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下丘脑外侧和内侧损伤不会急性影响棕色脂肪组织的产热作用。

Lateral and medial hypothalamic lesions do not acutely affect brown adipose tissue thermogenesis.

作者信息

Park I R, Coscina D V, Himms-Hagen J

机构信息

Department of Biochemistry, University of Ottawa, Faculty of Health Sciences, Ontario, Canada.

出版信息

Brain Res Bull. 1988 Nov;21(5):805-11. doi: 10.1016/0361-9230(88)90049-4.

DOI:10.1016/0361-9230(88)90049-4
PMID:3219612
Abstract

The acute effect of lateral (LH) and medial (MH) hypothalamic lesions on mitochondrial GDP binding in brown adipose tissue (BAT) (an index of thermogenic state) was studied one and two days postlesion. Groups of rats were lesioned, sham-lesioned, or unoperated and were all fasting. An additional group of unoperated rats had access to food throughout the study. The objective was to determine whether the hypermetabolic state and rapid weight loss known to be induced by LH lesions were attributable to the activation of BAT thermogenesis, and, if so, whether these effects were specific for LH lesions. No effect of either lesion on BAT thermogenic state could be detected at either time studied. Despite that fact, LH-lesioned rats, but not MH-lesioned rats, were hyperthermic at both times. We conclude that the prolonged hyperthermia which occurs shortly after LH lesions is not due to an activation of BAT thermogenesis. Instead, it can be likened to the febrile state in which an initial and brief activation of both nonshivering thermogenesis in BAT and shivering thermogenesis in muscles occurs only during the rising phase of the fever and is suppressed as soon as a stable hyperthermic state is reached. It thus appears unlikely that substantial and prolonged activation of BAT thermogenesis is a major mechanism that promotes exaggerated short-term weight loss in the LH-lesioned rat.

摘要

研究了下丘脑外侧(LH)和内侧(MH)损伤后1天和2天对棕色脂肪组织(BAT)中线粒体GDP结合(产热状态指标)的急性影响。将大鼠分组进行损伤、假损伤或不做处理,所有大鼠均处于禁食状态。另一组未做处理的大鼠在整个研究过程中可以进食。目的是确定已知由LH损伤诱导的高代谢状态和快速体重减轻是否归因于BAT产热的激活,如果是,这些影响是否是LH损伤所特有的。在所研究的两个时间点,均未检测到任何一种损伤对BAT产热状态有影响。尽管如此,LH损伤的大鼠在这两个时间点均体温过高,而MH损伤的大鼠则不然。我们得出结论,LH损伤后不久出现的持续性体温过高并非由于BAT产热的激活。相反,它类似于发热状态,即BAT中非寒战产热和肌肉中寒战产热的最初短暂激活仅发生在发热的上升阶段,一旦达到稳定的高温状态就会受到抑制。因此,BAT产热的大量和持续激活似乎不太可能是促进LH损伤大鼠短期内体重过度减轻的主要机制。

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