Evidence map›Paper›PMID 27018500›Full record

ReviewChannels (Austin, Tex.)2016

Leptin-mediated ion channel regulation: PI3K pathways, physiological role, and therapeutic potential.

Daniela Gavello, Emilio Carbone, Valentina Carabelli

Open access · goldAbstract readReview
In one paragraph

Review in Channels (Austin, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. eLife · 2022
    Article
  12. AMPA Receptor Function in Hypothalamic Synapses.Frontiers in synaptic neuroscience · 2022
    Review
  13. Article
  14. Leptin: an unappreciated key player in SLE.Clinical rheumatology · 2020
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Cognitive Impairment Due to Leptin Withdrawal in Rat Offspring of Dams with Maternal Diet-Induced Obesity.Medical science monitor : international medical journal of experimental and clinical research · 2018
    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

3 authors at 1 institution in 1 country.

Daniela Gavelloa Department of Drug Science , Lab of Cellular Physiology and Molecular Neuroscience, NIS Center of Excellence, University of Torino , Torino , Italy.
Emilio Carbonea Department of Drug Science , Lab of Cellular Physiology and Molecular Neuroscience, NIS Center of Excellence, University of Torino , Torino , Italy.
Valentina Carabellia Department of Drug Science , Lab of Cellular Physiology and Molecular Neuroscience, NIS Center of Excellence, University of Torino , Torino , Italy.
University of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leptin is produced by adipose tissue and identified as a "satiety signal," informing the brain when the body has consumed enough food. Specific areas of the hypothalamus express leptin receptors (LEPRs) and are the primary site of leptin action for body weight regulation. In response to leptin, appetite is suppressed and energy expenditure allowed. Beside this hypothalamic action, leptin targets other brain areas in addition to neuroendocrine cells. LEPRs are expressed also in the hippocampus, neocortex, cerebellum, substantia nigra, pancreatic β-cells, and chromaffin cells of the adrenal gland. It is intriguing how leptin is able to activate different ionic conductances, thus affecting excitability, synaptic plasticity and neurotransmitter release, depending on the target cell. Most of the intracellular pathways activated by leptin and directed to ion channels involve PI3K, which in turn phosphorylates different downstream substrates, although parallel pathways involve AMPK and MAPK. In this review we will describe the effects of leptin on BK, KATP, KV, CaV, TRPC, NMDAR and AMPAR channels and clarify the landscape of pathways involved. Given the ability of leptin to influence neuronal excitability and synaptic plasticity by modulating ion channels activity, we also provide a short overview of the growing potentiality of leptin as therapeutic agent for treating neurological disorders.

Indexed as

AnalgesicsAnimalsAnticonvulsantsAntidepressive AgentsGene ExpressionHumansIon ChannelsLeptinMiceNeuronsPhosphatidylinositol 3-KinasesPhosphorylationReceptors, LeptinSignal TransductionSynaptic TransmissionAnalgesicsAnticonvulsantsAntidepressive AgentsIon ChannelsLeptinPhosphatidylinositol 3-KinasesReceptors, LeptinCa2+ and TRP channelscell firingKATP and BK channelsLeptinNMDA and AMPA receptorsPI3K

Identifiers

PMID27018500
PMCPMC4954581
OpenAlexW2326795588

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.