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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
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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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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001-es BibID:	BIBFORM066140
035-os BibID:	(WOS)000401026600010 (Scopus)85019141123
Első szerző:	Marics Balázs (okleveles táplálkozástudományi szakember, dietetikus)
Cím:	Diet-induced obesity alters dural CGRP release and potentiates TRPA1-mediated trigeminovascular responses / Balázs Marics, Barna Peitl, Angelika Varga, Kitti Pázmándi, Attila Bácsi, József Németh, Zoltán Szilvássy, Gábor Jancsó, Mária Dux
Dátum:	2017
ISSN:	0333-1024
Megjegyzések:	Background: Clinical studies suggest a link between obesity and the primary headache disorder migraine. In our studywe aimed to reveal the effect of obesity on meningeal nociceptor function in rats receiving a high-fat, high-sucrose diet.Methods: Transient receptor potential ankyrin 1 (TRPA1) receptor activation-induced changes in meningeal blood flow,release of calcitonin gene-related peptide (CGRP) from trigeminal afferents and TRPA1 protein expression in thetrigeminal ganglia were measured in control and obese rats. Metabolic parameters of the animals were assessed bymeasuring glucose and insulin homeostasis as well as plasma cytokine concentrations.Results: The present experiments revealed an enhanced basal and TRPA1 receptor agonist-induced CGRP release frommeningeal afferents of obese insulin-resistant rats and an attenuated CGRP release to potassium chloride. Obesity wasalso associated with an augmented vasodilatation in meningeal arteries after dural application of the TRPA1 agonistacrolein, a reduction in TRPA1 protein expression in the trigeminal ganglia and elevations in circulating proinflammatorycytokines IL-1b and IL-6 in addition to increased fasting blood glucose and insulin concentrations.Conclusions: Our results suggest trigeminal sensitisation as a mechanism for enhanced headache susceptibility in obeseindividuals after chemical exposure of trigeminal nociceptors.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Obesity calcitonin gene-related peptide sensory neuron laser Doppler flowmetry headache transient receptor potential ankyrin 1
Megjelenés:	Cephalalgia. - 37 : 6 (2017), p. 581-591. -
További szerzők:	Peitl Barna (1972-) (orvos, farmakológus) Varga Angelika (1977-) (biológus) Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus) Bácsi Attila (1967-) (immunológus) Németh József (1954-) (vegyész, analitikus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Jancsó Gábor Dux Mária
Pályázati támogatás:	K-101873 OTKA 4.1.2.E-13/1/KONV-2013-0010 TÁMOP
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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