Beta 3-adrenoceptors in dog adipose tissue: studies on their involvement in the lipomobilizing effect of catecholamines.
Beta 3-adrenoceptors in dog adipose tissue: studies on their involvement in the lipomobilizing effect of catecholamines.
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狗脂肪组织中的β3-肾上腺素受体：关于它们参与儿茶酚胺的脂肪动员作用的研究。
DOI：
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发表时间：
1993
影响因子：
3.5
通讯作者：
M. Berlan
中科院分区：
文献类型：
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作者：
J. Galitzky;M. Reverte;C. Carpéné;M. Lafontan;M. Berlan
研究了犬脂肪组织中β_3肾上腺素能受体的存在及其对脂肪分解的调控作用。选择性β 3-肾上腺素能激动剂（BRL 37344、SR 58611 A和CGP 12177）和儿茶酚胺（异丙肾上腺素和去甲肾上腺素）激活分离脂肪细胞中的脂解（效力顺序：异丙肾上腺素> BRL 37344 >去甲肾上腺素> CGP 12177 > SR 58611 A）。非选择性β-AR拮抗剂可拮抗0.05 μ M BRL 37344的脂解作用，但选择性β 1-（CGP 20712 A）和β 2-（ICI 118551）拮抗剂无效。向清醒犬输注β 3-肾上腺素能激动剂可增加血浆非酯化脂肪酸水平，其效力顺序与脂解中定义的效力顺序相同。通过α 2-拮抗剂（0.01 mg/kg RX 821002 i. v.）给药诱导的脂质动员作用布萘洛尔（0.5 mg/kg）或CGP 20712 A和ICI 118551（各0.25 mg/kg）联合用药可抑制。0.05 mg/kg RX 821002的作用仅被相同的β-拮抗剂联合用药部分抑制，而布萘洛尔完全消除了该作用。在0.5 mg/kg剂量下，RX 821002的作用未被β-拮抗剂改变。由于输注儿茶酚胺（0.1、0.5或5 μ g/kg/min去甲肾上腺素或5 μ g/kg/min肾上腺素）引起的脂肪动员始终受到布萘洛尔或选择性β-受体拮抗剂组合的抑制。因此，狗脂肪细胞表达功能性β 3-AR。它们的刺激诱导脂质动员。外源性给药的儿茶酚胺的脂动化仅是由于β 1-或β 2-AR的募集。然而，只有在实现高水平的交感神经系统活性时，交感神经系统激活后释放的内源性儿茶酚胺才能刺激脂肪细胞中的β 3-AR。
The existence of beta 3-adrenoceptors in adipose tissue and their involvement in the control of lipolysis was investigated in dog. Selective beta 3-adrenergic agonists (BRL 37344, SR 58611A and CGP 12177) and catecholamines (isoproterenol and norepinephrine) activated lipolysis in isolated adipocytes (order of potency: isoproterenol > BRL 37344 > norepinephrine > CGP 12177 > SR 58611A). The lipolytic effect of 0.05 microM BRL 37344 was antagonized by the nonselective beta-AR antagonists, but the selective beta 1-(CGP 20712A) and beta 2-(ICI 118551) antagonists were ineffective. Infused to conscious dogs, beta 3-adrenergic agonists increased plasma nonesterified fatty acids levels with an order of potency equivalent to that defined in lipolysis. The lipomobilizing effect induced by the administration of an alpha 2-antagonist (0.01 mg/kg RX 821002 i.v.) was suppressed by bupranolol (0.5 mg/kg) or the combination of CGP 20712A and ICI 118551 (0.25 mg/kg each). The effect of 0.05 mg/kg RX 821002 was only partially suppressed by the same beta-antagonist combination, whereas bupranolol totally abolished it. At 0.5 mg/kg, the RX 821002 effect was not modified by beta-antagonists. The lipomobilization due to infusion of catecholamines (0.1, 0.5 or 5 micrograms/kg/min norepinephrine or 5 micrograms/kg/min epinephrine) was always suppressed by bupranolol or the combination of selective beta-antagonists. Thus dog adipocytes express functional beta 3-ARs. Their stimulation induces lipid mobilization. The lipomobilization of exogenously administered catecholamines is due only to the recruitment of beta 1- or beta 2-ARs. However, endogenous catecholamines released after sympathetic nervous system activation could stimulate beta 3-ARs in adipocytes only if a high level of sympathetic nervous system activity is realized.