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高脂喂养大鼠改变呼吸参数的机制不太可能通过颈动脉体 I 型细胞介导。

High Fat Feeding in Rats Alters Respiratory Parameters by a Mechanism That Is Unlikely to Be Mediated by Carotid Body Type I Cells.

机构信息

Department of Neuroscience, Cell Biology, & Physiology, Wright State University, Dayton, OH, USA.

Division of Biological Sciences, University of Missouri, Columbia, MO, USA.

出版信息

Adv Exp Med Biol. 2018;1071:137-142. doi: 10.1007/978-3-319-91137-3_17.

DOI:10.1007/978-3-319-91137-3_17
PMID:30357744
Abstract

The carotid bodies (CB) respond to changes in blood gases with neurotransmitter release, thereby increasing carotid sinus nerve firing frequency and ultimately correcting the pattern of breathing. It has previously been demonstrated that acute application of the adipokine leptin augments the hypoxic sensory response of the intact in-vitro CB (Pye RL, Roy A, Wilson RJ, Wyatt CN. FASEB J 30(1 Supplement):983.1, 2016) and isolated CB type I cell (Pye RL, Dunn EJ, Ricker EM, Jurcsisn JG, Barr BL, Wyatt CN. Arterial chemoreceptors in physiology and pathophysiology. Advances in experimental medicine and biology. Springer, Cham, 2015). This study's aim was to examine, in-vivo, if elevated leptin modulated CB function and breathing.Rats were fed high fat or control chow for 16-weeks. High fat fed (HFF) animals gained significantly more weight compared to control fed (CF) animals and had significantly higher serum leptin levels compared to CF. Utilizing whole-body plethysmography, HFF animals demonstrated significantly depressed breathing compared to CF at rest and during hypoxia. However, amplitudes in the change in breathing from rest to hypoxia were not significantly different between groups. CB type I cells were isolated and intracellular calcium levels recorded. Averaged and peak cellular hypoxic responses were not significantly different.Despite a small but significant rise in leptin, differences in breathing caused by high fat feeding are unlikely caused by an effect of leptin on CB type I cells. However, the possibility remains that leptin may have in-vivo postsynaptic effects on the carotid sinus nerve; this remains to be investigated.

摘要

颈动脉体(CB)通过神经递质释放对血液气体变化做出反应,从而增加颈动脉窦神经的发射频率,并最终纠正呼吸模式。先前已经证明,急性应用脂肪因子瘦素可增强完整体外 CB(Pye RL、Roy A、Wilson RJ、Wyatt CN。FASEB J 30(1 增刊):983.1,2016)和分离的 CB 型 I 细胞(Pye RL、Dunn EJ、Ricker EM、Jurcsisn JG、Barr BL、Wyatt CN。动脉化学感受器在生理学和病理生理学中的作用。实验医学和生物学进展。施普林格,瑞士,2015)的缺氧感觉反应。本研究的目的是体内研究瘦素是否调节 CB 功能和呼吸。大鼠喂养高脂肪或对照饲料 16 周。与对照喂养(CF)动物相比,高脂肪喂养(HFF)动物体重显著增加,血清瘦素水平显著高于 CF。利用全身 plethysmography,与 CF 相比,HFF 动物在休息和缺氧时呼吸明显减弱。然而,从休息到缺氧时呼吸变化的幅度在两组之间没有显著差异。分离 CB 型 I 细胞并记录细胞内钙水平。平均和峰值细胞缺氧反应没有显著差异。尽管瘦素略有但显著升高,但高脂肪喂养引起的呼吸差异不太可能是瘦素对 CB 型 I 细胞的作用所致。然而,瘦素可能对颈动脉窦神经有体内突触后效应的可能性仍然存在;这有待进一步研究。

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