Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Pharmacogenetic evidence that cd36 is a key determinant of the metabolic effects of pioglitazone

N Qi, L Kazdova, V Zidek, V Landa, V Kren, HA Pershadsingh, ES Lezin, NA Abumrad, M Pravenec, TW Kurtz

. 2002 ; 277 (50) : 48501-48507.

Jazyk angličtina Země Spojené státy americké

Typ dokumentu práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc13011063

Grantová podpora
NB6367 MZ0 CEP - Centrální evidence projektů

Pioglitazone, like other thiazolidinediones, is an insulin-sensitizing agent that activates the peroxisome proliferator-activated receptor gamma and influences the expression of multiple genes involved in carbohydrate and lipid metabolism. However, it is unknown which of these many target genes play primary roles in determining the antidiabetic and hypolipidemic effects of thiazolidinediones. To specifically investigate the role of the Cd36 fatty acid transporter gene in the insulin-sensitizing actions of thiazolidinediones, we studied the metabolic effects of pioglitazone in spontaneously hypertensive rats (SHR) that harbor a deletion mutation in Cd36 in comparison to congenic and transgenic strains of SHR that express wild-type Cd36. In congenic and transgenic SHR with wild-type Cd36, administration of pioglitazone was associated with significantly lower circulating levels of fatty acids, triglycerides, and insulin as well as lower hepatic triglyceride levels and epididymal fat pad weights than in SHR harboring mutant Cd36. Additionally, insulin-stimulated glucose oxidation in isolated soleus muscle was significantly augmented in pioglitazone-fed rats with wild-type Cd36 versus those with mutant Cd36. The Cd36 genotype had no effect on pioglitazone-induced changes in blood pressure. These findings provide direct pharmacogenetic evidence that in the SHR model, Cd36 is a key determinant of the insulin-sensitizing actions of a thiazolidinedione ligand of peroxisome proliferator-activated receptor gamma.

Bibliografie atd.

Literatura

000      
00000naa a2200000 a 4500
001      
bmc13011063
003      
CZ-PrNML
005      
20130327113059.0
007      
ta
008      
130325s2002 xxu ad f 000 0eng||
009      
AR
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxu
100    1_
$a Qi, N $u Department of Laboratory Medicine, University of California, San Francisco, USA
245    10
$a Pharmacogenetic evidence that cd36 is a key determinant of the metabolic effects of pioglitazone / $c N Qi, L Kazdova, V Zidek, V Landa, V Kren, HA Pershadsingh, ES Lezin, NA Abumrad, M Pravenec, TW Kurtz
504    __
$a Literatura
520    9_
$a Pioglitazone, like other thiazolidinediones, is an insulin-sensitizing agent that activates the peroxisome proliferator-activated receptor gamma and influences the expression of multiple genes involved in carbohydrate and lipid metabolism. However, it is unknown which of these many target genes play primary roles in determining the antidiabetic and hypolipidemic effects of thiazolidinediones. To specifically investigate the role of the Cd36 fatty acid transporter gene in the insulin-sensitizing actions of thiazolidinediones, we studied the metabolic effects of pioglitazone in spontaneously hypertensive rats (SHR) that harbor a deletion mutation in Cd36 in comparison to congenic and transgenic strains of SHR that express wild-type Cd36. In congenic and transgenic SHR with wild-type Cd36, administration of pioglitazone was associated with significantly lower circulating levels of fatty acids, triglycerides, and insulin as well as lower hepatic triglyceride levels and epididymal fat pad weights than in SHR harboring mutant Cd36. Additionally, insulin-stimulated glucose oxidation in isolated soleus muscle was significantly augmented in pioglitazone-fed rats with wild-type Cd36 versus those with mutant Cd36. The Cd36 genotype had no effect on pioglitazone-induced changes in blood pressure. These findings provide direct pharmacogenetic evidence that in the SHR model, Cd36 is a key determinant of the insulin-sensitizing actions of a thiazolidinedione ligand of peroxisome proliferator-activated receptor gamma.
536    __
$c Grant Number: P01 HL35018 (United States NHLBI NIH HHS)
536    __
$c Grant Number: R01 HL56028 (United States NHLBI NIH HHS)
536    __
$c Grant Number: R01 HL63709 (United States NHLBI NIH HHS)
536    __
$c Grant Number: R03 TW01236 (United States FIC NIH HHS)
590    __
$a bohemika - dle Pubmed
650    02
$a zvířata $7 D000818
650    12
$a antigeny CD36 $7 D018955
650    02
$a sekvence nukleotidů $7 D001483
650    02
$a northern blotting $7 D015152
650    02
$a DNA primery $7 D017931
650    02
$a glukosa $x metabolismus $7 D005947
650    02
$a hypoglykemika $x farmakologie $7 D007004
650    12
$a inzulin $x farmakologie $7 D007328
650    02
$a membránové glykoproteiny $x genetika $7 D008562
650    02
$a kosterní svaly $x metabolismus $x účinky léků $7 D018482
650    02
$a přenašeče organických aniontů $x genetika $7 D027361
650    02
$a farmakogenetika $7 D010597
650    02
$a krysa rodu Rattus $7 D051381
650    02
$a potkani inbrední SHR $7 D011918
650    02
$a sekvenční delece $7 D017384
650    02
$a thiazoly $x farmakologie $7 D013844
650    12
$a thiazolidindiony $7 D045162
650    12
$a inzulinová rezistence $7 D007333
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Kazdová, Ludmila, $d 1938- $7 xx0053119 $u Institute of Clinical and Experimantal Medicine, Prague, Czech Republic
700    1_
$a Zídek, Václav, $d 1951- $7 xx0088482 $u Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic
700    1_
$a Landa, Vladimír $7 xx0062600 $u Institutes of Molecular Genetics and Physiology, Czech Academy of Sciences, Prague, Czech Republic
700    1_
$a Křen, Vladimír $7 xx0070803 $u Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic
700    1_
$a Pershadsingh, HA $u Department of family Medicine, University of California, San Francisco, California, USA
700    1_
$a Lezin, ES $u Department of Veterans Affairs Medical Center, San Francisco, California, USA
700    1_
$a Abumrad, NA $u Department od Physiology and Biophysics, State University of New York, Stony Brook, New York, USA $7 gn_A_00000922
700    1_
$a Pravenec, Michal, $d 1953- $7 nlk20030127611 $u Institute of Phisiology, Czech Academy of Sciences, Prague, Czech Republic
700    1_
$a Kurtz, TW $u Department of Laboratory Medicine, University of California, San Francisco, USA
773    0_
$t Journal of Biological Chemistry $x 0021-9258 $g Roč. 277, č. 50 (2002), s. 48501-48507 $p J Biol Chem $w MED00002546
773    0_
$p J Biol Chem $g 277(50):48501-7, 2002 Dec 13 $x 0021-9258
910    __
$a ABA008 $b B 418 $y 4 $z 0
990    __
$a 20130325145300 $b ABA008
991    __
$a 20130327113321 $b ABA008
999    __
$a ok $b bmc $g 974071 $s 809332
BAS    __
$a 3
BMC    __
$x MED00002546 $i 0021-9258 $a 2002 $b 277 $c 50 $d 48501-48507 $m The Journal of biological chemistry
GRA    __
$a NB6367 $p MZ0
LZP    __
$c NLK110 $d 20130327 $a 2013-3/rp

Najít záznam

Citační ukazatele

Možnosti archivace