β-肾上腺素能激动剂对原位脂肪细胞线粒体膜电位的影响。
The effect of beta-adrenergic agonists on the membrane potential of fat-cell mitochondria in situ.
作者信息
Davis R J, Martin B R
出版信息
Biochem J. 1982 Sep 15;206(3):611-8. doi: 10.1042/bj2060611.
Abstract
- The accumulation of [3H]methyltriphenylphosphonium by isolated fat-cells was used to estimate the membrane potential of mitochondria in situ. 2. Adrenaline caused a large decrease in the accumulation of [3H]methyltriphenylphosphonium. Mitochondria in fat-cells incubated in the presence of adrenaline had a very low calculated membrane potential. This effect was also given by isoprenaline (a beta-adrenergic agonist) and was blocked by propranolol (a beta-adrenergic antagonist). 3. The effect of isoprenaline could be partially antagonized by the use of media with high albumin concentrations. Addition of sodium oleate to saturate the fatty acid-binding sites on the albumin reversed this antagonism. 4. It is proposed that the decrease in the calculated mitochondrial membrane potential is due to the uncoupling effect of the non-esterified fatty acids released by the stimulation of lipolysis observed in the presence of beta-adrenergic agonists.
摘要
- 利用分离的脂肪细胞对[³H]甲基三苯基鏻的摄取来估计原位线粒体的膜电位。2. 肾上腺素导致[³H]甲基三苯基鏻的摄取大幅减少。在肾上腺素存在下孵育的脂肪细胞中的线粒体计算出的膜电位非常低。异丙肾上腺素（一种β-肾上腺素能激动剂）也有此作用，且被普萘洛尔（一种β-肾上腺素能拮抗剂）阻断。3. 高白蛋白浓度的培养基可部分拮抗异丙肾上腺素的作用。添加油酸钠使白蛋白上的脂肪酸结合位点饱和可逆转这种拮抗作用。4. 有人提出，计算出的线粒体膜电位降低是由于在β-肾上腺素能激动剂存在下观察到的脂解刺激释放的非酯化脂肪酸的解偶联作用。
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