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Leptin Signaling in the Carotid Body Regulates a Hypoxic Ventilatory Response Through Altering TASK Channel Expression

Overview of attention for article published in Frontiers in Physiology, March 2018
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Title
Leptin Signaling in the Carotid Body Regulates a Hypoxic Ventilatory Response Through Altering TASK Channel Expression
Published in
Frontiers in Physiology, March 2018
DOI 10.3389/fphys.2018.00249
Pubmed ID
Authors

Fang Yuan, Hanqiao Wang, Jiaqi Feng, Ziqian Wei, Hongxiao Yu, Xiangjian Zhang, Yi Zhang, Sheng Wang

Abstract

Leptin is an adipose-derived hormone that plays an important role in the regulation of breathing. It has been demonstrated that obesity-related hypoventilation or apnea is closely associated with leptin signaling pathways. Perturbations of leptin signaling probably contribute to the reduced sensitivity of respiratory chemoreceptors to hypoxia/hypercapnia. However, the underlying mechanism remains incompletely understood. The present study is to test the hypothesis that leptin signaling contributes to modulating a hypoxic ventilatory response. The respiratory function was assessed in conscious obese Zucker rats or lean littermates treated with an injection of leptin. During exposure to hypoxia, the change in minute ventilation was lower in obese Zucker rats than chow-fed lean littermates or high fat diet-fed littermates. Such a change was abolished in all groups after carotid body denervation. In addition, the expression of phosphorylated signal transducers and activators of transcription 3 (pSTAT3), as well as putative O2-sensitive K+ channels including TASK-1, TASK-3 and TASK-2 in the carotid body, was significantly reduced in obese Zucker rats compared with the other two phenotype littermates. Chronic administration of leptin in chow-fed lean Zucker rats failed to alter basal ventilation but vigorously increased tidal volume, respiratory frequency, and therefore minute volume during exposure to hypoxia. Likewise, carotid body denervation abolished such an effect. In addition, systemic leptin elicited enhanced expression of pSTAT3 and TASK channels. In conclusion, these data demonstrate that leptin signaling facilitates hypoxic ventilatory responses probably through upregulation of pSTAT3 and TASK channels in the carotid body. These findings may help to better understand the pathogenic mechanism of obesity-related hypoventilation or apnea.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 19 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 19 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 5 26%
Student > Bachelor 2 11%
Lecturer 1 5%
Student > Doctoral Student 1 5%
Student > Master 1 5%
Other 1 5%
Unknown 8 42%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 2 11%
Nursing and Health Professions 2 11%
Agricultural and Biological Sciences 2 11%
Pharmacology, Toxicology and Pharmaceutical Science 1 5%
Chemical Engineering 1 5%
Other 3 16%
Unknown 8 42%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 11 April 2018.
All research outputs
#18,596,650
of 23,035,022 outputs
Outputs from Frontiers in Physiology
#8,235
of 13,775 outputs
Outputs of similar age
#256,387
of 330,042 outputs
Outputs of similar age from Frontiers in Physiology
#270
of 418 outputs
Altmetric has tracked 23,035,022 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 13,775 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.6. This one is in the 31st percentile – i.e., 31% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 330,042 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 11th percentile – i.e., 11% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 418 others from the same source and published within six weeks on either side of this one. This one is in the 26th percentile – i.e., 26% of its contemporaries scored the same or lower than it.