Bégin-Heick N, Heick H M
Can J Biochem. 1982 Sep;60(9):910-6. doi: 10.1139/o82-117.
The activation of brown adipose tissue adenylate cyclase by catecholamines was studied in genetically obese (ob/ob) and lean mice. In obese mice, the maximum activation of the enzyme by several beta-adrenergic agonists was only two-thirds that in lean mice and, as an activator, noradrenaline was only one-eighth as potent. The adenylate cyclase was also less responsive to guanine nucleotides. In these respects, the defect in catecholamine-stimulated adenylate cyclase was similar in both white and brown adipose tissue of the obese mouse. The enzyme in brown adipose tissue differed from that in white adipose tissue in its sensitivity to other beta-adrenergic agonists and in its requirement for Mg2+. It is suggested that this abnormal catecholamine-activated adenylate cyclase in brown adipose tissue may be relate to the thermoregulatory defect of the obese mouse and hence may contribute to the obesity syndrome.
在遗传性肥胖(ob/ob)小鼠和瘦小鼠中,研究了儿茶酚胺对棕色脂肪组织腺苷酸环化酶的激活作用。在肥胖小鼠中,几种β-肾上腺素能激动剂对该酶的最大激活程度仅为瘦小鼠的三分之二,而作为激活剂,去甲肾上腺素的效力仅为瘦小鼠的八分之一。腺苷酸环化酶对鸟嘌呤核苷酸的反应也较弱。在这些方面,肥胖小鼠的白色和棕色脂肪组织中,儿茶酚胺刺激的腺苷酸环化酶缺陷相似。棕色脂肪组织中的酶在对其他β-肾上腺素能激动剂的敏感性及其对Mg2+的需求方面与白色脂肪组织中的酶不同。有人认为,棕色脂肪组织中这种异常的儿茶酚胺激活的腺苷酸环化酶可能与肥胖小鼠的体温调节缺陷有关,因此可能导致肥胖综合征。