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Leptin decreases the expression of low-density lipoprotein receptor via PCSK9 pathway: linking dyslipidemia with obesity

Overview of attention for article published in Journal of Translational Medicine, September 2016
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  • In the top 25% of all research outputs scored by Altmetric
  • Good Attention Score compared to outputs of the same age (75th percentile)
  • High Attention Score compared to outputs of the same age and source (82nd percentile)

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37 Mendeley
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Title
Leptin decreases the expression of low-density lipoprotein receptor via PCSK9 pathway: linking dyslipidemia with obesity
Published in
Journal of Translational Medicine, September 2016
DOI 10.1186/s12967-016-1032-4
Pubmed ID
Authors

Ying Du, Sha Li, Chuan-Jue Cui, Yan Zhang, Sheng-Hua Yang, Jian-Jun Li

Abstract

Previous studies have suggested that people with obesity showed elevated serum levels of leptin as well as lipid dysfunction and proprotein convertase subtilisin/kexin type 9 (PCSK9) played an important role in the regulation of lipid metabolism recently. The aim of this study was to determine if leptin participated in regulating the uptake of low-density lipoproteins (LDL) in hepatocytes via PCSK9. HepG2 cells were treated with human recombinant leptin. The impact of leptin on cellular low density lipoprotein receptor (LDLR) and PCSK9 protein levels was determined by Western blot. Dil-LDL uptake assay was performed to examine the LDLR function. Specific small interfering RNAs (siRNAs) were used to interfere the expressions of target proteins. The expression of LDLR and LDL uptake could be significantly down-regulated by leptin treatment while the expressions of PCSK9 and hepatocyte nuclear factor 1α (HNF1α) were enhanced in HepG2 cells. Furthermore, inhibition of PCSK9 or HNF1α expression by siRNAs rescued the reduction of LDLR expression and LDL uptake by leptin. We found that leptin activated the p38 mitogen-activated protein kinase (p38MAPK) signaling pathway. Moreover, the changes of the expressions of HNF1α, PCSK9, LDLR, and LDL uptake induced by leptin could be blocked by p38MAPK inhibitor (SB203580). Additionally, leptin attenuated the up-regulation of LDLR caused by atorvastatin in HepG2 cells. These findings indicated firstly that leptin reduced LDLR levels in hepatocyte via PCSK9 pathway, suggesting that PCSK9 might be a alternative target for dyslipidemia in the obesity.

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X Demographics

The data shown below were collected from the profiles of 11 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 37 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Netherlands 1 3%
United States 1 3%
Unknown 35 95%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 9 24%
Researcher 8 22%
Student > Bachelor 5 14%
Student > Master 3 8%
Student > Doctoral Student 2 5%
Other 3 8%
Unknown 7 19%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 8 22%
Medicine and Dentistry 6 16%
Agricultural and Biological Sciences 4 11%
Pharmacology, Toxicology and Pharmaceutical Science 2 5%
Computer Science 2 5%
Other 4 11%
Unknown 11 30%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 7. 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 28 September 2016.
All research outputs
#5,209,170
of 24,989,834 outputs
Outputs from Journal of Translational Medicine
#910
of 4,532 outputs
Outputs of similar age
#80,750
of 329,205 outputs
Outputs of similar age from Journal of Translational Medicine
#13
of 68 outputs
Altmetric has tracked 24,989,834 research outputs across all sources so far. Compared to these this one has done well and is in the 79th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 4,532 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 10.8. This one has done well, scoring higher than 79% of its peers.
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 329,205 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 75% of its contemporaries.
We're also able to compare this research output to 68 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 82% of its contemporaries.