Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DISACCHARIDES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 577 records · Page 32Linked to original sources
PubMed2005

Banana lectin is unique in its recognition of the reducing unit of 3-O-beta-glucosyl/mannosyl disaccharides: a calorimetric study.

The binding of banana lectin (BanLec) to laminaribiose (Glcbeta1,3Glc) and a series of novel synthetic analogues was measured by titration calorimetry to assess the contribution of the hydroxyl groups of the reducing glycosyl moiety and its 3-O-beta-substituent to binding. Key areas of interaction involved the 1, 2, and 6 positions of the reducing-terminal hexose unit. The alpha-anomeric configuration of the reducing hexose was strongly favored over the beta-anomer. The 2-hydroxyl in the axial position (mannose) also enhanced binding, whereas the 6-hydroxymethyl group was essential, because xylopyranose in the reducing position was inactive. The 3-O-beta-glucosyl unit of methyl alpha-laminaribioside could be replaced by any of its monodeoxy derivatives. However, the 4'-deoxy derivative or axial hydroxy (galactosyl) substitution was somewhat detrimental to binding. 3-O-substitution with the (S)tetrahydropyranyl ring or a benzyl group had similar effect as 4'-deoxyglucosyl substitution. Surprisingly, p-nitrobenzyl or beta-xylosyl 3-O-substitution greatly enhanced binding of the reducing glucosyl or mannosyl derivative. Chemical syntheses of a number of novel disaccharides and analogues prepared for this study are described.

Calorimetry↗
PubMed1997

Heparin disaccharides inhibit tumor necrosis factor-alpha production by macrophages and arrest immune inflammation in rodents.

Inflammation is the clinical expression of chemical mediators such as the pro-inflammatory cytokine tumor necrosis factor (TNF-)-alpha produced by macrophages and other cells activated in the immune response. Hence, agents that can inhibit TNF-alpha may be useful in treating arthritis and other diseases resulting from uncontrolled inflammation. We now report that the cleavage of heparin by the enzyme heparinase I generates sulfated disaccharide (DS) molecules that can inhibit the production of TNF-alpha. Administration of nanogram amounts of the sulfated DS molecules to experimental animals inhibited delayed-type hypersensitivity to a skin sensitizer and arrested the joint swelling of immunologically induced adjuvant arthritis. Notably, the sulfated DS molecules showed a bell-shaped dose-response curve in vitro and in vivo: decreased effects were seen using amounts of the DS molecules higher than optimal. Thus, molecular regulators of inflammation can be released from the natural molecule heparin by the action of an enzyme.

Animals↗
PubMed1986

Intake and gastric emptying of mono- versus disaccharides by rats.

Eating and gastric emptying of mono- versus disaccharides were measured in rats which consumed each day a carbohydrate solution and, 5 h later, a restricted amount of a nutritionally adequate dry diet. When Wistar rats were offered 30% (wt/vol) sugar solutions for 60 min a day, energy intakes were smaller for glucose than for maltose or dextrin and smaller for invert sugar (fructose + glucose) than for sucrose. Sprague-Dawley rats consumed less energy from glucose than maltose when fed 60%, but not 15%, solutions of these sugars. Among Wistar rats accustomed to hypotonic carbohydrate meals, gastric emptying (kilocalories/minute) was slower for 30% glucose than 30% maltose and for 63% maltose than 21% maltose. These differences became obscured with continued exposure to highly hypertonic meals. Monosaccharides, being small, highly soluble molecules, can impart great osmolality to stomach contents. It appears that this osmotic property of monosaccharides tends to slow eating and gastric emptying.

Animals↗
PubMed1987

Apparent inability of channel catfish to utilize dietary mono- and disaccharides as energy sources.

Purified diets containing equivalent amounts of glucose, maltose, fructose, sucrose, corn starch and dextrin were fed to fingerling channel catfish (Icatalurus punctatus) to compare the growth responses to these various carbohydrates. The best growth response was achieved with dextrin and the next best with corn starch. Fish grew at the same rate when glucose, maltose or sucrose was the only dietary carbohydrate source. Dietary fructose resulted in the lowest growth rate. Feed efficiency and percent retained energy values followed the same pattern as growth rates. These data suggest that the catfish is apparently unable to utilize dietary mono- and disaccharides as energy sources. Oral carbohydrate tolerance tests using glucose, maltose, fructose, sucrose and dextrin were conducted with larger channel catfish. Oral glucose and maltose resulted in a persistent hyperglycemia indicative of a diabetic-like status. Fructose appeared to be poorly absorbed from the intestinal tract and did not appear to be converted to glucose. Oral administration of sucrose was followed by a gradual increase in plasma glucose, with no detectable fructose being absorbed until the 6-h period. Oral dextrin resulted in less than a two-fold increase in plasma glucose, which remained constant from 2 to 4 h after administration and then declined. These observations are consistent with the hypothesis that certain fishes, including the channel catfish, resemble diabetic animals by having insufficient insulin for maximum carbohydrate utilization.

Animals↗
PubMed1988

Short-chain fatty acid production from mono- and disaccharides in a fecal incubation system: implications for colonic fermentation of dietary fiber in humans.

An in vitro fecal incubation system was used to demonstrate how lactose, lactulose and monosaccharides (mainly constituents of dietary fiber) influence short-chain fatty acid production in colon. Short-chain fatty acids were formed from all mono- and disaccharides tested (except L-glucose): D-glucose, D-galactose, D-fructose, D-mannose, L-rhamnose, D-sorbitol, D-arabinose, D-xylose, D-ribose, D-galacturonate, D-glucuronate, lactose and lactulose. All saccharides increased acetate formation; propionate production was increased from rhamnose, arabinose, xylose, ribose, galacturonic and glucuronic acid, whereas the synthesis of butyrate was elevated in assays incubated with sorbitol, galacturonic and glucuronic acid, and to a lesser degree ribose. Isobutyrate, valerate, isovalerate and hexanoate were produced in increased amounts in assays incubated with albumin, but in fact decreased in many incubations with saccharides. It is speculated that saccharide fermentation always results in formation of acetate, and that the relative production of acetate, propionate and butyrate is related to the monosaccharide composition of dietary fiber available for colonic bacteria. However, the production of isobutyrate, valerate, isovalerate and hexanoate is probably not due to saccharide fermentation, but is rather of polypeptide origin.

Acetates↗
PubMed2003

The crystal structure of the complex between a disaccharide anthracycline and the DNA hexamer d(CGATCG) reveals two different binding sites involving two DNA duplexes.

The crystal structure of the complex formed between the anthracycline antibiotic 3'-deamino-3'- hydroxy-4'-(O-L-daunosaminyl)-4-demethoxydoxo rubicin (MEN 10755), an active disaccharide analogue of doxorubicin, and the DNA hexamer d(CGATCG) has been solved to a resolution of 2.1 A. MEN 10755 exhibits a broad spectrum of antitumor activities, comparable with that of the parent compound, but there are differences in the mechanism of action as it is active in doxorubicin-resistant tumors and is more effective in stimulating topoisomerase DNA cleavage. The structure is similar to previously crystallised anthracycline- DNA complexes. However, two different binding sites arise from drug intercalation so that the two halves of the self-complementary duplex are no longer equivalent. In one site both sugar rings lie in the minor groove. In the other site the second sugar protrudes out from the DNA helix and is linked, through hydrogen bonds, to guanine of a symmetry-related DNA molecule. This is the first structure of an anthracycline-DNA complex where an interaction of the drug with a second DNA helix is observed. We discuss the present findings with respect to the relevance of the amino group for DNA binding and to the potential role played by the second sugar in the interactions with topoisomerases or other cellular targets.

Animals↗
PubMed1995

Osmotic and physiological responses of mouse zygotes and human oocytes to mono- and disaccharides.

To survive cryopreservation, oocytes, zygotes and embryos must tolerate a sequence of volumetric contractions and expansions. These result as an egg or an embryo is exposed to a permeating cryoprotective additive, then to an increase followed by a decrease in the osmolality of its extracellular milieu as water freezes during cooling and then melts during warming, and finally to the dilution of the cryoprotective additive solution. Measurements of the extent to which mouse zygotes and human oocytes undergo osmotic contraction have been made by exposing them to solutions of monosaccharides (fructose, galactose, glucose) or disaccharides (maltose, sucrose, trehalose), ranging in concentration from 0.25 to 1.50 M. Mouse zygotes and human oocytes exhibit very similar responses to these solutions. Their volumes contract linearly as a function of 1/(osmolality) of the solutions, yielding estimates of non-osmotic volumes of 13-23%. Mouse zygotes exposed to 1.5 M concentrations of these solutions for 10 min lose 85% of their cell water. Yet > 75% of treated zygotes develop into hatching blastocysts. Human oocytes also appear to survive such extreme dehydration, based on a vital dye assay. These results suggest that solutions of various non-permeating saccharides can serve as osmotic buffers for the recovery of cryopreserved oocytes, zygotes and embryos.

Animals↗
PubMed2001

Correlative fine specificity of several Thomsen-Friedenreich disaccharide-binding proteins with an effect on tumor cell proliferation.

Epithelial cancer cells show increased cell surface expression of mucin antigens with aberrant O-glycosylation, notably type I core (Galbeta1-3GalNAcalpha), termed Thomsen-Friedenreich disaccharide (TFD), a chemically well-defined carbohydrate antigen with a proven link to malignancy. Several TFD-binding proteins influence the proliferation of cells to which they bind. We studied the fine specificity of TFD-binding proteins and its relationship with epithelial tumor cell proliferation. Competitive binding assays against asialoglycophorin showed that Agaricus bisporus lectin (ABL) and human anti-TFD monoclonal antibody (mAb) TF1 were inhibited only by TFD and its alpha-derivatives. Peanut agglutinin (PNA), mAb TF2, and mAb TF5 were also inhibited by other carbohydrates such as lacto-N-biose (Galbeta1-3GlcNAc), lactose, and (Mealpha or beta) Gal, indicating lower recognition of the axial C-4 hydroxyl group position of GalNAc from TFD, and the major relevance of the terminal Gal on interaction of these three TFD-binding proteins. In the direct glycolipid-binding assay, ABL bound mostly to alpha-anomeric TFD-bearing glycolipids, whereas PNA interacted mainly with beta-linked TFD. Of the three anti-TFD mAbs analyzed, all bound N5b (terminal beta-TFD), but only TF2 interacted with N6 (terminal alpha-TFD). These findings indicate that TFD-binding proteins that stimulate the proliferation of epithelial tumor cell lines recognize mainly a terminal beta-Gal region of beta-linked TFD, whereas ABL, which inhibits the proliferation of these tumor cells, binds mainly to subterminal GalNAc of alpha-anomeric TFD.

Animals↗
PubMed2006

A sulfated disaccharide derived from chondroitin sulfate proteoglycan protects against inflammation-associated neurodegeneration.

Chondroitin sulfate proteoglycan (CSPG), a matrix protein that occurs naturally in the central nervous system (CNS), is considered to be a major inhibitor of axonal regeneration and is known to participate in activation of the inflammatory response. The degradation of CSPG by a specific enzyme, chondroitinase ABC, promotes repair. We postulated that a disaccharidic degradation product of this glycoprotein (CSPG-DS), generated following such degradation, participates in the modulation of the inflammatory responses and can, therefore, promote recovery in immune-induced neuropathologies of the CNS, such as experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune uveitis (EAU). In these pathologies, the dramatic increase in T cells infiltrating the CNS is far in excess of the numbers needed for regular maintenance. Here, we show that CSPG-DS markedly alleviated the clinical symptoms of EAE and protected against the neuronal loss in EAU. The last effect was associated with a reduction in the numbers of infiltrating T cells and marked microglia activation. This is further supported by our in vitro results indicating that CSPG-DS attenuated T cell motility and decreased secretion of the cytokines interferon-gamma and tumor necrosis factor-alpha. Mechanistically, these effects are associated with an increase in SOCS-3 levels and a decrease in NF-kappaB. Our results point to a potential therapeutic modality, in which a compound derived from an endogenous CNS-resident molecule, known for its destructive role in CNS recovery, might be helpful in overcoming inflammation-induced neurodegenerative conditions.

Amino Acid Sequence↗
PubMed1980

The growth of Moniliformis (Acanthocephala) in rats fed on various monosaccharides and disaccharides.

Aspects of the course of infection, growth and reproductive activity of Moniliformis were studied in adult male and female rats fed on isoenergetic purified diets containing various sugars. When rats were infected and fed on experimental diets containing either 3% glucose or 3% galactose for 5 weeks, very little growth of worms and no signs of reproduction were observed. In contrast, Moniliformis grew well and showed many signs of normal reproduction when the rats were fed on diets containing either 3% fructose or 3% mannose. The ability of the worms to grow and reproduce was not lost by maintaining them first for 5 weeks in rats fed on diets containing 3% glucose and 3% galactose. When the diets of such rats were changed to ones containing 3% starch and 3% fructose, respectively, for a further 5 weeks, the worms grew and normal reproduction occurred. Similar experiments were carried out in which groups of infected rats were fed for 5 weeks on diets containing gradually increasing amounts of glucose (6-36%). It was not until the rats were fed on diets containing 24% glucose that the mean dry mass of the worms approached that of worms from rats fed on the diet containing 3% fructose; no host diet was found to be as effective a supporter of worm growth as 3% mannose. Under no circumstances, not even when the host's diet contained 36%, was galactose found to be a suitable sugar for supporting the growth and reproduction of Moniliformis. Results consistent with those recorded for worms from rats fed on the diets containing monosaccharides were obtained when infected rats were fed for 5 weeks on diets containing 3% of various disaccharides. Considerable growth and reproduction of Moniliformis occurred when sucrose was included in the host's diet, but not when lactose, maltose or trehalose was present. Several of these observations may be related to the fact that different sugars are absorbed at different rates from the intestinal tract. It is suggested that all of a given sugar, when present in the diet at a low concentration, may be removed rapidly from the anterior part of the small intestine with the result that none will be available to the parasites. Significant amounts, however, of those sugars that are absorbed more slowly may reach the region of the intestine in which the parasite normally lives.

Acanthocephala↗
PubMed1993

Identification of a benzyladenine disaccharide conjugate produced during shoot organogenesis in Petunia leaf explants.

Prior studies of benzyladenine (BA) metabolism in Petunia hybrida Vilm. leaf explants during shoot organogenesis revealed the presence of an abundant unidentified BA conjugate. The BA conjugate, compound C, made up to 39% of the total pool of BA conjugates in two Petunia lines and was associated with an increased shoot organogenic response when compared with a third Petunia line that did not produce any compound C. Structural analysis of compound C utilizing fast atom bombardment mass spectrometry, two methods of carbohydrate analysis, ultraviolet absorption spectra, and Fourier transform infrared spectra identified it as a new cytokinin conjugate, 6-benzylamino-9-[O-glucopyranosyl-(1-->3)-ribofuranosyl]-purine. Based on our prior biological studies and the similarity of this compound to related cytokinin conjugates, this disaccharide cytokinin conjugate may be part of the interconvertible pool of cytokinins active in Petunia shoot organogenesis.

Adenine↗
PubMed2000

Disaccharide-mediated regulation of sucrose:fructan-6-fructosyltransferase, a key enzyme of fructan synthesis in barley leaves.

Previous work has indicated that sugar sensing may be important in the regulation of fructan biosynthesis in grasses. We used primary leaves of barley (Hordeum vulgare cv Baraka) to study the mechanisms involved. Excised leaf blades were supplied in the dark with various carbohydrates. Fructan pool sizes and two key enzymes of fructan biosynthesis, sucrose (Suc):Suc-1-fructosyltransferase (1-SST; EC 2. 4.1.99) and Suc:fructan-6-fructosyltransferase (6-SFT; EC 2.4.1.10) were analyzed. Upon supply of Suc, fructan pool sizes increased markedly. Within 24 h, 1-SST activity was stimulated by a factor of three and 6-SFT-activity by a factor of more than 20, compared with control leaves supplemented with mannitol (Mit). At the same time, the level of mRNA encoding 6-SFT increased conspicuously. These effects were increased in the presence of the invertase inhibitor 2, 5-dideoxy-2,5-imino-D-mannitol. Compared with equimolar solutions of Suc, glucose (Glu) and fructose stimulated 6-SFT activity to a lesser extent. Remarkably, trehalose (Tre; Glc-alpha-1 and 1-alpha-Glc) had stimulatory effects on 6-SFT activity and, to a somewhat lesser extent, on 6-SFT mRNA, even in the presence of validoxylamine A, a potent trehalase inhibitor. Tre by itself, however, in the presence or absence of validoxylamine A, did not stimulate fructan accumulation. Monosaccharides phosphorylated by hexokinase but not or weakly metabolized, such as mannose (Man) or 2-deoxy-Glc, had no stimulatory effects on fructan synthesis. When fructose or Man were supplied together with Tre, fructan and starch biosynthesis were strongly stimulated. Concomitantly, phospho-Man isomerase (EC 5.3.1.8) activity was detected. These results indicate that the regulation of fructan synthesis in barley leaves occurs independently of hexokinase and is probably based on the sensing of Suc, and also that the structurally related disaccharide Tre can replace Suc as a regulatory compound.

Base Sequence↗
PubMed2005

Incorporation of a disaccharide nucleoside into the backbone of double-stranded DNA: crystallization and preliminary X-ray diffraction.

Incorporation of a disaccharide nucleoside into double-stranded DNA can be considered as a chemical (non-enzymatic) alternative for site-specific cleavage of DNA. Crystals of the sequence d(CGCGAATT*CGCG), where * is an incorporated ribose, were obtained by hanging-drop vapour diffusion and diffracted to 2.6 A. The crystals belong to the orthorhombic space group P222(1), with unit-cell parameters a = 41.52, b = 57.63, c = 81.39 A, indicating a new crystal packing motif for an oligonucleotide dodecamer sequence.

Crystallization↗
PubMed1984

alpha-L-Iduronidase deficiency in mucopolysaccharidosis type I against a radiolabelled sulfated disaccharide substrate derived from dermatan sulfate.

alpha-L-Iduronidase activity was assayed by incubation of a radiolabelled disaccharide, O-(alpha-L-idopyranosyluronic acid)-(1----3)-2,5 anhydro-D-[1,3H]-talitol 4-sulfate (IdoA-anT4S) derived from dermatan sulfate, with homogenates of leucocytes, cultured amniotic cells and skin fibroblasts from normal individuals and patients affected with an alpha-L-iduronidase-deficiency disorder (mucopolysaccharidosis type I, MPS I), parents of such patients and patients affected with other mucopolysaccharidoses. The assay clearly distinguished affected homozygotes from normal controls, heterozygotes and other mucopolysaccharidosis types. Preliminary results show that fibroblast homogenates from patients with the MPS I Hurler phenotype were virtually unable to hydrolyse IdoA-anT4S, whereas fibroblast homogenates from a patient with a relatively mild (Scheie) phenotype exhibited a residual activity with Vmax value of 2.5 pmol/min/mg protein and an apparent Km of 21 mumol/l compared to a range of 1020-2105 pmol/min/mg for Vmax and 12-35 mumol/l for Km for fibroblasts from normal controls.

Amniotic Fluid↗
PubMed1980

Microsomal glucosidases of rat liver. Partial purification and inhibition by disaccharides.

Further work on microsomal glucosidases of rat liver has confirmed that at least two enzymes are involved in the removal of glucose from the glucose-containing oligosaccharide. One acts on the oligosaccharide containing three glucose residues and another on the oligosaccharide which has one or two glucoses. The glucosidase which acts on (Glc)2(Man)9(GlcNAc)2 could be purified with a Concanavalin-A--Sepharose column following by electrofocusing. This purified preparation was active on the oligosaccharide containing one or two glucoses. Heat inactivation and inhibition by disaccharides was parallel for both activities. Inhibition of the glucosidase active on (Glc)3(Man)9(GlcNAC)2 was obtained with kojibiose which has an alpha 1-2 linkage, while the glucosidase acting on (Glc)1-2(Man)9-(GlcNAc)2 was inhibited by nigerose (alpha 1-3 linkage), maltose (alpha 1-4 linkage) and glucose at a higher concentration. None of the beta anomers inhibited. These results are consistent with an alpha configuration of the three glucoses of the dolichyl-diphosphate-linked oligosaccharide. Kojibiose was found to inhibit glucosidase action not only on the free oligosaccharide but also on protein-bound one.

Animals↗
PubMed1986

1H-NMR studies at 500 MHz of a neutral disaccharide and sulphated di-, tetra-, hexa- and larger oligosaccharides obtained by endo-beta-galactosidase treatment of keratan sulphate.

In the preceding paper in this journal, the major oligosaccharides obtained by endo-beta-galactosidase digestion of bovine corneal keratan sulphate were identified as a neutral disaccharide, GlcNAc beta 1-3Gal, and sulphated di-, tetra-, hexa-, octa- and decasaccharides based on the sequence (-3/4GlcNAc beta 1-3Gal beta 1-)n having 1, 3, 5, 7 and 9 sulphate groups, respectively. In the present study, these oligosaccharides have been analysed by 500-MHz 1H-NMR spectroscopy using spin-decoupling and two-dimensional correlated spectroscopy experiments. The NMR data confirm the beta-configuration of all the interglycosidic linkages and are consistent with an alternating sequence of----4GlcNAc and----3Gal, a non-reducing-end N-acetylglucosamine residue and a reducing-end galactose residue. The NMR data have also established that a sulphate group is linked to the C6 position of all sugar residues except the reducing-end galactose as follows: (Formula: see text). The signals of the protons attached to the sulphated carbon atoms show marked downfield shifts (approximately 0.4 ppm from equivalent protons of non-sulphated carbon atoms), while the protons at C5 vicinal to sulphated atoms show a change of 0.1-0.2 ppm and other protons of the sulphated monosaccharides show smaller changes in chemical shift (0.01-0.1 ppm). The proton at C4 of the non-sulphated reducing-end galactose linked at C3 also shows a significant change in chemical shift (0.03 ppm).

Animals↗
PubMed1987

Isolation and structural characterization of an 8-O-(4-amino-4-deoxy-beta-L-arabinopyranosyl)-3-deoxy-D-manno- octulosonic acid disaccharide in the lipopolysaccharide of a Proteus mirabilis deep rough mutant.

On short treatment of the lipopolysaccharide of a deep rough mutant of Proteus mirabilis (strain R45) with hydrochloric acid (0.01 M, 10 min, 100 degrees C) a compound was released which, on high-voltage paper electrophoresis, migrated slightly to the cathode (MGlcN = 0.19) and which stained with ninhydrin, alkaline silver nitrate and in the thiobarbituric acid assay. After purification and derivatization, its chemical structure was identified by combined gas-liquid chromatography/mass spectrometry and two-dimensional shift-correlated proton nuclear magnetic resonance spectroscopy as 8-O-(4-amino-4-deoxy-beta-L-arabinopyranosyl)-3-deoxy-D-manno-octu losonic acid. This disaccharide was also present in a wild-type strain of P. mirabilis.

Amino Sugars↗