Evidence map›Paper›PMID 21464566›Full record

ReviewNeuroendocrinology2011

Intracellular leptin-signaling pathways in hypothalamic neurons: the emerging role of phosphatidylinositol-3 kinase-phosphodiesterase-3B-cAMP pathway.

Abhiram Sahu

Open access · bronzeAbstract readReview
In one paragraph

Review in Neuroendocrinology, 2011. 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
3.4field-weighted citation impact, top 7% 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, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The Mechanism of Leptin Resistance in Obesity and Therapeutic Perspective.Advances in experimental medicine and biology · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Leptin signaling and leptin resistance.Medical review (2021) · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  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

1 author at 1 institution in 1 country.

Abhiram SahuDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh School of Medicine, Magee-Womens Research Institute, Pittsburgh, PA 15213, USA. asahu@pitt.edu
Magee-Womens Research Institute · US

Funding

Mechanisms of Leptin Signaling in the HypothalamusR01DK061499 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SAHU, ABHIRAM · 2003 to 2007
$1.4M
Phosphodiesterase-3B Signaling in the Hypothalamus and ObesityR01DK078068 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SAHU, ABHIRAM · 2010 to 2013
$1.3M
LEPTIN ACTION ON HYPOTHALAMIC PEPTIDES GOVERNING FEEDINGR01DK052844 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SAHU, ABHIRAM · 1999 to 2001
$519k
NIDDK NIH HHS DK52844NIDDK NIH HHS DK61499NIDDK NIH HHS DK78068NIDDK NIH HHS R01 DK052844NIDDK NIH HHS R01 DK061499NIDDK NIH HHS R01 DK078068
6 · The paper itself

Abstract

Leptin is secreted primarily by fat cells and acts centrally, particularly in the hypothalamus, to reduce food intake and body weight. Besides the classical JAK2 (Janus kinase-2)-STAT3 (signal transducer and activator of transcription-3) pathway, several non-STAT3 pathways play an important role in mediating leptin signaling in the hypothalamus. We have demonstrated that leptin action in the hypothalamus is mediated by an insulin-like signaling pathway involving stimulation of PI3K (phosphatidylinositol-3 kinase) and PDE3B (phosphodiesterase-3B), and reduction in cAMP levels, and that a PI3K-PDE3B-cAMP pathway interacting with the JAK2-STAT3 pathway constitutes a critical component of leptin signaling in the hypothalamus. It appears that defective regulation of multiple signaling pathways in the hypothalamus causes central leptin resistance, a major cause of obesity. In this regard, we have shown that leptin resistance in hypothalamic neurons following chronic central infusion of this hormone is associated with a defect in the PI3K-PDE3B-cAMP, and not due to compromised signaling in the JAK2-STAT3 pathway. Similarly, the PI3K, but not the STAT3, pathway is impaired in the hypothalamus during the development of diet-induced obesity. Additionally, our recent work suggests that suppressor of cytokine signaling-3 negatively regulates the PI3K pathway of leptin signaling in the hypothalamus, a mechanism expected to play a significant role in diet-induced obesity. Together, the PI3K-PDE3B-cAMP pathway appears to emerge as a major mechanism of leptin signaling in the hypothalamus in regulating energy balance.

Indexed as

Cyclic AMPCyclic Nucleotide Phosphodiesterases, Type 3HumansHypothalamusLeptinNeuronsPhosphatidylinositol 3-KinasesSignal TransductionCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 3LeptinPDE3B protein, humanPhosphatidylinositol 3-Kinases

Identifiers

PMID21464566
PMCPMC3130491
OpenAlexW2033220684

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.