Telemedicine screening adolescent metabolic syndrome in Greek schools.

Background: Using telemedicine in the school setting in Greece, we screened a representative adolescent sample for MetS (International Diabetes Federation criteria) and explored its associations with anthropometric, sociodemographic and behavioural parameters.

Materials And Methods: Cross-sectional data were obtained from 12- to 17-year-old high school students.

Results: The prevalence of MetS in 1578 adolescents (mean age ± SD 14.

An in-silico model of the biosynthesis of neurotransmitter glutamate, elucidates the complex regulatory role of glucocorticoids in neurotransmitter glutamate release.

An in-silico model, of the glucocorticoid regulated glutamate release, in rat hippocampal tissue, is constructed. The model permits the pseudo-steady state estimation of various fluxes, experimentally impossible to measure, from a set of measured rates. Estimates of the astrocytic pyruvate carboxylase reaction and the neuronal TCA cycle rates are correlated with different dexamethasone concentrations, in order to extrapolate explicit kinetic equations.

Metabolic flux analysis as a tool for the elucidation of the metabolism of neurotransmitter glutamate.

A flux analysis model for the metabolism of neurotransmitter glutamate is constructed, in order to study functional aspects of its metabolism. This work is based on the potassium [K(+)] evoked neurotransmitter glutamate released, as measured in a series of experiments of superfused rat or mouse brain preparations. These measurements are combined with data reported, concerning the metabolism of glutamate and its precursors, glutamine and glucose in rat cerebral cells in vivo.

Effects of dexamethasone on K(+)-evoked glutamate release from rat hippocampal slices.

Dexamethasone (DEX) at physiologically elevated (stress) concentration (1 microM) decreased K(+)-evoked glutamate release from rat hippocampal slices under superfusion in the presence of Ca2+. On the contrary 10 microM DEX increased this K(+)-evoked glutamate release while 0.1 microM DEX had no effect.

Determination of glutamate by high-performance liquid chromatography with fluorescence detection in superfusates of rat brain preparations.

A method is described for the determination of glutamate in superfusates of cortical or hippocampal rat brain slices. This method is based on the precolumn derivatization of amino acids with orthopthaldialdehyde and mercaptopropionic acid, separation by high-performance liquid chromatography, and detection by fluorescence. By adjusting the concentrations of reagents and with the minimum dilution of the sample, it was possible to reproducibly measure the Ca2+-dependent K+-evoked release of neurotransmitter glutamate in superfusates of brain slices.

Effectors of D-[3H]aspartate release from rat cerebellum.

The effect of aminooxyacetic acid (AOAA), NH4+, phenylsuccinate (Phs), ketone bodies (KB) and glutamine (Gln), that might interfere with the biosynthesis of neurotransmitter glutamate on the K(+)-evoked Ca(2+)-dependent release of D-[3H]aspartate from rat cerebellar slices was studied. Therefore slices were preincubated in a Krebs-Ringer-bicarbonate-glucose (KR) buffer, loaded with D-[3H]aspartate and superfused in the presence of Ca2+ or when Ca2+ was replaced by Mg2+ or in some cases by EGTA. AOAA, NH4+ and Phs increase the K(+)-evoked Ca(2+)-dependent release of radioactivity by 30%, 68% and 188% compared to the control respectively indicating that these agents are inhibitors of the K(+)-evoked Ca(2+)-dependent release of glutamate.

Regulatory sites and effectors of D-[3H]aspartate release from rat cerebral cortex.

To study the effect of agents interfering with the biosynthesis and/or the K(+)-evoked Ca(2+)-dependent release of neurotransmitter glutamate, rat cerebral slices were preincubated with Krebs-Ringer-HEPES-glucose-glutamine buffer (KRH buffer), loaded with D-[3H]aspartate and superfused with the preincubation medium in the presence or in the absence of Ca2+. The difference in radioactivity release divided by the basal release per min under the two conditions represented the K(+)-evoked Ca(2+)-dependent release. The agents used were: 1) Aminooxyacetic acid (AOAA), the inhibitor of transaminases, 2) Leucine (Leu), the inhibitor of phosphate activated glutaminase (PAG), 3) NH4+, the inhibitor of PAG, 4) Phenylsuccinic acid (Phs), the inhibitor of the mitochondrial ketodicarboxylate carrier, 5) ketone bodies, the inhibitors of glycolysis, 6) the absence of glutamine, the substrate of PAG.

Haloperidol reduces K(+)-evoked Ca(2+)-dependent D-[3H]aspartate release from rat hippocampal slices.

Rat hippocampal slices preloaded with D-[3H]aspartate, a non metabolizable analogue of L-glutamate, were superfused with artificial CSF. Depolarization was induced by 53.5 mM K+, in the presence of Ca2+ (1.

Incorporation of 15N from L-leucine into isoleucine by rat brain cerebral cortex slices.

The fate of leucine nitrogen in the central nervous system was investigated by incubating rat cerebral cortex slices in the presence of 0.5 mM each of L-[15N]-leucine, L-isoleucine, and L-valine. Analysis of the slices and incubation media for free amino acids by gas chromatography-mass spectrometry revealed that the 15N from leucine is incorporated into isoleucine only.

Effect of starvation or streptozotocin-diabetes on phosphate-activated glutaminase of different rat brain regions.

Phosphate-activated glutaminase (PAG) was assayed in homogenates of brain cerebellum, hippocampus or striatum from normal, starved for 48 h to 120 h or streptozotocin-diabetic rats. Only the hippocampal enzyme was increased (47%) by diabetes. Starvation had no effect in any of the regions studied.

Therapeutic effects of cetirizine in delayed pressure urticaria: clinicopathologic findings.

Cetirizine, a peripheral H1 antagonist, was administered to patients with delayed pressure urticaria in a double-blind, placebo-controlled, crossover study. Efficacy in reducing pressure-induced wheals and flares was evaluated. Histologic changes were also assessed with the skin window technique in weight-induced wheals.

Leucine: effector of phosphate activated glutaminase in rat cerebral cortex.

Phosphate activated glutaminase (PAG) was assayed in whole homogenate and synaptosomes of cerebral cortex from normal or fasted for 120 h rats. The specific activity (s.a.

Role of aspartate aminotransferase and mitochondrial dicarboxylate transport for release of endogenously and exogenously supplied neurotransmitter in glutamatergic neurons.

Evoked release of glutamate and aspartate from cultured cerebellar granule cells was studied after preincubation of the cells in tissue culture medium with glucose (6.5 mM), glutamine (1.0 mM), D[3H] aspartate and in some cases aminooxyacetate (5.

Evidence that aspartate aminotransferase activity and ketodicarboxylate carrier function are essential for biosynthesis of transmitter glutamate.

Based on the selective inhibition of glutamate release in cerebellar granule cells in primary cultures by the aspartate aminotransferase inhibitor, aminooxyacetic acid, and by the ketodicarboxylate carrier inhibitor, phenylsuccinate, a novel model for synthesis of transmitter glutamate is suggested: Glutamate is formed from glutamine in the mitochondrial intramembrane space by phosphate-activated glutaminase, transported across the inner membrane in exchange with aspartate, transaminated in the matrix to alpha-ketoglutarate, which via the ketodicarboxylate carrier is transferred to the cytoplasm, and transaminated to form transmitter glutamate. Such a mechanism would explain the functional role of aspartate aminotransferase in glutamatergic neurons.

Effects of fasting and diabetes on some enzymes and transport of glutamate in cortex slices or synaptosomes from rat brain.

Phosphate-activated glutaminase (PAG) and glutamic acid decarboxylase (GAD) were assayed in homogenates and synaptosomes obtained from starved (48 hr or 120 hr) and diabetic (streptozotocin) rat brain cortex. Glutamine synthetase (GS) was assayed in homogenates, microsomal and soluble fractions, from brain cortex of similarly treated rats. L-Glutamate uptake and exit rates were determined in cortex slices and synaptosomes under the same conditions.

Effects of branched chain amino acids, pyruvate, or ketone bodies on the free amino acid pool and release from brain cortex slices of normal and streptozotocin-diabetic rats.

Brain cortex slices from diabetic rats incubated in Krebs-Ringer-bicarbonate (KRB)--glucose medium show, compared to the normals, a 75% higher glutamine content. Branched chain amino acids (BCAA) added, at 0.5mM each, to this medium increase (53%) the glutamine content in the normal slices but have no effect on the glutamine content in the slices from diabetic rats.

Some aspects on amino acid metabolism in relation to glucose and ketone bodies in brain cortex slices of the rat.

Glucose is the major fuel of the adult brain under normal conditions. The most abundant free amino acids of the brain are: Glutamate, taurine N-acetylaspartate, glutamine, aspartate and 4-aminobutyrate. Deprivation of glucose from the incubation medium of brain cortex slices decreases mainly glutamate and glutamine content.

Effect of L-tryptophan injection in rats on some enzymes of amino acid metabolism in liver. I. In vitro studies of the effect of L-tryptophan and its metabolites on the extramitochondrial L-alanine: 2-ketoglutaric aminotransferase.

Fed and fasted rats were injected with L-tryptophan (12.5 mg/100 g body weight) and the specific activities of L-glutamic: NAD oxidoreductase (deaminating) (EC 1.4.

Influence of L-leucine on glutamate dehydrogenase activity in isolated rat diaphragm.

Glutamate dehydrogenase (NAD) activity was measured in liver and diaphragm mitochondria from 48 h fasted rats. Kinetic studies were performed with diaphragm enzyme and the effects of L-leu, ADP and L-ala on the K(1)m and V(1)max for NH(4)+, and α-ketoglutarate were evaluated. L-leucine increases by 2-8 fold the V(1)max for all three substrates with no significant changes in the K(1)m.

Amino acid and protein metabolism in diabetes mellitus.

In normal man, the fasting state is characterized by release of alanine and glutamine from muscle and in situ muscle catabolism of branched chain amino acids (lecucine, isoleucine, and valine). The alanine released by muscle is utilized by the liver for gluconeogenesis. Muscle nitrogen repletion occurs during protein feeding primarily by means of selective hepatic escape and muscle uptake of branched chain amino acids in ingested protein.

Effects of ketone bodies on amino acid metabolism in isolated rat diaphragm.

1. Diaphragms from 48h-starved rats were incubated in Krebs-Ringer bicarbonate medium at 37degreesC for 30min and then transferred into new medium and incubated for 1, 2 and 3 h. 2.