Cold exposure suppresses serum adiponectin levels through sympathetic nerve activation in mice
Cold exposure suppresses serum adiponectin levels through sympathetic nerve activation in mice
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DOI：
10.1038/oby.2006.130
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发表时间：
2006-07-01
期刊：
影响因子：
6.9
通讯作者：
Oka, Yoshitomo
中科院分区：
文献类型：
--
作者：
Imai, Junta;Katagiri, Hideki;Oka, Yoshitomo
目的：多项证据表明脂联素在糖脂代谢和动脉粥样硬化中具有重要作用。然而，调节血清脂联素水平和脂联素产生的机制仍未完全明确。我们的目的是确定脂联素的合成是否受到交感神经系统（SNS）的生理调节。
研究方法和步骤：将小鼠暴露于寒冷（4℃）环境中12小时和24小时，同时给予或不给予去甲肾上腺素合成抑制或泛β -肾上腺素能功能抑制，然后测量血清脂联素浓度以及各种白色脂肪组织（WAT）中脂联素和解偶联蛋白（UCP）1的表达水平。
结果：寒冷暴露显著降低了血清脂联素浓度，但未改变皮下或腹腔内脂肪组织的体重或白色脂肪组织大小。血清脂联素的降低与皮下、附睾和肠系膜脂肪组织中脂联素mRNA表达的减少有关。在这些脂肪组织中，UCP1表达显著增强，表明这些组织中的SNS被激活。给予α -甲基-对 -酪氨酸或SR59230A与普萘洛尔的组合可逆转寒冷暴露引起的这些组织中血清脂联素浓度和脂联素mRNA表达的降低。相反，在腹膜后脂肪中，寒冷暴露对脂联素和UCP1表达的影响非常微弱，且未被SNS抑制剂逆转。
讨论：SNS在体内生理调节白色脂肪组织中的血清脂联素水平和脂联素合成，尽管白色脂肪组织对SNS刺激的反应性存在显著差异。交感神经激活可能通过调节血清脂联素浓度参与代谢综合征的发生发展。
Objective: Several lines of evidence suggest important roles for adiponectin in glucose and lipid metabolism and atherosclerosis. However, the mechanisms regulating serum adiponectin levels and adiponectin production are still not completely understood. Our aim was to determine whether adiponectin synthesis is physiologically regulated by the sympathetic nervous system (SNS).Research Methods and Procedures: Mice were exposed to cold (4 degrees C) for 12 hours and for 24 hours with or without inhibition of noradrenaline synthesis or pan-beta adrenergic function, followed by measurement of serum adiponectin concentrations and levels of adiponectin and uncoupling protein (UCP) 1 expressions in various white adipose tissues (WATs).Results: Cold exposure significantly reduced serum adiponectin concentrations without changing body weights or WAT sizes in either subcutaneous or intra-abdominal fat tissues. The serum adiponectin reduction was associated with a decrease in adipionectin mRNA expression in subcutaneous, epididymal, and mesenteric fat tissues. In these adipose tissues, UCP1 expression was markedly enhanced, suggesting SNS activation in these tissues. Administration of alpha-methyl-p-tyrosine or a combination of SR59230A and propranolol reversed the cold-exposure-induced decreases in serum adiponectin concentrations and adiponectin mRNA expression in these tissues. In contrast, in retroperitoneal fat, the effects of cold exposure on adiponectin and UCP1 expressions were strikingly weak but were not reversed by SNS inhibitors.Discussion: SNS physiologically regulates serum adiponectin levels and adipionectin synthesis in WATs in vivo, although responsiveness to SNS stimulation differs markedly among WATs. Sympathetic activation might be involved in development of the metabolic syndrome by modulation of serum adiponectin concentrations.