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1.

001-es BibID:BIBFORM028198
Első szerző:Bajza Ágnes (biológus)
Cím:Block by nitrate tolerance of meal-induced insulin sensitization in conscious rabbits / Bajza Á., Németh J., Peitl B., Szilvássy Z.
Dátum:2011
ISSN:0160-2446
Megjegyzések:Hemodynamic nitrate tolerance has been shown to result in an insulin-resistant state. We studied whether nitrate tolerance induced by a 7-day continuous exposure to transdermal nitroglycerin influenced the meal-induced insulin sensitization phenomenon in rabbits. METHODS: Changes in insulin sensitivity in response to feeding in conscious rabbits were determined by rapid insulin sensitivity test, in both nitrate-tolerant and nitrate-intolerant animals. In a separate series of experiments with anesthetized rabbits with or without nitrate tolerance, the hyperinsulinemic euglycemic glucose clamping methods was used to study the effect of intraportal infusion of cholecystokinin (CCK) on whole-body insulin sensitivity. RESULTS: Rabbits with normal feeding exhibited a 46 ± 6% increase in insulin sensitivity as compared with their matching fasting controls. A 7-day period of treatment with patches releasing 0.07 mg of nitroglycerin per hour yielded nitrate tolerance and a state of insulin resistance and no increase in insulin sensitivity in response to food. Intraportal infusion of CCK8 (0.3-3.0 mikrog/kg over 20 minutes) resulted in a dose-dependent increase in insulin sensitivity in normal but not in nitrate-tolerant, fasted anesthetized animals. CONCLUSIONS: Nitrate tolerance blocks both the meal-induced insulin sensitization phenomenon and the insulin-sensitizing effect of intraportal CCK.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Cardiovascular Pharmacology. - 58 : 5 (2011), p. 508-513. -
További szerzők:Németh József (1954-) (vegyész, analitikus) Peitl Barna (1972-) (orvos, farmakológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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2.

001-es BibID:BIBFORM059983
Első szerző:Docsa Tibor (vegyész, biokémikus)
Cím:Insulin sensitivity is modified by a glycogen phosphorylase inhibitor : glucopyranosylidene-spiro-thiohydantoin in streptozotocin-induced diabetic rats / Tibor Docsa, Balázs Marics, József Németh, Csaba Hüse, László Somsák, Pál Gergely, Barna Peitl
Dátum:2015
ISSN:1568-0266
Megjegyzések:The major role of liver glycogen is to supply glucose to the circulation maintaining the normal blood glucose level. In muscle and liver the accumulation and breakdown of glycogen are regulated by the reciprocal activities of glycogen phosphorylase and glycogen synthase. Glycogen phosphorylase catalyses the key step of glycogen degradation and its activity can be inhibited by glucose and its analogues. Obviously, any readily accessible inhibitor of glycogen phosphorylase can be used as a potential therapy of non-insulin-dependent or type 2 diabetes. Hepatic glycogen phosphorylase has been identified as a new target for drugs that control blood glucose concentration. In our experiments glucopyranosylidene-spirothiohydantoin (TH) was tested on the insulin sensitivity and blood glucose level of control and streptozotocin-treated rats. The streptozotocin-treated rats failed to gain weight and exhibited stable hyperglycemia (4.7 ± 0.5 mmol/L glucose in control vs. 7.8 ± 0.5 mmol/L) and low plasma insulin levels (9.6 ± 1.9 [mű]IU/mL in control vs. 3.2 ± 2.2 [mű]IU/mL). When insulin supplementation with slow-release implants (2 IU/day) was started 8 weeks after streptozotocin injection, blood glucose concentration remained suppressed, plasma insulin level dramatically increased and the insulin sensitivity restored. TH administration significantly reduced the high blood glucose concentration and restored the insulin sensitivity of STZtreated rats.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Blood glucose
glycogen phosphorylase inhibitor
insulin implant
streptozotocin
Type 2 diabetes
Megjelenés:Current Topics In Medicinal Chemistry 15 : 23 (2015), p. 2390-2394. -
További szerzők:Marics Balázs (1986-) (okleveles táplálkozástudományi szakember, dietetikus) Németh József (1954-) (vegyész, analitikus) Hüse Csaba Somsák László (1954-) (vegyész) Gergely Pál (1947-) (biokémikus) Peitl Barna (1972-) (orvos, farmakológus)
Pályázati támogatás:OTKA-109450
OTKA
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3.

001-es BibID:BIBFORM049713
Első szerző:Drimba László (farmakológus)
Cím:In Vivo Preclinical Evaluation of a Promising Antiarrhythmic Agent, EGIS-7229 / László Drimba, Jozsef Nemeth, Réka Sári, Yin Di, Anikó Kovács, Gábor Szénási, Zoltán Szilvássy, Barna Peitl
Dátum:2013
ISSN:0272-4391
Megjegyzések:The basic hemodynamic, electrophysiological, and pharmacological effects of EGIS-7229(E-7229) were evaluated and compared with those of a pure "Class III" antiarrhythmic drug (GLG-V-13) inconscious rabbits. Both compounds decreased heart rate dose-dependently. Mean arterial blood pressurewas not influenced by E-7229; however, GLG-V-13 produced a significant elevation on this parameter. Leftventricular end-diastolic pressure was gradually increased by E-7229, while GLG-V-13 induced moreconsiderable elevation on that at intermediate doses. QT and QTcb were lengthened by both compounds;however, higher doses of E-7229 resulted in shortening of the prolonged QT and QTcb.Ventricular effectiverefractory period (VERP) was significantly prolonged by either drug studied. Threshold doses to produceQT50%, QTmax, VERP50%, and VERPmax were significantly higher for E-7229 compared with GLG-V-13.Significantly higher doses were required for E-7229 to induce arrhythmias. The safety ratio was comparablefor both of the compounds. E-7229 can exert multiple actions on cardiac ion channels with minimalinfluence on hemodynamic parameters and reduced proarrhytmic profile in our preclinical model.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
cardiac arrhythmias
preclinical drug development
cardiovascular safety
preclinical model
Megjelenés:Drug Developmet Research. - 74 : 3 (2013), p. 173-185. -
További szerzők:Németh József (1954-) (vegyész, analitikus) Sári Réka (farmakológus) Di, Yin Kovács Anikó Szénási Gábor Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
Pályázati támogatás:75965
OTKA
WNR7OS
WNR7OS
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4.

001-es BibID:BIBFORM042841
035-os BibID:PMID:23474828
Első szerző:Drimba László (farmakológus)
Cím:The role of acute hyperinsulinemia in the development of cardiac arrhythmias / László Drimba, Róbert Döbrönte, Csaba Hegedüs, Réka Sári, Yin Di, Joseph Németh, Zoltán Szilvássy, Barna Peitl
Dátum:2013
Megjegyzések:Patients with perturbed metabolic control are more prone to develop cardiac rhythm disturbances. The main purpose of the present preclinical study was to investigate the possible role of euglycemic hyperinsulinemia in development of cardiac arrhythmias. Euglycemic hyperinsulinemia was induced in conscious rabbits equipped with a right ventricular pacemaker electrode catheter by hyperinsulinemic euglycemic glucose clamp (HEGC) applying two different rates of insulin infusion (5 and 10 mIU/kg/min) and variable rate of glucose infusion to maintain euglycemia (5.5±0.5 mmol/l). The effect of hyperinsulinemia on cardiac electrophysiological parameters was continuously monitored by means of 12-lead surface ECG recording. Arrhythmia incidence was determined by means of programmed electrical stimulation (PES). The possible role of adrenergic activation was investigated by determination of plasma catecholamine levels and intravenous administration of a beta adrenergic blocking agent, metoprolol. All of the measurements were performed during the steady-state period of HEGC and subsequent to metoprolol administration. Both 5 and 10 mIU/kg/min insulin infusion prolonged significantly QTend, QTc, and Tpeak-Tend intervals. The incidence of ventricular arrhythmias generated by PES was increased significantly by euglycemic hyperinsulinemia and exhibited linear relationship to plasma levels of insulin. No alteration on plasma catecholamine levels could be observed; however, metoprolol treatment restored the prolonged QTend, QTc, and Tpeak-Tend intervals and significantly reduced the hyperinsulinemia-induced increase of arrhythmia incidence. Euglycemic hyperinsulinemia can exert proarrhythmic effect presumably due to the enhancement of transmural dispersion of repolarization. Metoprolol treatment may be of benefit in hyperinsulinemia associated with increased incidence of cardiac arrhythmias.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Naunyn-Schmiedeberg's Archives of Pharmacology. - 386 : 5 (2013), p. 435-444. -
További szerzők:Döbrönte Róbert Hegedűs Csaba (1983-) (Molekuláris biológus, Cera-Med Kft. Debrecen) Sári Réka (farmakológus) Di, Yin Németh József (1954-) (vegyész, analitikus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
Pályázati támogatás:GOP-1.2.1-08-2009-0023
Egyéb
NKFP_07-A2-2008-0260
Egyéb
GOP-1.1.2-07/1-2008-0004
Egyéb
TÁMOP-4.2.2.-08/1-2008-0014
TÁMOP
OM-00174/2008
Egyéb
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
GOP-1.1.1-07/1- 2008-0032
Egyéb
OTKA-75965
OTKA
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5.

001-es BibID:BIBFORM038424
Első szerző:Drimba László (farmakológus)
Cím:Beneficial Cardiac Effects of Cicletanine in Conscious Rabbits With Metabolic Syndrome / Drimba László, Hegedüs Csaba, Yin Din, Sári Réka, Németh József, Szilvássy Zoltán, Peitl Barna
Dátum:2012
ISSN:0160-2446
Megjegyzések:BACKGROUND AND PURPOSE: High-fat diet and consequent metabolic syndrome (MS) can lead to elevated risk for cardiac arrhythmias. This preclinical study was to investigate if cicletanine (CIC) could produce cardioprotective effects in conscious rabbits exhibiting the main symptoms of MS. METHODS: NZW rabbits that had undergone an 8-week-long cholesterol-enriched diet (1.5%) were instrumented with a pacemaker electrode and randomly assigned into 3 groups according to the oral treatment of either CIC (50 mg·kg) or sotalol (25 mg·kg) and their placebo b.i.d. over 5 days. Study groups were subjected to either "arrhythmia challenge" by programmed electrical stimulation in the "Arrhythmogenesis" study (N = 54) or global myocardial ischemia by rapid pacing in the "Ventricular Overdrive Pacing-induced Myocardial Ischemia" study (N = 18). The antiarrhythmic effect was evaluated by the establishment of the incidence of programmed electrical stimulation-induced arrhythmias. Proarrhythmia indicators (eg, QTc, Tpeak-Tend) were also measured to assess the cardiac safety profile of CIC. To evaluate the background of antiarrhythmic effect, cardiac cyclic nucleotide (cyclic 3',5'-guanosine monophosphate [cGMP], cyclic 3',5'-adenosine monophosphate [cAMP]) and nitric oxide content were determined. The antiischemic effect was characterized by change of intracavital ST segment. RESULTS: Cicletanine treatment significantly decreased the incidence of ventricular arrhythmias, increased cardiac cGMP and nitric oxide content and reduced cardiac cAMP level. Cicletanine did not modify significantly QTc and Tpeak-Tend interval. The ST-segment change in response to rapid pacing was reduced significantly by CIC. (P < 0.05). CONCLUSIONS: Cicletanine exerts beneficial cardiac effects in rabbits with symptoms of MS, which may be of influence with regard to the clinical application of the drug.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
cicletanine
cardiac arrhythmias
cardiac ischemia
metabolic syndrome
programmed electrical stimulation
cardiac nucleotides
nitric oxide
Megjelenés:Journal of Cardiovascular Pharmacology. - 60 : 2 (2012), p. 208-218. -
További szerzők:Hegedűs Csaba (1983-) (Molekuláris biológus, Cera-Med Kft. Debrecen) Yin, Din Sári Réka (farmakológus) Németh József (1954-) (vegyész, analitikus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
Pályázati támogatás:NKFP_07-A2-2008-0260
EGYÉB
GOP-1.1.2-07/1-2008-0004
EGYÉB
GOP-1.1.1-07/1-2008-0032
EGYÉB
GOP-1.2.1-08-2009-0023
EGYÉB
OTKA-75965
OTKA
TÁMOP-4.2.2.- 08/1-2008-0014
TÁMOP
OM-00174/2008
EGYÉB
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6.

001-es BibID:BIBFORM042635
Első szerző:Fürjes Gergely
Cím:Thrittene radioimmunoassay : description and application of a novel method / G. Fürjes, G. K. Tóth, B. Peitl, R. Pórszász, B. Lelesz, R. Sári, A. Tóth, Z. Szilvássy, J. Németh
Dátum:2012
Megjegyzések:In the present paper the development andapplication of a novel thrittene radioimmunoassay (RIA)are described. 125I-labeling of Tyr(0)-thrittene was performedby the iodogen-method and the mono-iodinatedpeptide, as RIA tracer, was separated by reversed-phasehigh performance liquid chromatography (HPLC). TheRIA results show that the antiserum used in the radioimmunoassayturned to be C-terminal specific, without significantaffinity to other members of the somatostatinpeptide hormone family. Detection limit of the assay was0.2 fmol/ml. This highly specific and sensitive thritteneRIA was used to investigate the distribution of thrittene inthe rat gastrointestinal tract and other tissue samples. Differentareas of the gastrointestinal tract and other tissueswere removed from rats and after extraction the sampleswere processed for thrittene radioimmunoassay. Highestconcentrations were found in the duodenum samplesfollowed by jejunum and ileum, however, all the examinedtissues contained highly enough thrittene for themeasurement.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény hazai lapban
Megjelenés:Journal of Radioanalytical and Nuclear Chemistry. - 292 : 1 (2012), p. 113-118. -
További szerzők:Tóth Gábor K. Peitl Barna (1972-) (orvos, farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Lelesz Beáta (1989-) (molekuláris biológus) Sári Réka (farmakológus) Tóth Attila (1971-) (biológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Németh József (1954-) (vegyész, analitikus)
Pályázati támogatás:75965
OTKA
Internet cím:DOI
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7.

001-es BibID:BIBFORM061364
035-os BibID:(WOS)000365744800007 (Scopus)84948683402
Első szerző:Hegedűs Csaba (Molekuláris biológus, Cera-Med Kft. Debrecen)
Cím:Effect of long-term olanzapine treatment on meal-induced insulin sensitization and on gastrointestinal peptides in female Sprague-Dawley rats / Csaba Hegedűs, Diána Kovács, Rita Kiss, Réka Sári, József Németh, Zoltán Szilvássy, Barna Peitl
Dátum:2015
ISSN:0269-8811
Megjegyzések:Meal-induced insulin sensitization (MIS), an endogenous adaptive mechanism is activated post-prandially. Reduced MIS leads to diabetes, but itsactivation improves insulin sensitivity. MIS is preserved to single olanzapine administration, therefore we aimed to investigate the chronic effect ofolanzapine on fasted-state insulin sensitivity and on MIS in female Sprague?Dawley rats. Daily food and water intake, stool and urine production andbody weight were determined. The MIS was characterized by a rapid insulin sensitivity test. Fasting hepatic and peripheral insulin sensitivity weredetermined by a hyperinsulinaemic euglycaemic glucose clamping supplemented with radiotracer technique. Fasted and post-prandial blood sampleswere obtained for plasma insulin, leptin, ghrelin, amylin, GLP-1, GIP, PYY and PP determination. Adiposity was characterized by weighing intraabdominaland inguinal fat pads. Olanzapine caused hepatic insulin resistance and a reduced metabolic clearance rate of insulin, but the MIS retainedits function. Body weight and adiposity were enhanced, but olanzapine failed to increase food intake. Fasting insulin and leptin were elevated and thepost-prandial reduction in ghrelin level was inhibited by olanzapine.The MIS remained functionally intact after long-term olanzapine treatment. Altered insulin, leptin and ghrelin levels indicate olanzapine-inducedmetabolic derangements. Pharmacological activation of MIS could potentially be exploited to treat or prevent olanzapine-induced insulin resistance.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
olanzapine
insulin resistance
obesity
ghrelin
leptin
Megjelenés:Journal Of Psychopharmacology. - 29 : 12 (2015), p. 1271-1279. -
További szerzők:Kovács Diána Klára (1985-) (Molekuláris biológus) Kiss Rita (1974-) (laboratóriumi diagnosztika szakorvos) Sári Réka (farmakológus) Németh József (1954-) (vegyész, analitikus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
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8.

001-es BibID:BIBFORM057941
Első szerző:Hegedűs Csaba (Molekuláris biológus, Cera-Med Kft. Debrecen)
Cím:Investigation of the metabolic effects of chronic clozapine treatment on CCK-1 receptor deficient Otsuka Long Evans Tokushima Fatty (OLETF) rats / Csaba Hegedűs, Diána Kovács, László Drimba, Réka Sári, Angelika Varga, József Németh, Zoltán Szilvássy, Barna Peitl
Dátum:2013
ISSN:0014-2999
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal of Pharmacology. - 718 : 1-3 (2013), p. 188-196. -
További szerzők:Kovács Diána Klára (1985-) (Molekuláris biológus) Drimba László (farmakológus) Sári Réka (farmakológus) Varga Angelika (1977-) (biológus) Németh József (1954-) (vegyész, analitikus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
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9.

001-es BibID:BIBFORM020274
Első szerző:Horváth Péter
Cím:Changes in tracheo-bronchial sensory neuropeptide receptor gene expression pattern in rats with cisplatin-induced sensory neuropathy / Péter Horváth, Zoltán Szilvássy, Barna Peitl, Judit Szilvássy, Zsuzsanna Helyes, János Szolcsányi, József Németh
Dátum:2006
ISSN:0143-4179
Megjegyzések:AbstractAn attenuated neurogenic broncho-constriction underpinned by a decrease in sensory neuropeptide release has been shown to be characteristic of cisplatin-induced neuropathy. The present work was to explore if beyond neuropeptide release, cisplatin at a treatment schedule attaining sensory neuropathy, produced changes in the expression of the receptors of sensory neuropeptides such as somatostatin, calcitonin gene-related peptide (CGRP) and substance P (SP) in bronchial tissue of the rat. Twenty-four Wistar rats were divided into three groups. The animals in the "Treatment groups 1 and 2" were given cisplatin (1.5mgkg(-1)) and mannitol (75mgkg(-1)) over 5 days. The rats in the "Control" group were given mannitol+isotonic saline. Four animals from each group were used to study the expression pattern of the neuropeptide receptors in bronchial tissue. The levels of somatostatin receptor 4 (SSTR 4), neurokinin 1 (NK1), neurokinin 2 (NK2) and CGRP receptor expression were examined by quantitative real time polymerase chain reaction (RT-PCR) method, 11 and 22 days after the last cisplatin/vehicle dose. The cisplatin treatment significantly increased plasma somatostatin immunoreactivity and the expression of SSTR4 receptor detected both on the 11th and 22nd post-treatment days with no change in either CGRP, NK1, and NK2 receptor gene expression or plasma CGRP and substance P levels. We conclude that cisplatin neuropathy is accompanied by an increase in plasma somatostatin immunoreactivity with an increase in SSTR4 expression in rats.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
tracheo-bronchial
neuropeptide receptor
cisplatin-induced
Megjelenés:Neuropeptides. - 40 : 1 (2006), p. 77-83. -
További szerzők:Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus) Szilvássy Judit (1960-2022) (fül- orr- gégész) Helyes Zsuzsanna Szolcsányi János (Pécs) Németh József (1954-) (vegyész, analitikus)
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10.

001-es BibID:BIBFORM061365
Első szerző:Kovács Diána Klára (Molekuláris biológus)
Cím:Meal-induced insulin sensitization is preserved after acute olanzapine administration in female Sprague-Dawley rats / Diána Kovács, Csaba Hegedűs, Rita Kiss, Réka Sári, József Németh, Zoltán Szilvássy, Barna Peitl
Dátum:2015
ISSN:0028-1298
Megjegyzések:Olanzapine, an atypical antipsychotic, can acutely induce fasting insulin resistance, but we do not know whether it is able to modulate the meal-induced insulin sensitization (MIS). Two main experimental groups (control and olanzapine-treated) were created with two subgroups (fasted and re-fed) within each. After oral vehicle/olanzapine administration, the first meal size and duration and the total amount of consumed food was recorded in conscious rats. Then, under anaesthesia, the carotid artery and jugular vein was prepared and cannulated to obtain samples for blood glucose and hormone determination as well as for insulin/glucose infusion, respectively. Basal insulin sensitivity and MIS was determined by homeostasis model assessment (HOMA) calculation and by rapid insulin sensitivity test, respectively. In fasted animals, olanzapine increased blood glucose and plasma insulin and reduced basal insulin sensitivity, but it failed to modify other hormone levels. Postprandial leptin and glucose-dependent insulinotropic polypeptide (GIP) levels increased, and ghrelin level decreased significantly (p?<?0.05) both in vehicle- and olanzapine-treated groups, but plasma insulin increased only in vehicle-treated animals. Furthermore, decrement in ghrelin level was attenuated in olanzapine-treated animals compared to controls. There was no significant change in the first meal size and duration or in the total amount of food consumed. Olanzapine had no effect on the MIS. We demonstrated that olanzapine can induce insulin resistance without weight gain in healthy rats. Furthermore, the MIS was preserved after acute olanzapine treatment. The blunted postprandial ghrelin and insulin response could contribute to the effect of olanzapine on feeding behaviour. Pharmacological induction of MIS may improve the olanzapine-induced insulin resistance.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Olanzapine
Insulin sensitivity
Satiety
Ghrelin
Gut hormones
Megjelenés:Naunyn-Schmiedebergs Archives Of Pharmacology. - 388 : 5 (2015), p. 525-530. -
További szerzők:Hegedűs Csaba (1983-) (Molekuláris biológus, Cera-Med Kft. Debrecen) Kiss Rita (1974-) (laboratóriumi diagnosztika szakorvos) Sári Réka (farmakológus) Németh József (1954-) (vegyész, analitikus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
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11.

001-es BibID:BIBFORM048149
Első szerző:Kovács Diána Klára (Molekuláris biológus)
Cím:Identification of PPARγ ligands with One-dimensional Drug Profile Matching / Diána Kovács, Zoltán Simon, Péter Hári, András Málnási-Csizmadia, Csaba Hegedűs, László Drimba, József Németh, Réka Sári, Zoltán Szilvássy, Barna Peitl
Dátum:2013
ISSN:1177-8881
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Drug Design, Development and Therapy [electronic resources]. - 7 (2013), p. 917-928. -
További szerzők:Simon Zoltán (1935-) Hári Péter Málnási-Csizmadia András Hegedűs Csaba (1983-) (Molekuláris biológus, Cera-Med Kft. Debrecen) Drimba László (farmakológus) Németh József (1954-) (vegyész, analitikus) Sári Réka (farmakológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
Pályázati támogatás:NKFP_07-A2-2008-0260
Egyéb
GOP-1.1.2-07/1-2008-0004
Egyéb
TÁMOP-4.2.2.-08/1-2008-0014
TÁMOP
OM-00174/2008
Egyéb
GOP-1.1.1-07/1-2008-0032
Egyéb
GOP-1.1.1-07/1-2008-0021
Egyéb
GOP-1.2.1-08-2009-0023
Egyéb
KDOP-1.2.1-11-2011-0003
Egyéb
GOP-1.1.1-11-2012-0435
Egyéb
75965
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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12.

001-es BibID:BIBFORM066474
Első szerző:Marics Balázs (okleveles táplálkozástudományi szakember, dietetikus)
Cím:Diet-induced obesity enhances TRPV1-mediated neurovascular reactions in the dura mater / Marics B., Peitl B., Pázmándi K., Bácsi A., Németh J., Oszlács O., Jancsó G., Dux M.
Dátum:2017
ISSN:0017-8748
Megjegyzések:Objective: Exploring the pathophysiological changes in transient receptor potential vanilloid 1 (TRPV1) receptor of the trigeminovascular system in high-fat, high-sucrose (HFHS) diet-inducedobesity of experimental animals.Background: Clinical and experimental observations suggest a link between obesity and migraine. Accumulating evidence indicates that metabolic and immunological alterations associated with obesity may potentially modulate trigeminovascular functions. A possible target for obesity-induced pathophysiological changes is the TRPV1/capsaicin receptor which is implicated in the pathomechanism of headaches in a complex way.Methods: Male Sprague-Dawley rats were fed a regular (n = 25) or HFHS diet (n = 26) for 20 weeks. At the end of the dietary period, body weight of the animals was normally distributed in both groups and it was significantly higher in animals on HFHS diet. Therefore, experimental groups were regarded as control and HFHS diet-induced obese groups. Capsaicin-induced changes in meningeal blood flow and release of calcitonin gene-related peptide (CGRP) from dural trigeminal afferents were measured in control and obese rats. The distribution of TRPV1- and CGRP-immunoreactive meningeal sensory nerves was also compared in whole mount preparations of the dura mater. Metabolic parameters of the animals were assessed by examining glucose and insulin homeostasis as well as plasma cytokine concentrations.Results: HFHS diet was accompanied by reduced food consumption and greater fluid and energy intakes in addition to increased body weight of the animals. HFHS diet increased fasting blood glucose and insulin concentrations as well as levels of circulating proinflammatory cytokines interleukin-1? and interleukin-6. In obese animals, dural application of the archetypal TRPV1 agonist capsaicin resulted in significantly augmented vasodilatory and vasoconstrictor responses as compared to controls. Diet-induced obesity was also associated with enhanced basal and capsaicin- induced CGRP release from meningeal afferents ex vivo. Except for minor morphological changes, the distribution of dural TRPV1- and CGRP-immunoreactive afferents was similar in control and obese animals.Conclusions: Our results suggest that obesity induced by long-term HFHS diet results in sensitization of the trigeminovascular system. Changes in TRPV1-mediated vascular reactions and CGRP release are pathophysiological alterations that may be of relevance to the enhanced headache susceptibility of obese individuals.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
headache
obesity
transient receptor potential vanilloid 1
calcitonin gene-related peptide
meningeal blood flow
trigeminal nociception
Megjelenés:Headache 57 : 3 (2017), p. 441-454. -
További szerzők:Peitl Barna (1972-) (orvos, farmakológus) Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus) Bácsi Attila (1967-) (immunológus) Németh József (1954-) (vegyész, analitikus) Oszlács Orsolya Jancsó Gábor Dux Mária
Pályázati támogatás:OTKA K-101873
OTKA
OTKA K119597
OTKA
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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