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1 型发作性睡病患者暴露于寒冷后功能性棕色脂肪组织和交感神经活性。

Functional brown adipose tissue and sympathetic activity after cold exposure in humans with type 1 narcolepsy.

机构信息

Department of Clinical Physiology, Nuclear Medicine and PET, Rigshospitalet, Denmark.

Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark.

出版信息

Sleep. 2018 Aug 1;41(8). doi: 10.1093/sleep/zsy092.

Abstract

STUDY OBJECTIVES

To investigate the activity of brown adipose tissue (BAT) in patients with type 1 narcolepsy during cold exposure using two separate scans of sympathetic and metabolic activity of BAT to evaluate whether orexin deficiency leads to altered nonshivering thermoregulation in narcolepsy.

METHODS

Seven patients with type 1 narcolepsy and seven healthy controls underwent two consecutive scans after 2 hr cold exposure: 123I-meta-iodo-benzyl-guanidine (123I-MIBG) single photon emission computed tomography and18F-2-deoxy-glucose (18F-FDG) positron emission tomography and computed tomography to visualize sympathetic innervation and metabolic activity of BAT, respectively. Plasma levels of eight hormones regulating BAT activity were measured before and after 2 hr in the cold.

RESULTS

18F-FDG-uptake and uptake of 123I-MIBG in BAT after 2 hr cold exposure were observed in all individuals, but the activity of BAT was not significantly different between patients with type 1 narcolepsy and healthy controls (p > 0.05). Plasma levels of GLP-1 were higher in patients with type 1 narcolepsy compared with controls (p < 0.05), but not altered by cold adaptation in patients and controls (p > 0.05). FGF21 concentrations decreased after 2 hr cold exposure in both patients with type 1 narcolepsy and healthy participants (p < 0.05).

CONCLUSIONS

Sympathetic and metabolic activity of BAT was observed after cold exposure in patients with type 1 narcolepsy. Increased GLP-1 in narcolepsy may suggest autonomic dysfunction with metabolic changes. We conclude that BAT is functional after cold exposure in spite of the loss of orexinergic neurons in narcolepsy.

摘要

研究目的

通过两次分别扫描棕色脂肪组织(BAT)的交感神经和代谢活性,来研究 1 型发作性睡病患者在冷暴露下 BAT 的活性,以评估食欲素缺乏是否会导致发作性睡病的非颤抖体温调节发生改变。

方法

7 例 1 型发作性睡病患者和 7 例健康对照者在冷暴露 2 小时后连续进行两次扫描:123I-间碘苄胍(123I-MIBG)单光子发射计算机断层扫描和 18F-2-脱氧葡萄糖(18F-FDG)正电子发射断层扫描和计算机断层扫描,分别用于观察 BAT 的交感神经支配和代谢活性。在冷暴露前和冷暴露 2 小时后测量调节 BAT 活性的八种激素的血浆水平。

结果

在所有个体中均观察到 BAT 在冷暴露 2 小时后 18F-FDG 和 123I-MIBG 的摄取,但 1 型发作性睡病患者与健康对照者之间 BAT 的活性无显著差异(p > 0.05)。与对照组相比,1 型发作性睡病患者的 GLP-1 水平较高(p < 0.05),但在患者和对照组中均不受冷适应的影响(p > 0.05)。1 型发作性睡病患者和健康参与者在冷暴露 2 小时后 FGF21 浓度均降低(p < 0.05)。

结论

在 1 型发作性睡病患者中,冷暴露后观察到 BAT 的交感神经和代谢活性。发作性睡病中 GLP-1 的增加可能提示自主神经功能障碍伴代谢变化。我们的结论是,尽管在发作性睡病中丧失了食欲素能神经元,但 BAT 在冷暴露后仍具有功能。

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