Carpene C, Berlan M, Lafontan M
J Lipid Res. 1983 Jun;24(6):766-74.
The response of the hamster adipocyte to various lipolytic (beta-adrenergic) and antilipolytic (alpha(2)-adrenergic and adenosine-dependent) stimuli was studied during the development and after cold-induced regression of fat stores. Alpha(2)-adrenergic binding ([(3)H]clonidine binding sites) was also investigated. Adipocytes came from young animals (4-5 weeks), adults (20-25 weeks), and adults submitted to a 6-week cold exposure (6 degrees C) that promoted a large decrease in fat stores and in fat cell size. The lipolytic response induced by isoproterenol (beta-agonist) was equivalent in the different groups. Adenosine and alpha(2)-adrenergic antilipolytic effects were estimated through the inhibition of theophylline-induced lipolysis by phenylisopropyladenosine and clonidine, respectively. The adenosine effect was unchanged in all the groups. In contrast, the alpha(2)-adrenergic effect, which was not present in young hamsters, increased simultaneously with fat cell size, was fully effective in adult hamsters, and had completely disappeared in small adipocytes from cold-exposed hamsters. In fat cell ghosts, alpha(2)-adrenoceptors ([(3)H]clonidine binding sites), followed similar modifications: they increased with fat cell enlargement and disappeared after cell size reduction following cold exposure. These results suggest that: 1) the increased alpha(2)-adrenergic antilipolytic response which is concomitant with fat cell enlargement could partly explain the growth-related decrease in the previously reported lipolytic effect of epinephrine; 2) the alpha(2)-receptivity of the adipocyte seems to be strictly fat cell size-dependent while the beta-adrenergic and adenosine responses are unaffected; and 3) the regulation in the adipocytes of the adenosine, alpha(2)- and beta-receptors seems to be unrelated.-Carpene, C., M. Berlan, and M. Lafontan. Influence of development and reduction of fat stores on the antilipolytic alpha(2)-adrenoceptor in hamster adipocytes: comparison with adenosine and beta-adrenergic lipolytic responses.
在仓鼠脂肪储备的发育过程中以及冷诱导脂肪储备消退后，研究了仓鼠脂肪细胞对各种脂解（β-肾上腺素能）和抗脂解（α₂-肾上腺素能和腺苷依赖性）刺激的反应。还研究了α₂-肾上腺素能结合（[³H]可乐定结合位点）。脂肪细胞来自幼龄动物（4 - 5周）、成年动物（20 - 25周）以及经历6周冷暴露（6℃）的成年动物，冷暴露促使脂肪储备和脂肪细胞大小大幅减少。异丙肾上腺素（β-激动剂）诱导的脂解反应在不同组中相当。分别通过苯异丙基腺苷和可乐定对茶碱诱导的脂解的抑制作用来评估腺苷和α₂-肾上腺素能抗脂解作用。腺苷的作用在所有组中均未改变。相反，幼龄仓鼠不存在的α₂-肾上腺素能作用，随脂肪细胞大小同时增加，在成年仓鼠中完全有效，而在冷暴露仓鼠的小脂肪细胞中则完全消失。在脂肪细胞空壳中，α₂-肾上腺素能受体（[³H]可乐定结合位点）呈现类似变化：它们随脂肪细胞增大而增加，在冷暴露后细胞大小减小后消失。这些结果表明：1）与脂肪细胞增大同时出现的增强的α₂-肾上腺素能抗脂解反应可能部分解释了先前报道的肾上腺素脂解作用与生长相关的降低；2）脂肪细胞的α₂-受体敏感性似乎严格依赖于脂肪细胞大小，而β-肾上腺素能和腺苷反应不受影响；3）脂肪细胞中腺苷、α₂-和β-受体的调节似乎无关。——卡尔佩内，C.，M. 贝尔兰，和 M. 拉丰坦。脂肪储备的发育和减少对仓鼠脂肪细胞抗脂解α₂-肾上腺素能受体的影响：与腺苷和β-肾上腺素能脂解反应的比较
