Evidence map›Paper›PMID 24115476›Full record

ArticleJournal of the American Society of Nephrology : JASN2014

A pegylated leptin antagonist ameliorates CKD-associated cachexia in mice.

Wai W Cheung, Wei Ding, Sujana S Gunta, Yong Gu, Rinat Tabakman, Leah N Klapper, Arieh Gertler, Robert H Mak

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

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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

8 authors at 3 institutions in 3 countries.

Wai W CheungDivision of Pediatric Nephrology, University of California, San Diego, La Jolla, California;
Wei Ding
Sujana S Gunta
Yong Gu
Rinat Tabakman
Leah N Klapper
Arieh Gertler
Robert H Mak
University of California, San Diego · USFudan University · CNHebrew University of Jerusalem · IL

Funding

NIDDK NIH HHS U01 DK-3012
6 · The paper itself

Abstract

Elevated serum leptin levels correlate with inflammation and predict changes in lean body mass in patients with CKD, and activation of the melanocortin system by leptin signaling mediates the pathophysiology of CKD-associated cachexia. We tested whether treatment with a pegylated leptin receptor antagonist (PLA) attenuates cachexia in mice with CKD. CKD and Sham mice received vehicle or PLA (2 or 7 mg/kg per day). At these doses, PLA did not influence serum leptin levels in mice. Treatment with 7 mg/kg per day PLA stimulated appetite and weight gain, improved lean mass and muscle function, reduced energy expenditure, and normalized the levels of hepatic TNF-α and IL-6 mRNA in mice with CKD. Furthermore, treatment with 7 mg/kg per day PLA attenuated the CKD-associated increase in the transcriptional and protein abundance of uncoupling proteins that mediates thermogenesis, and it normalized the molecular signatures of processes associated with muscle wasting in CKD, including proteolysis, myogenesis and muscle regeneration, and expression of proinflammatory muscle cytokines, such as IL-1α, -1β, and -6 and TNF-α. Our results suggest that leptin antagonism may represent a viable therapeutic strategy for cachexia in CKD.

Indexed as

AnimalsAnorexiaCachexiaEnergy MetabolismGene ExpressionLeptinMaleMiceMice, Inbred C57BLMuscle, SkeletalReceptors, LeptinRenal Insufficiency, ChronicSignal TransductionWeight LossLeptinleptin receptor, mouseReceptors, Leptin

Identifiers

PMID24115476
PMCPMC3871780
OpenAlexW2117140357

What OpenQuestion holds

Textmetadata
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.