Evidence map›Paper›PMID 31803004›Full record

ArticleFrontiers in neuroscience2019

Leptin-Mediated Sympathoexcitation in Obese Rats: Role for Neuron-Astrocyte Crosstalk in the Arcuate Nucleus.

Xuefei Liu, Hong Zheng

Abstract read
In one paragraph

Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

  1. Review
  2. Astrocyte involvement in metabolic regulation and disease.Trends in endocrinology and metabolism: TEM · 2025
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Loss of leptin receptor-expressing cells in the hindbrain decreases forebrain leptin sensitivity.American journal of physiology. Endocrinology and metabolism · 2020
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Xuefei LiuDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD, United States.
Hong ZhengDivision of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAccumulated evidence indicates that obesity is associated with enhanced sympathetic activation. Hypothalamic leptin-mediated signaling may contribute to the exaggerated sympathoexcitation of obesity. The goal of this study was to investigate the "neuron-astrocyte" interaction affecting leptin-mediated sympathoexcitation within the arcuate nucleus (ARCN) of the hypothalamus in obese rats. METHODS AND

resultsObesity was induced by high-fat diet (HFD, 42% of calories from fat) in Sprague Dawley rats. Twelve weeks of HFD produced hyperleptinemia, hyperlipidemia, and insulin resistance. In anesthetized rats, microinjections of leptin into the ARCN induced increases in heart rate (HR), renal sympathetic nerve activity (RSNA), and mean arterial pressure (MAP) in both control and HFD rats. However, microinjections of leptin in HFD rats elicited higher responses of RSNA and arterial pressure than control-fed rats. It also caused the inhibition of astrocytes within the ARCN using an astrocytic metabolic inhibitor, fluorocitrate, and reduced leptin-induced sympathetic activity and blood pressure responses. Moreover, the expression of the leptin receptor in the ARCN of HFD-fed rats was significantly increased compared to rats fed a control diet. Immunohistochemistry analysis revealed leptin receptor localization from both neurons and astrocytes of the ARCN. HFD rats exhibited increased protein expression of glial fibrillary acidic protein (GFAP) in the ARCN. We also found that the expression of astrocyte-specific glutamate transporters and excitatory amino acid transporter 1 (EAAT1) and 2 (EAAT2) were decreased within the ARCN of the HFD rats. In cultured astrocytic C6 cells, 24 h of leptin treatment increased the protein expression of GFAP and reduced the expression of EAAT1 and EAAT2.

conclusionThe results suggest that central leptin signaling occurs via neuron-astrocyte interactions in the ARCN and contributing to the exaggerated sympathoexcitation observed in obese rats. The effects may be mediated by the action of leptin on regulating astrocytic glutamate transporters within the ARCN of the hypothalamus.

Indexed as

glial cellshypothalamusleptinobesitysympathetic nerve activity

Identifiers

PMID31803004
PMCPMC6877670

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.