Evidence map›Paper›PMID 24749060›Full record

ArticleMolecular metabolism2014

Improved metabolic phenotype of hypothalamic PTP1B-deficiency is dependent upon the leptin receptor.

Ryan C Tsou, Kimberly S Rak, Derek J Zimmer, Kendra K Bence

Abstract read
In one paragraph

Article in Molecular metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

  1. Review
  2. Endothelial Dysfunction in Obesity and Therapeutic Targets.Advances in experimental medicine and biology · 2024
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. GMolecular metabolism · 2019
    Article
  12. Review
  13. The Leptin Receptor Complex: Heavier Than Expected?Frontiers in endocrinology · 2017
    Review
  14. Article
  15. Leptin signalling pathways in hypothalamic neurons.Cellular and molecular life sciences : CMLS · 2016
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

4 authors.

Ryan C TsouDepartment of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Kimberly S RakDepartment of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Derek J ZimmerDepartment of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Kendra K BenceDepartment of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.

Funding

VIRAL VECTOR COREP30DK019525 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Patrick Seale · 1986 to 2026
$48.3M
SYSTEMS AND INTEGRATIVE BIOLOGYT32GM007517 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI GOLD, JOSHUA I · 1985 to 2017
$8.0M
Neuronal Protein Tyrosine Phosphatases in MetabolismR01DK082417 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI BENCE, KENDRA · 2009 to 2015
$2.6M
The role of PTP1B in leptin receptor-dependent and -independent regulation of eneF31NS074684 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI TSOU, RYAN · 2011 to 2013
$116k
NIDDK NIH HHS P30 DK019525NIDDK NIH HHS R01 DK082417NIGMS NIH HHS T32 GM007517NINDS NIH HHS F31 NS074684
6 · The paper itself

Abstract

Protein tyrosine phosphatase 1B (PTP1B) is a known regulator of central metabolic signaling, and mice with whole brain-, leptin receptor (LepRb) expressing cell-, or proopiomelanocortin neuron-specific PTP1B-deficiency are lean, leptin hypersensitive, and display improved glucose homeostasis. However, whether the metabolic effects of central PTP1B-deficiency are due to action within the hypothalamus remains unclear. Moreover, whether or not these effects are exclusively due to enhanced leptin signaling is unknown. Here we report that mice with hypothalamic PTP1B-deficiency (Nkx2.1-PTP1B(-/-)) display decreased body weight and adiposity on high-fat diet with no associated improvements in glucose tolerance. Consistent with previous reports, we find that hypothalamic deletion of the LepRb in mice (Nkx2.1-LepRb(-/-)) results in extreme hyperphagia and obesity. Interestingly, deletion of hypothalamic PTP1B and LepRb (Nkx2.1-PTP1B(-/-):LepRb(-/-)) does not rescue the hyperphagia or obesity of Nkx2.1-LepRb(-/-) mice, suggesting that hypothalamic PTP1B contributes to the central control of energy balance through a leptin receptor-dependent pathway.

Indexed as

BAT, Brown adipose tissueCNTF, Ciliary neurotrophic factorCre, Cre recombinasedb/db, Leptin receptor-deficient miceGTT, Glucose tolerance testHFD, High-fat dietHPA, hypothalamus–pituitary–adrenalHypothalamusIL-6, Interleukin-6ITT, Insulin tolerance testJAK2, Janus kinase 2LepRb, Leptin receptor long formLeptinNkx2.1, NK2 homeobox 1 protein or thyroid transcription factor-1Obesityob/ob, leptin-deficient micePhosphatasePI3K, Phosphatidylinositol 3-kinasePOMC, ProopiomelanocortinPrdm16, PR domain containing 16PTP1B, Protein tyrosine phosphatase 1BPTPs, Protein tyrosine phosphatasesSHP2, Src homology 2 domain-containing protein tyrosine phosphataseSTAT3, Signal transducer and activator of transcription 3UCP1, Uncoupling protein 1WAT, White adipose tissue

Identifiers

PMID24749060
PMCPMC3986631

What OpenQuestion holds

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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.