Evidence map›Paper›PMID 22535963›Full record

ArticleThe Journal of biological chemistry2012

Catestatin (chromogranin A(352-372)) and novel effects on mobilization of fat from adipose tissue through regulation of adrenergic and leptin signaling.

Gautam K Bandyopadhyay, Christine U Vu, Stefano Gentile, Howon Lee, Nilima Biswas, Nai-Wen Chi, Daniel T O'Connor, Sushil K Mahata

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

36 citing papers in PubMed, 77 citations in OpenAlex.

  1. Trial
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  7. Review
  8. The Role of Catestatin in Preeclampsia.International journal of molecular sciences · 2024
    Review
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  12. Review
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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 2 institutions in 1 country.

Gautam K BandyopadhyayVeterans Affairs San Diego Healthcare System, San Diego, California 92161, USA. gbandyopadhyay@ucsd.edu
Christine U Vu
Stefano Gentile
Howon Lee
Nilima Biswas
Nai-Wen Chi
Daniel T O'Connor
Sushil K Mahata
University of California, San Diego · USVA San Diego Healthcare System · US

Funding

Hypertensive kidney disease: Novel pathogenic and therapeutic pathwayR01DK094894 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI VAINGANKAR, SUCHETA M · 2012 to 2015
$1.4M
Chromaffin Cell physiology: Novel molecular approachesR01DA011311 · NIDA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MAHATA, SUSHIL K · 2005 to 2009
$922k
NIDA NIH HHS R01 DA011311NIDDK NIH HHS R01 DK094894
6 · The paper itself

Abstract

Chromogranin A knock-out (Chga-KO) mice display increased adiposity despite high levels of circulating catecholamines and leptin. Consistent with diet-induced obese mice, desensitization of leptin receptors caused by hyperleptinemia is believed to contribute to the obese phenotype of these KO mice. In contrast, obesity in ob/ob mice is caused by leptin deficiency. To characterize the metabolic phenotype, Chga-KO mice were treated with the CHGA-derived peptide catestatin (CST) that is deficient in these mice. CST treatment reduced fat depot size and increased lipolysis and fatty acid oxidation. In liver, CST enhanced oxidation of fatty acids as well as their assimilation into lipids, effects that are attributable to the up-regulation of genes promoting fatty acid oxidation (Cpt1α, Pparα, Acox, and Ucp2) and incorporation into lipids (Gpat and CD36). CST did not affect basal or isoproterenol-stimulated cAMP production in adipocytes but inhibited phospholipase C activation by the α-adrenergic receptor (AR) agonist phenylephrine, suggesting inhibition of α-AR signaling by CST. Indeed, CST mimicked the lipolytic effect of the α-AR blocker phentolamine on adipocytes. Moreover, CST reversed the hyperleptinemia of Chga-KO mice and improved leptin signaling as determined by phosphorylation of AMPK and Stat3. CST also improved peripheral leptin sensitivity in diet-induced obese mice. In ob/ob mice, CST enhanced leptin-induced signaling in adipose tissue. In conclusion, our results implicate CST in a novel pathway that promotes lipolysis and fatty acid oxidation by blocking α-AR signaling as well as by enhancing leptin receptor signaling.

Indexed as

AdipocytesAdipose TissueAnimalsAnti-Obesity AgentsCatecholaminesChromogranin AFatty AcidsGene ExpressionLeptinLipolysisMaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMice, ObeseAnti-Obesity AgentsCatecholaminesChromogranin Achromogranin A (344-364)chromogranin A, mouseFatty AcidsLeptinPeptide FragmentsReceptors, Adrenergic, alpha

Identifiers

PMID22535963
PMCPMC3391131
OpenAlexW2033183800

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.