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At least 1,099 records · Page 61Linked to original sources
PubMed1986

Effect of glucose and other hexoses on efferent discharges of brown adipose tissue nerves.

The activity of sympathetic nerves innervating interscapular brown adipose tissue of the rat was recorded. Intravenous administrations of glucose (100-300 mg/kg) enhanced the nerve activity. However, mannose, fructose, or galactose (300 mg/kg) showed no effect, suggesting the response is related to diet-induced thermogenesis in the brown adipose tissue.

Adipose Tissue, Brown↗
PubMedDate not supplied

Different metabolism of hexose sugars and sucrose in wound fluid and in fibroblast cultures derived from granulation tissue, hypertrophic scar and keloid.

Viscose cellulose sponge implants in the rat and fibroblast cultures established from granulation tissue, hypertrophic scar, or keloid were treated with different concentrations of glucose, fructose, galactose, mannose, and sucrose. The concentrations of the above-mentioned sugars in wound fluid and cell culture medium were examined at the termination of experiments by liquid chromatography. Results showed that glucose was present in wound fluid in relatively low levels. In addition to glucose, only mannose was found in wound fluid. On the other hand, cell culture studies showed that virtually all the added sugars were found in cell culture medium. The most prominent exception was the decreased concentration of mannose in keloid fibroblast cultures. In addition, glucose concentration in culture medium of keloid fibroblasts was constantly very low except in mannose-treated cultures where the consumption of glucose was dose-dependently decreased compared to increased mannose concentration. Similarly, increased concentrations of galactose and mannose resulted in dose-dependent lowered consumption of glucose in granulation tissue and hypertrophic scar fibroblasts. These findings suggest that the sugar metabolism may differ in various fibroblast cultures. Further, at least in our wound model, only glucose and mannose are present in wound fluid, and excess sugar is rapidly cleared from wound fluid.

Animals↗
PubMed1970

Renal and intestinal hexose transport in familial glucose-galactose malabsorption.

Glucose transport by jejunal mucosa in vitro and kidney in vivo was investigated in a 3 yr old patient with congenital glucose-galactose malabsorption, her family, and 16 normal volunteers. Glucose transport by normal human jejunal mucosa was concentrative, saturable, sodium and energy dependent, and exhibited competitive inhibition. Biopsy specimens from six normal controls and an asymptomatic 5 yr old brother of the proband accumulated glucose to concentrations 16 times that in the incubation medium. The proband's mucosa was unable to concentrate glucose throughout a 60 min incubation period. Both of her parents and a half sister demonstrated impaired glucose transport. Their values fell between normal and those of the proband. Influx of glucose was impaired but efflux of glucose from the mucosa of these three heterozygotes was identical with that in three normal controls. A kinetic analysis indicated a reduced capacity (V(max)), but a normal affinity (K(m)) for glucose transport by their intestinal mucosa. All subjects accumulated fructose similarly.Renal glucose transport was investigated using renal glucose titration techniques. A partial defect in renal glucose reabsorption was found in the proband. Her brother's titration curve was similar to that of seven normal volunteers. We conclude that familial glucose-galactose malabsorption is inherited as an autosomal recessive trait, that heterozygotes for this disorder are detectable and demonstrate a reduced capacity for glucose transport, and that absent intestinal glucose transport is accompanied by partial impairment of renal glucose transport.

Adolescent↗
PubMed1985

The influence of insulin and insulin-like growth factor-I on hexose transport by Sertoli cells.

Insulin stimulates the synthesis of lactate by cultured Sertoli cells prepared from rats aged 13 days, to a much greater extent if glucose is present in the incubation medium than when it is absent. Insulin also stimulates the transport of 3-O-methyl-D-[14 C]glucose into cultured Sertoli cells. This increased transport results from a decrease in the Michaelis-Menten constant (Km) of methylglucose for the transport system without change in maximum velocity (Vmax). Moreover, insulin stimulates influx of the glucose analog and is without effect on efflux. Insulin does not alter transport of methylglucose in peritubular fibroblasts or in mixed populations of germ cells. It was observed that whereas insulin stimulates transport of methylglucose at micromolar concentrations, insulin-like growth factor I (IGF I) exerts the same effect at nanomolar (physiological) concentrations. Moreover, the response to insulin plus IGF I is the same as the maximal responses to either hormone alone. In view of the effects of insulin and IGF I on glucose transport by Sertoli cells and in view of the importance of lactate as a substrate for germ cells, it is suggested that IGF I may be important for the development of normal germinal epithelium in rat testes.

3-O-Methylglucose↗
PubMed1975

Effect of alloxan on permeability and hexose transport in rat pancreatic islets.

The in vitro effect of alloxan exposure on the permeability of collagenase isolated rat pancreatic islets to sucrose, D-mannitol, and L-glucose has been investigated. Determination of changes in cell volume with a non-wash double label isotope procedure indicates that alloxan treatment exerts no measurable effect on permeability to sucrose, D-mannitol, or L-glucose as compared to nonalloxan-treated islets. In addition, neither prior exposure nor the concomitant presence of alloxan alters the rate of D-glucose or 3-0-methyl-D-glucose transport into rat pancreatic islets. It is concluded that the in vitro effect of alloxan on abolishing glucose-induced insulin release in isolated rat pancreatic islets does not appear to be the result of permeability changes to small organic molecules or alteration in the transport of D-glucose into the beta-cell.

Alloxan↗
PubMed1986

Total synthesis of chain-length-uniform dolichyl phosphates and their fitness to accept hexoses in the enzymatic formation of lipoglycans.

Dolichols of defined uniform chain length (C35, C45, and C55) and geometry were prepared by total synthesis according to the following principle: (E,E)-Farnesol, activated as its 4-tolyl sulfone, is condensed with 8-chloroneryl benzyl ether, the sulfonyl group removed and the ether linkage cleaved by lithium/triethylamine. The resulting elongated prenol is converted again to its corresponding 4-toly/sulfone; at this stage isomers are removed by chromatography. After several cycles of this C10-elongation sequence the synthesis is completed in the same way but using 8-chlorocitronellyl benzyl ether as building block to introduce the saturated alpha-isoprene unit. The dolichols obtained were chemically phosphorylated (POCl3/Et3N). Both, the alcohols and their phosphate esters, are characterized spectroscopically. 1H- and 13C-NMR data are recorded for qualitative and stereochemical comparison with natural dolichols. The authentic dolichyl phosphates (Dol-7-P, Dol-9-P, and Dol-11-P) were assayed relative to the natural dolichyl phosphate mixture from pig liver as acceptors for transglycosylation from nucleoside diphosphate sugars (glucose, mannose) by standardized membrane vesicle preparations from plants (Volvox) and animals (liver). Even the shortest chain dolichyl 7-phosphate has full activity in this lipoglycan-forming reaction.

Chemical Phenomena↗