Schimmel R J, McCarthy L, Dzierzanowski D
Am J Physiol. 1985 Nov;249(5 Pt 1):C456-63. doi: 10.1152/ajpcell.1985.249.5.C456.
This communication reports the effects of the exotoxin of Bordetella pertussis (pertussis toxin) on hamster brown fat cells. Pertussis toxin significantly increased the lipolytic and respiratory responses to isoproterenol but did not increase the basal rates of either of these processes. In contrast, the stimulation of respiration by the alpha-adrenergic agent phenylephrine was not altered by pertussis toxin. The inhibitory effects of adenosine on stimulated lipolysis, respiration, and adenylate cyclase activity were completely abolished by pertussis toxin, as was the ability of methylxanthines or adenosine deaminase to potentiate isoproterenol stimulation of respiration or lipolysis. These effects of pertussis toxin were associated with an ADP ribosylation of a single membrane protein having a molecular weight of approximately 41. These data demonstrate that pertussis toxin can prevent the inhibitory action of adenosine on brown fat cells and suggest that the effects of the nucleoside on these cells results from inhibition of adenylate cyclase. We further suggest that the enhanced responses to isoproterenol in pertussis-treated adipocytes results from a blockade of the action of endogenous adenosine. In addition to blocking adenosine action, pertussis toxin also abolished the antilipolytic effect of insulin. However, because the antilipolytic effect of insulin was prevented by adenosine deaminase and 3-isobutyl-1-methylxanthine and restored by 2-chloroadenosine, we conclude that insulin action on these cells is dependent on adenosine. Thus pertussis toxin blockade of insulin action appears to be secondary to blockade of adenosine action.
本通讯报道了百日咳博德特氏菌外毒素(百日咳毒素)对仓鼠棕色脂肪细胞的作用。百日咳毒素显著增强了对异丙肾上腺素的脂解和呼吸反应,但并未提高这些过程的基础速率。相比之下,α-肾上腺素能剂去氧肾上腺素对呼吸的刺激作用不受百日咳毒素影响。百日咳毒素完全消除了腺苷对刺激的脂解、呼吸和腺苷酸环化酶活性的抑制作用,甲基黄嘌呤或腺苷脱氨酶增强异丙肾上腺素对呼吸或脂解刺激的能力也被消除。百日咳毒素的这些作用与一种分子量约为41的单一膜蛋白的ADP核糖基化有关。这些数据表明,百日咳毒素可阻止腺苷对棕色脂肪细胞的抑制作用,并提示核苷对这些细胞的作用是通过抑制腺苷酸环化酶实现的。我们进一步认为,经百日咳毒素处理的脂肪细胞对异丙肾上腺素反应增强是由于内源性腺苷作用受阻。除了阻断腺苷作用外,百日咳毒素还消除了胰岛素的抗脂解作用。然而,由于胰岛素的抗脂解作用可被腺苷脱氨酶和3-异丁基-1-甲基黄嘌呤阻止,并可被2-氯腺苷恢复,我们得出结论,胰岛素对这些细胞的作用依赖于腺苷。因此,百日咳毒素对胰岛素作用的阻断似乎是腺苷作用阻断的继发效应。