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001-es BibID:	BIBFORM020242
Első szerző:	Peitl Barna (orvos, farmakológus)
Cím:	Meal-induced enhancement in insulin sensitivity is not triggered by hyperinsulinemia in rats / Barna Peitl, Róbert Döbrönte, József Németh, Csaba Pankucsi, Réka Sári, Angelika Varga, Zoltán Szilvássy
Dátum:	2009
Megjegyzések:	Several reports confirmed the phenomenon of postprandial increase in whole-body insulin sensitivity. Although the initial step of this process is unknown, the pivotal role of postprandial hyperinsulinemia has strongly been suggested. The aim of the present study was to determine whether hyperinsulinemia per se induces insulin sensitization in healthy male Wistar rats. Rapid insulin sensitivity test (RIST) were performed in fasted, anesthetized rats before and during stable hyperinsulinemia achieved by hyperinsulinemic euglycemic glucose clamping (HEGC) with insulin infused either through the jugular vein (systemic HEGC) or into the portal circulation (portal HEGC) at a rate of 3 mU/(kg min). Insulin sensitivity expressed by the rapid insulin sensitivity (RIST) index (in milligrams per kilogram) was characterized by the total amount of glucose needed to maintain prestudy blood glucose level succeeding an intravenous bolus infusion of 50 mU/kg insulin over 5 minutes. In fasted animals, the RIST index was 37.4 +/- 3.1 mg/kg. When hyperinsulinemia mimicking the postprandial state was achieved by systemic HEGC, the RIST index (39.7 +/- 10.6 mg/kg) showed no significant changes as compared with the pre-HEGC values. Hyperinsulinemia achieved by portal insulin infusion also failed to modify the RIST index (35.7 +/- 4.3 mg/kg). The results demonstrate that acute hyperinsulinemia, no matter how induced, does not yield any sensitization to the hypoglycemic effect of insulin.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban insulin insulin sensitivity hyperinsulinemia
Megjelenés:	Metabolism: Clinical and Experimental. - 58 : 3 (2009), p. 328-332. -
További szerzők:	Döbrönte Róbert Németh József (Pécs) Pankucsi Csaba (farmakológus) Sári Réka (farmakológus) Varga Angelika (1977-) (biológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
Pályázati támogatás:	HO7-BEL 74162 Egyéb K75965 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM028449
Első szerző:	Szilvássy Zoltán (belgyógyász, farmakológus, klinikai farmakológus)
Cím:	Insulin resistance occurs in parallel with sensory neuropathy in streptozotocin-induced diabetes in rats : differential response to early vs late insulin supplementation / Szilvássy Z., Németh J., Kovács P., Paragh G., Sári R., Vígh L., Peitl B.
Dátum:	2012
Megjegyzések:	We investigated whether progressive sensory neuropathy was accompanied by changes in whole-body insulin sensitivity (WBIS) in rats made diabetic by streptozotocin (STZ). The effects of early and late insulin supplementation were also studied. The STZ-treated rats failed to gain weight and exhibited stable hyperglycemia and low plasma insulin levels with a decrease in nerve conduction velocity (NCV) measured in A and C fibers of the saphenous nerve. A decreased sensory neuropeptide (SNP) release such as that of substance P, somatostatin, and calcitonin gene-related peptide determined from organ fluid of tracheal preparations subjected to electrical field stimulation also occurred in diabetic animals. These features were accompanied by a decrease in WBIS measured by hyperinsulinemic-euglycemic glucose clamping and a decrease in insulin-stimulated glucose uptake in cardiac and gastrocnemius muscle. When insulin supplementation with slow-release implants (2 IU/d) was started 4 weeks after STZ injection, blood glucose level normalized. Both insulin sensitivity and sensory nerve function reflected in either NCV or SNP release completely recovered by the 12th post-STZ week. When the insulin implants were applied from the eighth post-STZ week, both WBIS and glucose uptake remained significantly decreased, with a seriously impaired NCV and SNP release with strong hyperglycemia. Late insulin supplementation, however, even by using double implantation from the 10th post-STZ week, was unable to restore blood glucose, WBIS, NCV, and SNP release by the 12th week. Insulin resistance occurs in parallel with sensory neuropathy in STZ-diabetic rats. Both can be improved by early but not late insulin supplementation.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Metabolism. - 61 : 6 (2012), p. 776-786. -
További szerzők:	Németh József (1954-) (vegyész, analitikus) Kovács Péter (1947-) (belgyógyász, kardiológus, klinikai farmakológus) Paragh György (1953-) (belgyógyász) Sári Réka (farmakológus) Vígh László (orvos Szeged) Peitl Barna (1972-) (orvos, farmakológus)
Pályázati támogatás:	TÁMOP-4.2.2.-08/1-2008-0014 TÁMOP 75965 OTKA NKFP_07-A2-2008-0260 Egyéb GOP-1.1.207/1-2008-0004 Egyéb OM00174/2008 Egyéb GOP-1.1.1-07/1-2008-0032 Egyéb GOP-1.2.1-082009-0023 Egyéb
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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