Nitric oxide production from rat adipocytes is modulated by beta3-adrenergic receptor agonists and is involved in a cyclic AMP-dependent lipolysis in adipocytes
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
16413212
DOI
10.1016/j.niox.2005.06.006
PII: S1089-8603(05)00099-6
Knihovny.cz E-zdroje
- MeSH
- 1-methyl-3-isobutylxanthin farmakologie MeSH
- adenin analogy a deriváty farmakologie MeSH
- agonisté adrenergních receptorů farmakologie MeSH
- agonisté beta-3-adrenergních receptorů * MeSH
- AMP cyklický metabolismus MeSH
- donory oxidu dusnatého farmakologie MeSH
- guanosinmonofosfát cyklický analogy a deriváty farmakologie MeSH
- inhibitory adenylylcyklasy MeSH
- kolforsin farmakologie MeSH
- krysa rodu Rattus MeSH
- lipolýza * účinky léků MeSH
- oxid dusnatý biosyntéza MeSH
- potkani Wistar MeSH
- S-nitroso-N-acetylpenicilamin farmakologie MeSH
- tukové buňky účinky léků metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 1-methyl-3-isobutylxanthin MeSH
- 8-bromocyclic GMP MeSH Prohlížeč
- 9-(tetrahydro-2-furyl)-adenine MeSH Prohlížeč
- adenin MeSH
- agonisté adrenergních receptorů MeSH
- agonisté beta-3-adrenergních receptorů * MeSH
- AMP cyklický MeSH
- donory oxidu dusnatého MeSH
- guanosinmonofosfát cyklický MeSH
- inhibitory adenylylcyklasy MeSH
- kolforsin MeSH
- oxid dusnatý MeSH
- S-nitroso-N-acetylpenicilamin MeSH
It is established that the modulation of beta(3)-adrenoceptor function could be associated with impairment of lipolysis in white fat and be responsible for disturbed lipid metabolism. Though two isoforms of nitric oxide synthase (NOS) were reported in adipocytes, the role of nitric oxide (NO) in adipose tissue is still ambiguous. The present work was directed to study the interplay between NO production and beta-adrenoceptor/cyclic AMP (cAMP) pathway on lipid mobilization (glycerol and nonesterified fatty acids, NEFA) in cultures of rat adipocytes isolated from epididymal white adipose tissue. beta-Nonselective (isoprenaline) and beta(3)-selective (BRL-37344) agonists and the postadrenoceptor agents such as dibutyryl-cAMP, forskolin, and 3-isobutyl-1-methylxanthine significantly increased nitrite, glycerol, and NEFA levels with BRL-37344 being the most potent. Conversely, addition of beta-nonselective (propranolol) or beta(3)-selective (bupranolol) antagonist or the adenylyl cyclase inhibitor (SQ 22,536) significantly reduced beta-agonist-induced NO production and lipolysis. For beta-adrenoceptor agonists, antagonists, and their pairs, there was a positive correlation between medium nitrite and glycerol or NEFA with r(2) being 0.90 and 0.84, respectively. The possible relationship between NO and lipolysis was revealed after adipocyte treatment with nonspecific (N(omega)-nitro-l-arginine methyl ester, l-NAME) and specific (aminoguanidine) NOS inhibitors. Both l-NAME and aminoguanidine significantly inhibited the lipolytic effect of BRL-37344. Moreover, NO-donor (S-nitroso-N-acetylpenicillamine) at higher concentration increased basal glycerol and NEFA levels. 8-bromo-cyclic GMP had no effect on adipocyte lipolysis. These data suggest that beta-adrenergic lipolysis, specifically beta(3)-adrenoceptor effect, which is realized via the adenylyl cyclase/cAMP/protein kinase A signaling cascade, involves NO production downstream of beta(3)-adrenoceptor/cAMP pathway.
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