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Nat Med:美学者揭示交感神经系统驱动身体生热作用

摘要 : 2017年4月17日,国际学术权威刊物自然出版集团旗下子刊《Nature Medicine》杂志在线发表了美国西奈山伊坎医学院Christoph Buettner教授的一项最新研究,研究显示身体生热作用的主要驱动力是由大脑控制的交感神经系统,而此前人们曾猜测巨噬细胞在生热作用中发挥重大作用。

 2017年4月17日,国际学术权威刊物自然出版集团旗下子刊《Nature Medicine》杂志在线发表了美国西奈山伊坎医学院Christoph Buettner教授的一项最新研究,研究显示身体生热作用的主要驱动力是由大脑控制的交感神经系统,而此前人们曾猜测巨噬细胞在生热作用中发挥重大作用。

人体调节热量产生的过程称为生热作用,这是目前研究糖尿病和治疗肥胖症的主要方向。在利用免疫系统治疗糖尿病和胰岛素耐受性方面,虽然科学家做出了很多努力,但对于人类的代谢疾病尚未开发出疗效突出的药物。研究人员认为,要想彻底根治糖尿病和肥胖症,可能还需要从恢复大脑和自主神经系统对生热作用和新陈代谢的控制能力方面着手。

研究团队重点研究了儿茶酚胺,包括去甲肾上腺素、肾上腺素和多巴胺,其参与生热作用调节,并通过β受体增加氧耗量而产热,同时可促进褐色脂肪组织的分解。而褐色脂肪组织正是人体的产热器,可消耗能量产生热量,调节体温。

研究人员确认,大脑可通过交感神经系统产生儿茶酚胺,而巨噬细胞无法产生儿茶酚胺。

比特纳表示,生热作用是新陈代谢过程,将之作为靶标来开发药物,可消耗人体能量,减少肥胖,改善糖尿病,因此,研究大脑和交感神经系统对生热作用的影响,对理解新陈代谢过程具有非常重要的意义。

原文链接:

Alternatively activated macrophages do not synthesize catecholamines or contribute to adipose tissue adaptive thermogenesis

原文摘要:

Adaptive thermogenesis is the process of heat generation in response to cold stimulation. It is under the control of the sympathetic nervous system, whose chief effector is the catecholamine norepinephrine (NE). NE enhances thermogenesis through β3-adrenergic receptors to activate brown adipose tissue and by 'browning' white adipose tissue. Recent studies have reported that alternative activation of macrophages in response to interleukin (IL)-4 stimulation induces the expression of tyrosine hydroxylase (TH), a key enzyme in the catecholamine synthesis pathway, and that this activation provides an alternative source of locally produced catecholamines during the thermogenic process. Here we report that the deletion of Th in hematopoietic cells of adult mice neither alters energy expenditure upon cold exposure nor reduces browning in inguinal adipose tissue. Bone marrow–derived macrophages did not release NE in response to stimulation with IL-4, and conditioned media from IL-4-stimulated macrophages failed to induce expression of thermogenic genes, such as uncoupling protein 1 (Ucp1), in adipocytes cultured with the conditioned media. Furthermore, chronic treatment with IL-4 failed to increase energy expenditure in wild-type, Ucp1−/− and interleukin-4 receptor-α double-negative (Il4ra−/−) mice. In agreement with these findings, adipose-tissue-resident macrophages did not express TH. Thus, we conclude that alternatively activated macrophages do not synthesize relevant amounts of catecholamines, and hence, are not likely to have a direct role in adipocyte metabolism or adaptive thermogenesis.

来源: Nature Medicine 浏览次数:0

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