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胍乙啶诱导的去交感神经雏鸭的线粒体氧化能量代谢

Mitochondrial oxidative energy metabolism in guanethidine-induced sympathectomized ducklings.

作者信息

Filali-Zegzouti Younes, Rouanet Jean-Louis, Fechtali Toufiq, Roussel Damien

机构信息

Université Moulay Ismail de Meknès, EPPE-FST, Errachidia, Morocco.

出版信息

Gen Physiol Biophys. 2014;33(1):91-7. doi: 10.4149/gpb_2013072. Epub 2013 Dec 13.

DOI:10.4149/gpb_2013072
PMID:24334534
Abstract

Here we investigate the possible involvement of the sympathetic nervous system in the respiratory properties of intermyofibrillar and subsarcolemmal mitochondrial populations from heart and gastrocnemius muscles. Mitochondrial oxidative phosphorylation was assessed polarographically by using succinate (plus rotenone), and ascorbate plus N,N,N',N'-tetramethyl-p-phenyl-enediamine (plus antimycin) as respiratory substrates. We report that chronic chemical sympathectomy with guanethidine (150 mg/kg, daily for 3 weeks) induced a marked decrease in whole body metabolic and heart rates, in plasma metabolites (fatty acids and glucose) and norepinephrine levels. Guanethidine treatment decreased mainly the oxidative phosphorylation capacity of subsarcolemmal mitochondria in heart, irrespective of the substrate used. In contrast, both mitochondrial populations were affected by the treatment in skeletal muscle. This suggests that sympathetic nervous system activity can alter the energetic status of muscle cells, and to some extent play a thermogenic role in birds.

摘要

在此,我们研究交感神经系统可能参与心脏和腓肠肌肌原纤维间及肌膜下线粒体群体呼吸特性的情况。通过极谱法,使用琥珀酸(加鱼藤酮)以及抗坏血酸加N,N,N',N'-四甲基对苯二胺(加抗霉素)作为呼吸底物来评估线粒体氧化磷酸化。我们报告称,用胍乙啶进行慢性化学交感神经切除术(150毫克/千克,每日一次,持续3周)导致全身代谢率和心率显著降低,血浆代谢物(脂肪酸和葡萄糖)以及去甲肾上腺素水平也降低。胍乙啶处理主要降低了心脏肌膜下线粒体的氧化磷酸化能力,无论使用何种底物。相比之下,骨骼肌中的两种线粒体群体均受该处理影响。这表明交感神经系统活动可改变肌肉细胞的能量状态,并在一定程度上在鸟类中发挥产热作用。

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