BETA-ADRENERGIC STIMULATION OF BROWN ADIPOCYTE PROLIFERATION

BETA-ADRENERGIC STIMULATION OF BROWN ADIPOCYTE PROLIFERATION
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DOI:
10.1152/ajpcell.1988.254.1.c175
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发表时间:
1988-01-01
影响因子:
--
通讯作者:
BUKOWIECKI, LJ
BUKOWIECKI, LJ
中科院分区:
其他
文献类型:
--
作者:
GELOEN, A;COLLET, AJ;BUKOWIECKI, LJ

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采用氚化胸腺嘧啶定量光子放射自显影技术研究了褐色脂肪组织(BAT)生长的机制。为了确定介导棕色脂肪细胞增殖和分化的肾上腺素能途径的性质,低温暴露(4天,4℃)的影响。C) 25℃处理大鼠对BAT生长的影响。C与去甲肾上腺素(一种混合激动剂)、异丙肾上腺素(a . β。-激动剂)和苯基肾上腺碱(一种-激动剂)。通过渗透微型泵(0.375 .mu)连续给药。Mol /h (4 d)皮下植入。冷暴露显著增强棕色脂肪细胞前体细胞(间质细胞和前脂肪细胞)和内皮细胞的有丝分裂活性,形成大量毛细血管。去甲肾上腺素不仅对有丝分裂活性有影响,而且对各种细胞类型之间的标记分布也有影响。异丙肾上腺素完全再现了去甲肾上腺素对标记指数和细胞类型标记频率的影响。相反,苯肾上腺素不刺激细胞分裂。这些结果表明,去甲肾上腺素在温暖暴露的大鼠中触发棕色脂肪细胞和内皮细胞的协调增殖,这与冷暴露后观察到的情况相似。他们还认为,寒冷暴露会增加交感神经释放的去甲肾上腺素,从而刺激BAT的生长,这种神经激素会通过β激活BAT前体细胞中的有丝分裂。肾上腺素的途径。
The mechanisms of brown adipose tissue (BAT) growth were studied by quantitative photonic radioautography using tritiated thymidine to follow mitotic activity. To identify the nature of the adrenergic pathways mediating brown adipocyte proliferation and differentiation, the effects of cold exposure (4 days at 4.degree. C) on BAT growth were compared with those induced by treating rats at 25.degree. C with norepinephrine (a mixed agonist), isoproterenol (a .beta.-agonist), and phenylephinine (an .alpha.-agonist). The drugs were continuously administered via osmotic minipumps (0.375 .mu.mol/h during 4 days) implanted subcutaneously. Cold exposure markedly enhanced the mitotic activity in brown adipocyte precursor cells (interstitial cells and preadipocytes) and endothelial cells forming the numerous capillaries. Norepinephrine mimicked the effects of cold exposure, not only on the mitotic activity, but also on the distribution of the labeling among the various cellular types. Isoproterenol entirely reproduced the effects of norepinephrine both on the labeling index and on the cellular type labeling frequency. In contrast, phenylephrine did not stimulate cell division. These results demonstrate that norepinephrine triggers a coordinated proliferation of brown adipocytes and endothelial cells in warm-exposed rats that is similar to that observed after cold exposure. They also suggest that cold exposure stimulates BAT growth by increasing the release of norepinephrine from sympathetic nerves and that the neurohormone activates mitoses in BAT precursor cells via .beta.-adrenergic pathways.