escherichia coli sacculi of different cell shapes and dimensions was determined both in rod-shaped cells and in filaments induced by temperature shift of a division mutant or by addition of cephalexin or nalidixic acid. The average chain length found in most of these sacculi was between 70 and 100 hexosamines long. Small spherical 'mini' cells had chain lengths similar to those of the isogenic rod-like cells. (+info)A unique primary structure, cDNA cloning and function of a galactose-specific lectin from ascidian plasma. (7/3083)
The complete amino acid sequence of a galactose-specific lectin from the plasma of the ascidian Halocynthia roretzi has been determined by sequential Edman degradation analysis of peptide fragments derived by proteolytic fragmentation and chemical cleavage of the reductive S-pyridylethylated lectin. Peptide fragments were separated by reverse-phase HPLC. The N-terminal and C-terminal amino acid sequences were determined by Edman degradation and enzymatic digestion. The H. roretzi plasma lectin is a single-chain protein consisting of 327 amino acids and four disulfide bonds, one of which was found to be cross-linked intramolecularly. A comparison of the amino acid sequence of the H. roretzi plasma lectin with the sequences of other proteins reveals that the H. roretzi lectin has a structure consisting of a twice-repeated sequence, a fibrinogen-related sequence and a C-type lectin-homologous sequence. The above amino acid sequence was verified by cDNA cloning of this lectin. Three cDNA clones that have single ORFs encoding the lectin precursor were isolated from an H. roretzi hepatopancreas cDNA library. The deduced amino acid sequences in the three cDNA clones contain the same sequence of the mature lectin molecule and the same putative signal sequence. In addition, it was demonstrated that this lectin can enhance phagocytosis by H. roretzi hemocytes. Thus, the plasma lectin is constructed into an oligomer structure via intermolecular disulfide bonds and plays a role in the biological defense of H. roretzi as a defense molecule. (+info)Orotate decreases the inhibitory effect of ethanol on galactose elimination in the perfused rat liver. (8/3083)
1. The galactose-elimination rate in perfused livers from starved rats was decreased in the presence of ethanol (2-28mM) to one-third of the control values. Orotate injections partly reversed the effect of ethanol, so that the galactose-elimination rate was about two-thirds of the control values. Orotate alone had no effect on the galactose-elimination rate. 2. Ethanol increased [galactose 1-phosphate] and [UDP-galactose], and decreased (UDP-glucose] and [UTP], both with and without orotate. Orotate increased [UTP], [UDP-galactose], both with and without ethanol. The increase of [galactose 1-phosphate] in the presence of ethanol was inhibited by orotate. Orotate alone had no appreciable effect on [galactose 1-phosphate]. 3. Both the effect of ethanol and that of orotate on the galactose-elimination rate can be accounted for by assuming inhibition of galactokinase by galactose 1-phosphate with Ki about 0.2mM, the inhibition being either non-competitive or uncompetitive. 4. The primary effect of ethanol seems to be inhibition of UDP-glucose epimerase (EC 5.1.3.2), followed by accumulation of UDP-galactose, trapping of UDP-glucose and increase of [galactose 1-phosphate]. Orotate decreased the effect of ethanol, probably by increasing [UDP-glucose]. (+info)There are two main types of galactosemia:
1. Classical galactosemia: This is the most severe form of the disorder, and it is characterized by a complete lack of the enzyme galactose-1-phosphate uridylyltransferase (GALT). Without GALT, galactose builds up in the blood and tissues, leading to serious health problems.
2. Dialectical galactosemia: This form of the disorder is less severe than classical galactosemia, and it is characterized by a partial deficiency of GALT. People with dialectical galactosemia may experience some symptoms, but they are typically milder than those experienced by people with classical galactosemia.
Symptoms of galactosemia can include:
* Diarrhea
* Vomiting
* Jaundice (yellowing of the skin and eyes)
* Fatigue
* Poor feeding in infants
* Developmental delays
If left untreated, galactosemia can lead to a range of complications, including:
* Liver disease
* Kidney disease
* Increased risk of infections
* Delayed growth and development
The diagnosis of galactosemia is typically made through a combination of physical examination, medical history, and laboratory tests. Treatment for the disorder typically involves a strict diet that limits or eliminates galactose-containing foods, such as milk and other dairy products. In some cases, medication may also be prescribed to help manage symptoms.
Overall, early diagnosis and treatment of galactosemia are important for preventing or minimizing the risk of complications associated with this condition.
Galactose
Galactose mutarotase
Galactose (EP)
Galactose oxidase
Galactose 1-phosphate
Uridine diphosphate galactose
Glucose-galactose malabsorption
Galactose epimerase deficiency
Galactose 1-dehydrogenase
UDP-galactose translocator
Galactose-6-sulfurylase
Methyl-α-D-galactose
DTDP-galactose 6-dehydrogenase
Galactose 1-dehydrogenase (NADP+)
Galactose-6-phosphate isomerase
Galactose-1-phosphate uridylyltransferase
GDP-L-galactose phosphorylase
Undecaprenyl-phosphate galactose phosphotransferase
Galactose-1-phosphate thymidylyltransferase
Galactose-3-O-sulfotransferase
Galactose binding lectin domain
L-galactose 1-dehydrogenase
Galactose-1-phosphate uridylyltransferase deficiency
Galactose-alpha-1,3-galactose
UDP-galactose-UDP-N-acetylglucosamine galactose phosphotransferase
DTDP-4-amino-4,6-dideoxy-D-galactose acyltransferase
Galactosaminogalactan
Chronic diarrhea of infancy
Levee Blues
Glycan
Galactose-1-phosphate uridyltransferase blood test: MedlinePlus Medical Encyclopedia
RCSB PDB - 3OB8: Structure of the beta-galactosidase from Kluyveromyces lactis in complex with galactose
2-deoxy-2-fluoro-beta-D-galactose | C6H11FO5 | CID 7191874 - PubChem
Letters: Milk and Mortality : Study used wrong assumption about galactose content of fermented dairy products - WUR
Galactose and Hepatic Metabolism in Malnutrition and Sepsis in Man | Clinical Science | Portland Press
Glucose galactose malabsorption - Genes and Disease - NCBI Bookshelf
The Big Apple: "The Milky Way is a hard place to be if you're galactose-intolerant"
Galactose Assay
Galactose tolerance test and methotrexate-induced liver fibrosis and cirrhosis in patients with psoriasis - PubMed
Genetic and Functional Aspects of Galactose Metabolism in Escherichia coli K-12 - Joshua Lederberg - Profiles in Science
Effect of Galactose and Glucose Levels and Sorbinil Treatment on myo-Inositol Metabolism and Na+-K+ Pump Activity in Cultured...
The fine specificity of mannose-binding and galactose-binding lectins revealed using outlier motif analysis of glycan array...
"Starvation and Particle Effects on the Galactose Transport System of a" by Henry Kenneth Lowery
Brain Dump - 2015.02.15 - Casein & Galactose - 3.5 to Life
Genetic and Functional Aspects of Galactose Metabolism in Escherichia coli K-12 - Digital Collections - National Library of...
Finding step glcU for D-galactose catabolism in Caulobacter crescentus NA1000
DailyMed - NIFEDIPINE tablet, extended release
D-galactose might protect against ionizing radiation by stimulating oxidative metabolism and modulating redox homeostasis. | J...
Borrelia burgdorferi - Wikipedia
Nutrition and Diet Research Progress - Page 5 - Nova Science Publishers
Sweeteners - sugars: MedlinePlus Medical Encyclopedia
Simultaneous utilization of galactose and glucose by Saccharomyces cerevisiae mutant strain for ethanol production<...
Lentils, raw Nutrition
"Efficacy of galactose and adalimumab in patients with resistant focal " by Howard Trachtman, Suzanne Vento et al.
Is LSD sacred? | Grasscity Forums - The #1 Marijuana Community Online
CATH Superfamily 2.60.120.260
Glucose and galactose7
- Glucose Galactose Malabsorption (GGM) is a rare metabolic disorder caused by a defect in glucose and galactose transport across the intestinal lining. (nih.gov)
- GGM is characterized by severe diarrhea and dehydration as early as the first day of life and can result in rapid death if lactose (milk sugar), sucrose (table sugar), glucose, and galactose are not removed from the diet. (nih.gov)
- Normally within the space enclosed by the small intestine (called the lumen), lactose is broken down into glucose and galactose by an enzyme called lactase, while sucrose is broken down into glucose and fructose by an enzyme called sucrase. (nih.gov)
- Usually the mutations carried by GGM individuals result in nonfunctional truncated SGLT1 proteins or in the improper placement of the proteins such that they can not transport glucose and galactose out of the intestinal lumen. (nih.gov)
- The glucose and galactose, if left untransported, draw water out of the body into the intestinal lumen, resulting in diarrhea. (nih.gov)
- Because lactose is composed of glucose and galactose, which have equal molecular weight, this decrease in lactose would lead to 1.25 g/100 g of galactose formed (equal to the 1.3 g/100 g in the quoted paper). (wur.nl)
- It is made up of glucose and galactose. (nih.gov)
Lactose5
- In normal diets, most galactose comes from the breakdown ( metabolism ) of lactose, which is found in milk and dairy products. (medlineplus.gov)
- The paper quoted by the authors shows a decrease in lactose from 4.8 g/100 g to 2.3 g/100 g (loss of 2.5 g/100 g) in yoghurt compared with milk,2 with an increase in galactose of 1.3 g/100 g. (wur.nl)
- Galactose intolerant" is portmanteau of "galaxy" and "lactose intolerant," and it's often used in puns with "Milky Way. (barrypopik.com)
- The signals of α/β-lactose and α/β-galactose were separately observed in the 1 H NMR spectra. (mdpi.com)
- Galactose is primarily part of a larger sugar called lactose, which is found in all dairy products and many baby formulas. (nih.gov)
Galactosemia4
- This technology includes selective inhibitors of the human enzyme galactokinase (EC 2.7.1.6), which may be useful for the treatment of Galactosemia and other diseases caused by aberrant galactose metabolism, including cancer. (nih.gov)
- Treatment of Galactosemia and other diseases caused by aberrant galactose metabolism, including some cancers. (nih.gov)
- UDP-galactose 4'-epimerase (GALE)-deficient galactosemia is an autosomal recessive disorder with clinical manifestations ranging from asymptomatic, where enzyme deficiency is restricted to peripheral blood, to severe, with a generalized GALE deficiency affecting multiple tissues. (umaryland.edu)
- Misfolding of galactose 1-phosphate uridylyltransferase can result in type I galactosemia. (nih.gov)
Saccharomyces1
- The authors report a novel ethanogenic strain capable of fermenting galactose, Saccharomyces cerevisiae. (elsevierpure.com)
Proteins1
- This chemical reaction also produces another form of galactose (UDP-galactose) that is used to build galactose-containing proteins and fats. (nih.gov)
Metabolism6
- 1. Hepatic carbohydrate metabolism was studied by an intravenous galactose test in control patients, malnourished non-septic patients, patients with prolonged severe sepsis and patients after recovery from sepsis. (portlandpress.com)
- Neuroblastoma cells were used to analyze the effect of galactose supplementation on myo -inositol metabolism, polyol accumulation, and Na +- K + pump activity. (diabetesjournals.org)
- Treatment of the galactose-containing media with 0.4 mM sorbinil partially prevented the galactose-mediated decreases in myo -inositol metabolism and content. (diabetesjournals.org)
- The effects of long-term galactose supplementation on myo -inositol metabolism, polyol accumulation, and Na +- K + -ATPase transport activity in cultured neuroblastoma cells are similar to the effects of high concentrations of glucose. (diabetesjournals.org)
- D-galactose might protect against ionizing radiation by stimulating oxidative metabolism and modulating redox homeostasis. (bvsalud.org)
- These compounds inhibit the first step in galactose metabolism, thereby eliminating the build-up of toxic metabolites during the aberrant metabolism of galactose, as well as inhibitor the entry of galactose into glycolysis and other downstream assays. (nih.gov)
Enzyme called1
- The GALT gene provides instructions for making an enzyme called galactose-1-phosphate uridylyltransferase. (nih.gov)
Amino Acids1
- Most changes in the GALT gene alter single protein building blocks (amino acids) in galactose-1-phosphate uridylyltransferase. (nih.gov)
Uridyltransferase1
- Galactose-1-phosphate uridyltransferase is a blood test that measures the level of a substance called GALT, which helps break down milk sugars in your body. (medlineplus.gov)
Utilization1
- In a mixed sugar (galactose+glucose) condition, the existence of glucose retarded galactose utilization however, 120g/L of the mixed sugar was completely consumed within 60h at any galactose concentration. (elsevierpure.com)
Fermentation1
- From this result, the ethanol fermentation efficiency of the novel S. cerevisiae strain using the galactose base of red algae was superior to the fermentation efficiency when using the wild type strain, and the novel strain was found to have resistance to the major inhibitors generated during the saccharification process. (elsevierpure.com)
Lactase1
- Yoghurt therefore contains the same amount of galactose as milk (and in lactase non-persistent people may lead to even higher galactose intakes). (wur.nl)
Fermentative1
- This mutant yeast strain exhibited exceptional fermentative performance on galactose and a mixture of galactose and glucose. (elsevierpure.com)
Mutations1
- Most of these mutations severely reduce or eliminate the activity of galactose-1-phosphate uridylyltransferase. (nih.gov)
Compounds1
- As a result, galactose-1-phosphate and related compounds can build up to toxic levels in the body. (nih.gov)
Metabolic1
- 6. It is suggested that alterations in hepatic blood flow and the metabolic fate of galactose within the liver may explain the changes in the metabolic response to galactose observed in malnourished or septic patients. (portlandpress.com)
Dairy products2
- Michaëlsson and colleagues' proposed mechanism for the effect of milk intake on the risk of mortality and fractures is based on the assumption that fermented dairy products (which had the opposite effects to those of non-fermented milk) are free of galactose.1 For most fermented dairy products, however, this is untrue. (wur.nl)
- Overall, the galactose intake from fermented dairy products (soured milk and yoghurt in the paper) is equal to that from regular dairy products, which makes the authors' proposed mechanism highly unlikely. (wur.nl)
Milk1
- Following exposure to milk, which contains high levels of galactose, affected infants may experience rapid onset and progression of potentially lethal symptoms. (nih.gov)
Diets1
- All patients were on galactose-restricted diets. (nih.gov)
Liver1
- 2. Blood galactose half-life was not significantly increased in the septic group despite abnormal liver-function tests, whereas it was approximately doubled in the malnourished patients. (portlandpress.com)
Abstract1
- abstract = "The present paper explores the antioxidant and antiaging properties of agar extracted from Laminaria digitata (L. digitata) on a D-galactose (D-Gal)-induced mouse model. (elsevier.com)
Subjects2
- 3. The rise in blood glucose after galactose injection was less in both the septic and malnourished groups, as compared with that in the control subjects. (portlandpress.com)
- While none of the adalimumab-treated subjects achieved the primary outcome, 2 subjects in the galactose and 2 in the standard medical therapy arm had a 50 % reduction in proteinuria without a decline in eGFR. (childrensmercy.org)
Decrease1
- Exposing neuroblastoma cells to 30 mM galactose causes a decrease in the levels of phosphatidylinositol that is partially restored by the addition of sorbinil. (diabetesjournals.org)
Experimental1
- The experimental treatments - adalimumab, galactose, standard medical therapy-- were administered for 26 weeks. (childrensmercy.org)
Content2
- The galactose content of (semi)hard cheeses is somewhat lower because the curd is washed during production, but cheese is not usually free from galactose. (wur.nl)
- The effect of galactose on the intracellular content of galactitol and myo -inositol was concentration dependent. (diabetesjournals.org)
Patients2
- Efficacy of galactose and adalimumab in patients with resistant focal " by Howard Trachtman, Suzanne Vento et al. (childrensmercy.org)
- Efficacy of galactose and adalimumab in patients with resistant focal segmental glomerulosclerosis: report of the font clinical trial group. (childrensmercy.org)
Blood1
- Without this substance, the body cannot break down galactose, and the substance builds up in the blood. (medlineplus.gov)
Product1
- The protein product of SGLT1 then moves the glucose and the galactose from the lumen of the small intestine into intestinal cells. (nih.gov)
Step1
- Galactose-1-phosphate uridylyltransferase is responsible for one step in a chemical process that breaks down galactose into other molecules that can be used by the body. (nih.gov)
Body1
- This enzyme enables the body to process a simple sugar called galactose, which is present in small amounts in many foods. (nih.gov)
Form1
- Specifically, this enzyme converts a modified form of galactose (galactose-1-phosphate) to glucose, which is another simple sugar. (nih.gov)
Cells3
- Extracellular myo -inositol accumulation and incorporation into phospholipid decreased by 20-30% in cells grown in 30 mM galactose. (diabetesjournals.org)
- The activity of the Na +- K + pump was decreased by 20% in cells cultured in 30 mM galactose and was partially protected by sorbinil treatment. (diabetesjournals.org)
- A shortage of this enzyme prevents cells from processing galactose obtained from the diet. (nih.gov)
Activity1
- The Duarte variant reduces but does not eliminate the activity of galactose-1-phosphate uridylyltransferase. (nih.gov)
Hard1
- The Milky Way is a hard place to be if you're galactose-intolerant" was posted on Twitter by God (Not a Parody, Actually God) on December 29, 2011. (barrypopik.com)
Study1
- We developed a systematic approach, called outlier-motif analysis, for extracting fine-specificity information from glycan-array data, and we applied the method to the study of four commonly used lectins: two mannose binders (concanavalin A and Lens culinaris) and two galactose binders (Bauhinia purpurea and peanut agglutinin). (nih.gov)
Found1
- We found broader specificity for bauhinea purpurea (BPL) than previously reported, showing that BPL can bind terminal N-acetylgalactosamine (GalNAc) and penultimate β-linked galactose under certain limitations. (nih.gov)