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At least 973 records · Page 54Linked to original sources
PubMed1988

Hexose metabolism in pancreatic islets: regulation of mitochondrial hexokinase binding.

A major fraction of hexokinase was found to be bound, presumably to mitochondria, in both normal and tumoral rat pancreatic islet cells examined after either mechanical disruption or digitonin treatment. Spermidine enhanced the binding and glucose 6-phosphate caused the release of hexokinase to and from islet mitochondria, in a manner comparable to that seen in parotid or brain homogenates. In hepatocytes, some hexokinase, but no glucokinase, was found in the bound form. In islet cells, however, the pattern of glucokinase binding was similar to that of hexokinase. It is speculated that the preferential location of both hexokinase and glucokinase on mitochondria may favor the maintenance of a high cytosolic ATP content in islet cells.

Animals↗
PubMed1992

Hexose metabolism in pancreatic islets. Regulation of NAD-isocitrate dehydrogenase activity.

D-Glucose causes a preferential stimulation of mitochondrial oxidative events relative to glycolysis in pancreatic islets. The possible participation of a Ca(2+)-induced activation of NAD-isocitrate dehydrogenase in this process was investigated. The activity of the enzyme in rat islet homogenates was measured through the generation of either NADH or 2-ketoglutarate. In the absence of Ca2+ and ADP, half-maximal velocities were recorded at isocitrate and NAD+ concentrations close to 1.2 and 0.5 mM, respectively. At isocitrate concentrations in the 0.15-1.5 mM range, ADP (1.0 mM) markedly increased the reaction velocity recorded in the absence of Ca2+ and conferred to the enzyme the property of being activated by Ca2+, with a Ka for Ca2+ somewhat below 1.0 microM. From these data and by comparison with the activity of 2-ketoglutarate dehydrogenase, it is proposed that activation of NAD-isocitrate dehydrogenase by such factors as ADP and Ca2+ may be required in order to match, in nutrient-stimulated islets, the rates of 2-ketoglutarate generation and oxidative decarboxylation.

Animals↗
PubMed1996

Myofibril-bound muscle phosphofructokinase is less sensitive to inhibition by ATP than the free enzyme, but retains its sensitivity to stimulation by bisphosphorylated hexoses.

Phosphofructokinase activity is modulated by allosteric effectors and macromolecular interactions (e.g. binding to myofibrillar components). The aim of this study was to determine the effects of ATP and bisphosphorylated sugars upon phosphofructokinase in the presence of myofibrils. Myofibrils were prepared from resting and electrically stimulated rat muscle. Dephosphorylation of myofibrils was performed with alkaline phosphatase acid. Purified rabbit skeletal muscle phosphofructokinase was used for all experiments. Myofibrils from resting muscle showed a higher capacity to bind phosphofructokinase and a lower phosphate content than myofibrils from stimulated muscle. Dephosphorylation of myofibrils did not increase their binding capacity. Myofibrils greatly counteracted the inhibition of phosphofructokinase by high concentrations of ATP, without affecting maximum activity. In the presence of myofibrils, both glucose 1,6-bisphosphate and fructose 2,6-bisphosphate additionally activated muscle phosphofructokinase. We suggest that the binding of phosphofructokinase to myofibrils in combination with increasing glucose 1,6-bisphosphate concentration could be important in the enhancement of the glycolytic flux that takes place during muscle contraction.

Adenosine Triphosphate↗
PubMed2004

Pyridinium-carbaldehyde: active Maillard reaction product from the reaction of hexoses with lysine residues.

Besides the formation of the aminotriazine N6-[4-(3-amino-1,2,4-triazin-5-yl)-2,3-dihydroxybutyl]-L-lysine, the reaction of [1-13C]D-glucose with lysine and aminoguanidine leads to the generation of 6-[2-([[amino(imino)methyl]hydrazono]methyl)pyridinium-1-yl]-L-norleucine (14-13C1). The dideoxyosone N6-(2,3-dihydroxy-5,6-dioxohexyl)-L-lysine was shown to be a precursor in the formation of 14-13C1, which proceeds via the reactive carbonyl intermediate 6-(2-formylpyridinium-1-yl)-L-norleucine (13-13C1). In order to study the reactivity of 13-13C1, the model compound 1-butyl-2-formylpyridinium (18) was prepared in a two-step procedure starting from 2-pyridinemethanol. The reaction of the pyridinium-carbaldehyde 18 with L-lysine yielded the Strecker analogous degradation product 2-(aminomethyl)-1-butylpyridinium and another compound, which was shown to be as 1-butyl-2-[(2-oxopiperidin-3-ylidene)methyl]pyridinium. Reaction of 18 with the C-H acidic 4-hydroxy-5-methylfuran-3(2H)-one leads to the formation of the condensation product 1-butyl-2-[hydroxy-(4-hydroxy-5-methyl-3-oxofuran-2(3H)-ylidene)methyl]-pyridinium.

Aldehydes↗
PubMed2000

Action of acid on 6-thio-hexose derivatives. Synthesis of 1,6-epithio-hexofuranoses.

Reaction of 5,6-anhydro-1,2-O-isopropylidene-3-O-methanesulfonyl-3-L-idofuranose+ ++ with thioacetic acid in pyridine gave 6-S-acetyl-1,2-O-isopropylidene-3-O-methanesulfonyl-6-thio-3-L-idofur anose, which was deacetylated and the resultant thiol was converted into 1,2-O:5,6-O,S-diisopropylidene-3-O-methanesulfonyl-3-L-idofuran ose. Alkaline cleavage of the mesyl group gave 1,2-O: 5,6-O,S-diisopropylidene-3-L-idofuranose, which on treatment with hot dilute hydrochloric acid gave, after acetylation, 2,3,5-tri-O-acetyl-1,6-dideoxy-1,6-epithio-alpha-L-idofuranose+ ++ and not the expected idopyranose isomer. 1,2:3,5-Di-O-isopropylidene-6-O-toluene-p-sulfonyl-alpha-D-glucofuranose was converted into 6-S-acetyl-1,2:3,5-di-O-isopropylidene-6-thio-alpha-D-glucofuranose; conversion into the 6-thiol and isomerisation in acidified acetone gave 1,2-O:5,6-O,S-diisopropylidene-6-thio-alpha-D-glucofuranose. Acid treatment of this diacetal, or the isomeric 1,2:3,5-di-O-isopropylidene-6-thio-alpha-D-glucofuranose, followed by acetylation gave 2,3,5-tri-O-acetyl-1,6-dideoxy-1,6-epithio-beta-D-glucofuranose. Similar treatment of 1,2:3,4-di-O-isopropylidene-6-thio-alpha-D-galactopyranose gave 2,3,5-tri-O-acetyl-1,6-dideoxy-1,6-epithio-alpha-D-galactofuranose .

Carbohydrates↗
PubMed1977

Preparative syntheses of 2,6-dideoxy-alpha-L-lyxo-hexose (2-deoxy-alpha-L-fucose) and its D-ribo epimer (digitoxose).

Methyl 4,6-O-benzylidene-2-deoxy-alpha-D-ribo-hexopyranoside (1) is converted into methyl 3,4-di-O-benzoyl-6-bromo-2,6-dideoxy-alpha-D-ribo-hexopyranoside (3) via the 3-O-benzoyl derivative (2) of 1 by subsequent treatment with N-bromosuccinimide. Compound 3 is the key intermediate in high-yielding, preparative syntheses of the title dideoxy sugars, which are constituents of many antibiotics, Dehydrohalogenation of 3 affords the 5,6-unsaturated glycoside 7, which undergoes stereospecific reduction by hydrogen with net inversion at C-5 to give methyl 3,4-di-O-benzoyl-2,6-dideoxy-beta-L-lyxo-hexopyranoside (8), whereas reductive dehalogenation of 3 provides the corresponding D-ribo derivative 4. The unprotected glycosides 9 (L-lyxo) and 5 (D-ribo) are readily obtained by catalytic transesterification, and mild, acid hydrolysis gives the crystalline title sugars 10 (L-lyxo) and 6 (D-ribo) in 45 and 57% overall yield from 1 without the necessity of chromatographic purification at any of the steps.

Chemical Phenomena↗
PubMed2003

The absolute configuration of 1-carboxyethyl substituents on common hexoses by circular dichroism.

Determination of the absolute configuration of the 1-carboxyethyl substituent on a monosaccharide by circular dichroism measurements was found to be a sensitive and simple method. It relies on comparison of the spectrum of a 1-carboxyethyl substituted sugar or sugar derivative with the spectra of (R)- and (S)-lactic acid in the region 200-260 nm in which the (R)- and (S)-configuration give negative and positive deltaepsilon, respectively. The oligo- or poly-saccharide containing a 1-carboxyethyl substituted sugar is hydrolyzed to monomers and the 1-carboxyethyl substituted sugar isolated by chromatography. The CD spectrum obtained for the 1-carboxyethyl substituted sugar in water solution at pH 2 is then compared with spectra of (R)- and (S)-lactic acid. The sign for the absorption and a maximum of comparable intensity and appearance around 210 nm, identify the stereochemistry.

Circular Dichroism↗
PubMed1984

Hexose transport modification of rat hearts during development of chronic diabetes.

Transport of 3-o-methylglucose into hearts of chronic diabetic rats was studied to determine if loss of transporter activity could be accounted for by higher concentrations of citrate and triglyceride and to determine if 7 days post alloxan was a representative time period for study of myocardial changes in chronic diabetes. Chronic diabetes was induced in rats by rapid i.v. injection of alloxan (37.5 mg/kg body weight), and the rats were studied 1 to 5 weeks afterward. Basal sugar transport rate in isolated perfused hearts declined after 2 weeks of diabetes and was nearly undetectable at 3 to 5 weeks. Stimulation of transport by insulin was also very low. Triglyceride concentrations were 50% of normal and G6P concentrations were elevated, but citrate concentrations were not different from control. Results of these studies showed that tissue triglyceride and citrate concentrations were not correlated with transport inhibition in chronic diabetic rat hearts. Loss of basal transport activity and lowered insulin sensitivity in these hearts is more likely due to a loss of transporters from the sarcolemma. These studies also show that transport rate and metabolite concentrations continue to change over 5 weeks of diabetes, and, therefore, one time point cannot be defined as representative of chronic diabetes.

Animals↗