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| DC Field | Value | Language |
|---|---|---|
| dc.creator | Solà, Anna M. | - |
| dc.creator | Roselló-Catafau, Joan | - |
| dc.creator | Gelpí, Emili | - |
| dc.creator | Hotter, Georgina | - |
| dc.date | 2008-02-18T18:19:44Z | - |
| dc.date | 2008-02-18T18:19:44Z | - |
| dc.date | 2001-02 | - |
| dc.date.accessioned | 2017-01-31T01:00:11Z | - |
| dc.date.available | 2017-01-31T01:00:11Z | - |
| dc.identifier | Gut. 2001 February; 48(2): 168–175. | - |
| dc.identifier | http://dx.doi.org/10.1136/gut.48.2.168 | - |
| dc.identifier | 0017-5749 | - |
| dc.identifier | http://hdl.handle.net/10261/2972 | - |
| dc.identifier | 10.1136/gut.48.2.168 | - |
| dc.identifier.uri | http://dspace.mediu.edu.my:8181/xmlui/handle/10261/2972 | - |
| dc.description | [BACKGROUND AND AIMS] Inhibition of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) by nitric oxide (NO) in intestinal preconditioning could modify the rate of formation of glycolytic intermediates. Fructose-1,6-biphosphate (F16BP) is a glycolytic intermediate that protects tissue from ischaemia/reperfusion injury. We evaluated if F16BP may be endogenously accumulated as a consequence of GAPDH inhibition by NO during intestinal preconditioning in rats. | - |
| dc.description | [METHODS] We assessed: (1) effect of preconditioning on F16BP content; (2) effect of NO on GAPDH activity before and during sustained ischaemia; and (3) protective effect of F16BP in control, ischaemic, and preconditioned animals with or without administration of N-nitro-L-arginine methyl ester (L-NAME), NO donor, or F16BP. | - |
| dc.description | [RESULTS] Preconditioned rats showed a significant transient decrease in GAPDH activity and also maintained basal F16BP levels longer than ischaemic rats. L-NAME administration to preconditioned rats reversed these effects. F16BP administration to ischaemic rats decreased protein release in the perfusate. Administration of F16BP to L-NAME treated rats attenuated the harmful effect of L-NAME. | - |
| dc.description | [CONCLUSIONS] Our study indicates that F16BP may be endogenously accumulated in preconditioned rats as a consequence of inhibition of GAPDH by NO, and this may contribute to the protection observed in intestinal preconditioning. | - |
| dc.description | This work was supported by grant FIS 98/002901. A Sola was supported by a grant from Institut d’Investigacions Biomèdiques August Pi I Sunyer. | - |
| dc.description | Peer reviewed | - |
| dc.format | 75510 bytes | - |
| dc.format | 74796 bytes | - |
| dc.format | 48177 bytes | - |
| dc.format | 46852 bytes | - |
| dc.format | 20011 bytes | - |
| dc.format | 154667 bytes | - |
| dc.format | 55006 bytes | - |
| dc.format | image/jpeg | - |
| dc.format | image/jpeg | - |
| dc.format | image/jpeg | - |
| dc.format | image/jpeg | - |
| dc.format | image/jpeg | - |
| dc.format | application/pdf | - |
| dc.format | image/jpeg | - |
| dc.language | eng | - |
| dc.publisher | BMJ Publishing Group | - |
| dc.relation | http://dx.doi.org/10.1136/gut.48.2.168 | - |
| dc.rights | openAccess | - |
| dc.subject | Fructose-1,6-biphosphate | - |
| dc.subject | Glyceraldehyde- 3-phosphate dehydrogenase | - |
| dc.subject | Intestinal preconditioning | - |
| dc.subject | Ischaemia/reperfusion injury | - |
| dc.subject | Nitric Oxide | - |
| dc.title | Fructose-1,6-biphosphate in rat intestinal preconditioning: involvement of nitric oxide | - |
| dc.type | Artículo | - |
| Appears in Collections: | Digital Csic | |
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