The role of the sympathetic nervous system in the regulation of leptin synthesis in C57BL/6 mice
The role of the sympathetic nervous system in the regulation of leptin synthesis in C57BL/6 mice
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DOI：
10.1016/s0014-5793(99)00049-6
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发表时间：
1999-02-12
期刊：
影响因子：
3.5
通讯作者：
Summers, RJ
中科院分区：
文献类型：
--
作者：
Evans, BA;Agar, L;Summers, RJ
本研究的目的是确定瘦素合成是否受交感神经系统调节，如果是，β-肾上腺素能受体是否介导这种作用。我们发现，利血平的交感神经阻滞会增加棕色脂肪组织中的瘦素 mRNA 水平，但不会增加白色脂肪组织中的瘦素 mRNA 水平，而急性寒冷暴露会使棕色脂肪组织中的瘦素表达降低 10 倍，使白色脂肪组织中的瘦素表达降低 2 倍。普萘洛尔和 SR 59230A 联合使用可以预防寒冷引起的瘦素 mRNA 减少，但单独使用任何一种拮抗剂都无法预防，这表明 β(3)-肾上腺素能受体和经典 β(1)/β(2)-肾上腺素能受体均介导对交感神经刺激的反应。循环瘦素水平反映了白色脂肪组织的合成，但不反映棕色脂肪组织的合成。 (C) 1999 年欧洲生化学会联合会。
The objectives of this study were to determine whether leptin synthesis is regulated by the sympathetic nervous system and if so whether beta-adrenergic receptors mediate this effect. We show that sympathetic blockade by reserpine increases leptin mRNA levels in brown but not white adipose tissue, while acute cold-exposure decreases leptin expression 10-fold in brown adipose tissue and 2-fold in white adipose tissue. The cold-induced reduction in leptin mRNA can be prevented by a combination of propranolol and SR 59230A but not by either antagonist alone, indicating that beta(3)-adrenergic receptors and classical beta(1)/beta(2)-adrenergic receptors both mediate responses to sympathetic stimulation. Circulating leptin levels reflect synthesis in white adipose tissue but not in brown adipose tissue. (C) 1999 Federation of European Biochemical Societies.