Evidence map›Paper›PMID 30429087›Full record

ArticleEBioMedicine2018

A renal-cerebral-peripheral sympathetic reflex mediates insulin resistance in chronic kidney disease.

Wei Cao, Meng Shi, Liling Wu, Zhichen Yang, Xiaobing Yang, Hongfa Liu, Xin Xu, Youhua Liu, Christopher S Wilcox, Fan Fan Hou

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 11% of its field
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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Chronic kidney disease combined with metabolic syndrome is a non-negligible risk factor.Therapeutic advances in endocrinology and metabolism · 2024
    Review
  8. Adipose tissue metabolic changes in chronic kidney disease.Immunometabolism (Cobham, Surrey) · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Wei CaoDivision of Nephrology, Nanfang Hospital, 1838 North Guangzhou Avenue, Guangzhou 510515, PR China.
Meng ShiDivision of Nephrology, Nanfang Hospital, 1838 North Guangzhou Avenue, Guangzhou 510515, PR China.
Liling WuDivision of Nephrology, Nanfang Hospital, 1838 North Guangzhou Avenue, Guangzhou 510515, PR China.
Zhichen YangDivision of Nephrology, Nanfang Hospital, 1838 North Guangzhou Avenue, Guangzhou 510515, PR China.
Xiaobing YangDivision of Nephrology, Nanfang Hospital, 1838 North Guangzhou Avenue, Guangzhou 510515, PR China.
Hongfa LiuDivision of Nephrology, Nanfang Hospital, 1838 North Guangzhou Avenue, Guangzhou 510515, PR China.
Xin XuDivision of Nephrology, Nanfang Hospital, 1838 North Guangzhou Avenue, Guangzhou 510515, PR China.
Youhua LiuDivision of Nephrology, Nanfang Hospital, 1838 North Guangzhou Avenue, Guangzhou 510515, PR China.
Christopher S WilcoxDivision of Nephrology and Hypertension, Georgetown University Medical Central, 3800 Reservoir Road, NW, 6 PHC Bldg, F6003, Washington, DC 20007, USA. Electronic address: wilcoxch@georgetown.edu.
Fan Fan HouDivision of Nephrology, Nanfang Hospital, 1838 North Guangzhou Avenue, Guangzhou 510515, PR China.. Electronic address: ffhouguangzhou@163.com.
Georgetown University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin resistance (IR) complicates chronic kidney disease (CKD). We tested the hypothesis that CKD activates a broad reflex response from the kidneys and the white adipose tissue to impair peripheral glucose uptake and investigated the role of salt intake in this process.

methods5/6-nephrectomized rats were administered normal- or high-salt for 3 weeks. Conclusions were tested in 100 non-diabetic patients with stage 3-5 CKD.

findingsHigh-salt in 5/6-nephrectomized rats decreased insulin-stimulated 2-deoxyglucose uptake >25% via a sympathetic nervous system (SNS) reflex that linked the IR to reactive oxygen species (ROS) and the renin-angiotensin system (RAS) in brain and peripheral tissues. Salt-loading in CKD enhanced inflammation in adipose tissue and skeletal muscle, and enhanced the impairment of insulin signaling and Glut4 trafficking. Denervation of the kidneys or adipose tissue or deafferentation of adipose tissue improved IR >40%. In patients with non-diabetic CKD, IR was positively correlated with salt intake after controlling for cofounders (r = 0.334, P = 0.001) and was linked to activation of the RAS/SNS and to impaired glucose uptake in adipose tissue and skeletal muscle, all of which depended on salt intake.

interpretationCKD engages a renal/adipose-cerebral-peripheral sympathetic reflex that activates the RAS/ROS axes to promote IR via local inflammation and impaired Glut4 trafficking that are enhanced by high-salt intake. The findings point to a role for blockade of RAS or α-and-β-adrenergic receptors to reduce IR in patients with CKD. FUND: National Natural Science Foundation of China.

Indexed as

BrainInsulin ResistanceRenal Insufficiency, ChronicRenin-Angiotensin SystemSignal TransductionSympathetic Nervous SystemAdipose TissueAnimalsDisease Models, AnimalMaleMuscle, SkeletalRatsRats, Sprague-DawleyAdipose tissueChronic kidney diseaseInsulin resistanceRenin-angiotensin systemSaltSympathetic reflex

Identifiers

PMID30429087
PMCPMC6286258
OpenAlexW2899857987

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.