Together with the development of peritoneal dialysis (PD), appropriate animal models play an important role in the investigation of physiological, pathophysiological and clinical aspects of PD. However, there is still not an ideal experimental PD animal model. In this study, 45 Sprague-Dawley rats were divided into three groups. Grou p 1 (n=15) was receiving daily peritoneal injection through the catheter connected to the abdominal cavity, using PD solution containing 3.86 % D-glucose. Group 2 (n=15) was receiving daily peritoneal injection of 0.9 % physiological saline through a catheter. Group 3 (n=15), which was subjected to sham operation, served as controls. Our results showed that WBC counts in peritoneal effluent of Group 1 were slightly higher than those of Group 2 and control group, respectively (p<0.05). However, there was no episode of infection in any group. In addition, there was no significant difference in neutrophils fractions among these three groups. Hematoxylin-eosin and Masson’s trichrome staining demonstrated a dramatic increase in thickness of the mesothelium-to-muscle layer of peritoneum exposed to high glucose (Group 1) compared to Group 2 and controls (p<0.01). These data indicated that we established a novel rat model of PD with a modified catheter insertion method. This model is more practical, easy to operate, not too expensive and it will facilitate the investigate of long-term effects of PD., Y.-M. Peng ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
The diabetogenic effect of prolactin observed in patients with pathological hyperprolactinaemia was verified in healthy subjects. Plasma prolactin elevation was induced by administration of a dopamine antagonist drug domperidone (Motilium 10 mg orally, 9 subjects) and 2 h later the oral glucose tolerance test was performed. The influence of dopamine receptor stimulation on glucose homeostasis was tested by dopamine infusion (0.3 mg in saline or 20 % glucose, 1 g/min for 60 min, 11 subjects). After the blockade of dopamine receptors, a significant and prolonged increase of prolactin concentration was found. However, the levels of glucose, insulin, and C- peptide either before or after the glucose load were not different from control ones. The decreased number of insulin receptors (1.97±0.41 vs 0.51 ±0.14 pmol per 2.109 red blood cells) was compensated by increased affinity (0.51 ±0.17 vs 1.00±0.22 K* 108 mol.-1 per 1]) of insulin receptors. The stimulation of dopamine receptors showed a negligible effect on glucose regulation. It may be suggested that an endogenous increase of prolactin concentration in the physiological range does not participate in the regulation of glucose homeostasis in healthy subjects.
The aim of the experiment was to investigate the mechanism of harmful alloxan action in vivo. 75 mg/kg b.w. of this diabetogenic agent were administered to fasting rats. Two minutes later the animals were decapitated. It was observed that alloxan caused a distinct rise in blood insulin and glucose levels with a concomitant drop of free fatty acids. The amount of sulfhydryl groups in the liver of alloxan-treated rats was decreased and glutathione peroxidase activity was substantially higher. These results indicate that some changes observed in alloxan-induced diabetes can not only be the consequence of B cells damage by alloxan but may also be the result of its direct influence on other tissues. It was also observed that glucose given 20 min before alloxan injection only partially protected against the deleterious effects of alloxan.
Maghemite (γ-Fe2O3) nanoparticles, 12 nm in size, were prepared by co-precipitation of Fe(II) and Fe(III) chlorides with ammonium hydroxide and oxidation with hydrogen peroxide. To achieve stability and biocompatibility, obtained particles were coated with silica, to which glucose and ascorbic acid were bound by different mechanisms. The composite particles were thoroughly characterized by transmission electron microscopy, dynamic light scattering, elemental analysis, and FT-Raman and fluorescence spectroscopy to determine composition, morphology, size and its distribution, ζ-potential, and scavenging of peroxyl and hydroxyl radicals. As the particles showed promising antioxidative properties, they may have a possible application as a stable magnetically controlled scavenger of reactive oxygen species., M. Moskvin, D. Horák., and Obsahuje bibliografii
The effects of metabolisable sugars sucrose and glucose along with non-metabolisable isomers of sucrose palatinose and turanose were tested. Rate of oxygen evolution (P), electron transport rate (ETR), and photochemical quenching (qp) showed substantial decrease after 24 and 48 h by glucose and sucrose treatments, whereas there was no effect on all these parameters by the treatment with palatinose and turanose. Also the Fv/Fm ratio remained constant through the time of studies revealing that the maximal photochemical capacity of the cells was unchanged. Non-photochemical quenching (qN) showed a decrease compared to the control values by all the treatments. Hence P and Chl fluorescence parameter were affected only by those sugars which are used in the metabolic pathways and not by sugar analogues. and A. K. Sinha, T. Roitsch.
Cyanobacteria Spirulina platensis and Nostoc linckia were grown in the presence of 5 mM and 50 mM glucose or 5 mM mannose, non-metabolisable glucose analogue that effectively triggers the repression of photosynthesis. Glucose evoked active cyanobacterial growth but chlorophyll (Chl) content decreased to some extent and porphyrins were excreted. The content of monogalactosyldiacylglycerol decreased in glucose-grown cyanobacteria and that of phosphatidylglycerol increased substantially. Mannose inhibited cyanobacteria growth as well as Chl synthesis, however, phosphatidylglycerol contents were higher than in respective control samples. In cyanobacterial cells glucose may not only inhibit photosynthetic processes, but also cause structural transformations of membranes which may be necessary for the activity of respiratory electron transport chain components under heterotrophic conditions. and N. F. Mykhaylenko ... [et al.].
We investigated whether hypoxia altered the utilization of fructose-1,6-bisphosphate as a gluconeogenic or glycolytic intermediate in superfused media from hog carotid artery. Using 13C-NMR, we found that although 3-13C-iactate production from l-13C-glucose increased compared to that under well-oxygenated conditions, the conversion of exogenously applied l,6-13C-fructose-l,6-bisphosphate to glucose (gluconeogenesis) or to 3-13C-lactate was not significantly affected by hypoxia. Since hypoxia alters the rate of glucose conversion to lactate but not the conversion of fructose-1,6-bisphosphate to glucose, we conclude that glycolysis and glycogenolysis may continue to be compartmentalized during hypoxia and that a high rate of gluconeogenesis can occur even during hypoxia.
Apolipoprotein A-V plays an important role in the determination of plasma triglyceride (TG) concentration. We aimed to determine whether polymorphisms -1131T>C (rs662799) and 56C>G (rs3135506) of the APOA5 gene have an impact on the course of postprandial lipemia induced by a fat load and a fat load with added glucose. Thirty healthy male volunteers, seven heterozygous for the -1131C variant and three for the 56G variant (HT) carriers, and 20 wild-type (WT) carriers underwent two 8-hour tests of postprandial lipemia – one after an experimental breakfast consisting of 75 g of fat and second after a breakfast consisting of 75 g of fat and 25 g of glucose. HT carriers had a higher postprandial response after fat load than WT carriers (AUC TG: 14.01±4.27 vs. 9.84±3.32 mmol*h/l,
respectively, p=0.016). Glucose added to the test meal suppressed such a difference. Heterozygous carriers of the variants of APOA5 (-1131C and 56G) display more pronounced postprandial lipemia after pure fat load than WT carriers. This statistically significant difference disappears when glucose is added to a fat load, suggesting that meal composition modulates the effect of these polymorphisms on the magnitude of postprandial lipemia.
Lipoprotein lipase (LPL) is a key factor determining the clearance of triglycerides from the circulation. The enzyme activity is tissue-specifically regulated by insulin, but it is not clear yet how insulin regulates the total LPL activity in the circulation. To answer such question, we measured LPL activity using the intravenous fat tolerance test (IVFTT) that was carried out 1 h before as well as 2 h and 4 h after oral administration of glucose (75 g) in eleven healthy male volunteers. In control experiments, no glucose was given to the subjects. Glucose administration resulted in an expected increase in plasma glucose and insulin and in a suppression of non-esterified fatty acid concentration. The LPL activity assessed in IVFTT as a k2 rate constant did not change in control experiments and decreased to 78 % and 73 % of baseline values 2 h and 4 h after glucose administration, respectively (p=0.01). Similarly, LPL activity measured in the plasma after intravenous injection of heparin at the end of the experiments was 16 % lower (p<0.05) after glucose administration. In conclusion, LPL activity is already downregulated in vivo 2 h after glucose administration. The results of our study indicate that repeated IVFTT is a promising approach for studying acute changes in LPL activity., E. Jindřichová, S. Kratochvílová, J. Kovář., and Obsahuje bibliografii a bibliografické odkazy
In order to elucidate the direct effect of glucose on lipolysis in isolated rat adipocytes, cells were incubated in a buffer with different concentrations of this sugar: 2, 8 or 16 mmol/l. The increase in glucose concentration from 2 mmol/l to 8 or 16 mmol/l enhanced basal lipolysis by 30% and 47 %, respectively. Epinephrine-induced lipolysis (1 m mol/l) was also increased by 31 % and 32 %, when glucose concentration was increased from 2 mmol/l to 8 or 16 mmol/l, respectively. The rise in lipolysis caused by glucose was restricted by H-89 (an inhibitor of protein kinase A, 30 µmol/l), but insulin (1 nmol/l) had no inhibitory action. The augmentation of lipolysis by glucose did not require its metabolism (as demonstrated using 2-deoxyglucose) and was due to the action of this sugar on the final steps of the lipolytic cascade, particularly on protein kinase A. However, short-term exposure of adipocytes to higher glucose concentrations did not restrict the inhibitory action of insulin on lipolysis induced by epinephrine., T. Szkudelski, K. Szkudelska., and Obsahuje bibliografii