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Induction of uncoupling protein-2 mRNA by triiodothyronine in rat liver
Radka Bolehovská, Monika Pospíšilová, David Rychtrmoc, Lenka Hubálková, Zuzana Červinková
Jazyk angličtina Země Česko
Typ dokumentu práce podpořená grantem
- MeSH
- energetický metabolismus MeSH
- exprese genu MeSH
- glycerolfosfátdehydrogenasa MeSH
- jaterní mitochondrie * enzymologie genetika metabolismus MeSH
- játra enzymologie metabolismus účinky léků MeSH
- messenger RNA izolace a purifikace MeSH
- potkani Wistar MeSH
- reaktivní formy kyslíku MeSH
- trijodthyronin * farmakokinetika farmakologie krev terapeutické užití MeSH
- uncoupling protein 2 * účinky léků MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- práce podpořená grantem MeSH
Uncoupling protein-2, discovered in 1997, is the first described homologue of uncoupling protein-1. Uncoupling proteins increase the permeability of inner mitochondrial membrane for protons, decrease the efficiency of energy conversion, inhibit the ATP synthesis and stimulate energy release in form of heat. Uncoupling proteins also increase the substrate oxidation and reduce production of reactive oxygen species in mitochondria. The present study was conducted to assess the effects of acute treatment with triiodothyronine on uncoupling protein-2 mRNA levels in Wistar rats. Intraperitoneal injection of one dose of triiodothyronine (200 μg/kg rat body weight) increased mRNA expression of uncoupling protein-2 in liver tissue almost 2-fold after 12 h. Concentrations of total triiodothyronine and free triiodothyronine in serum were increased 122-fold and 76-fold, respectively. These results suggest that gene coding uncoupling protein-2 is gene inducible in the liver shortly after single administration of T3. Data about the kinetics of T3 mediated induction of UCP-2 mRNA during the first 24 h after treatment were not available in literature so far and therefore constitute our priority findings.
Citace poskytuje Crossref.org
Literatura
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- $a Uncoupling protein-2, discovered in 1997, is the first described homologue of uncoupling protein-1. Uncoupling proteins increase the permeability of inner mitochondrial membrane for protons, decrease the efficiency of energy conversion, inhibit the ATP synthesis and stimulate energy release in form of heat. Uncoupling proteins also increase the substrate oxidation and reduce production of reactive oxygen species in mitochondria. The present study was conducted to assess the effects of acute treatment with triiodothyronine on uncoupling protein-2 mRNA levels in Wistar rats. Intraperitoneal injection of one dose of triiodothyronine (200 μg/kg rat body weight) increased mRNA expression of uncoupling protein-2 in liver tissue almost 2-fold after 12 h. Concentrations of total triiodothyronine and free triiodothyronine in serum were increased 122-fold and 76-fold, respectively. These results suggest that gene coding uncoupling protein-2 is gene inducible in the liver shortly after single administration of T3. Data about the kinetics of T3 mediated induction of UCP-2 mRNA during the first 24 h after treatment were not available in literature so far and therefore constitute our priority findings.
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