Evidence map›Paper›PMID 21343257›Full record

ArticleEndocrinology2011

Differential acute and chronic effects of leptin on hypothalamic astrocyte morphology and synaptic protein levels.

Cristina García-Cáceres, Esther Fuente-Martín, Emma Burgos-Ramos, Miriam Granado, Laura M Frago, Vicente Barrios, Tamas Horvath, Jesús Argente, Julie A Chowen

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 101 citations in OpenAlex.

  1. Review
  2. Hypothalamic regulation of energy homeostasis: Quo vadis.Reviews in endocrine & metabolic disorders · 2026
    Review
  3. Astrocyte involvement in metabolic regulation and disease.Trends in endocrinology and metabolism: TEM · 2025
    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

9 authors at 5 institutions in 2 countries.

Cristina García-CáceresDepartment of Endocrinology, Hospital Infantil Universitario Niño Jesús, Avenida Menéndez Pelayo, 65, 28009 Madrid, Spain.
Esther Fuente-Martín
Emma Burgos-Ramos
Miriam Granado
Laura M Frago
Vicente Barrios
Tamas Horvath
Jesús Argente
Julie A Chowen
Centro de Investigación Biomédica en Red · ESHospital Infantil Universitario Niño Jesús · ESInstituto de Salud Carlos III · ESUniversidad Autónoma de Madrid · ESYale University · US

Funding

Developmental insulin/leptin signaling determines set-point of the adult melanocoR01DK080000 · NIDDK · YALE UNIVERSITY · PI HORVATH, TAMAS L · 2008 to 2011
$1.5M
NIDDK NIH HHS R01 DK080000
6 · The paper itself

Abstract

Astrocytes participate in neuroendocrine functions partially through modulation of synaptic input density in the hypothalamus. Indeed, glial ensheathing of neurons is modified by specific hormones, thus determining the availability of neuronal membrane space for synaptic inputs, with the loss of this plasticity possibly being involved in pathological processes. Leptin modulates synaptic inputs in the hypothalamus, but whether astrocytes participate in this action is unknown. Here we report that astrocyte structural proteins, such as glial fibrillary acidic protein (GFAP) and vimentin, are induced and astrocyte morphology modified by chronic leptin administration (intracerebroventricular, 2 wk), with these changes being inversely related to modifications in synaptic protein densities. Similar changes in glial structural proteins were observed in adult male rats that had increased body weight and circulating leptin levels due to neonatal overnutrition (overnutrition: four pups/litter vs. control: 12 pups/litter). However, acute leptin treatment reduced hypothalamic GFAP levels and induced synaptic protein levels 1 h after administration, with no effect on vimentin. In primary hypothalamic astrocyte cultures leptin also reduced GFAP levels at 1 h, with an induction at 24 h, indicating a possible direct effect of leptin. Hence, one mechanism by which leptin may affect metabolism is by modifying hypothalamic astrocyte morphology, which in turn could alter synaptic inputs to hypothalamic neurons. Furthermore, the responses to acute and chronic leptin exposure are inverse, raising the possibility that increased glial activation in response to chronic leptin exposure could be involved in central leptin resistance.

Indexed as

AnimalsAnimals, NewbornAstrocytesBlotting, WesternCells, CulturedCell SizeDose-Response Relationship, DrugFemaleGlial Fibrillary Acidic ProteinHypothalamusImmunohistochemistryInfusions, IntraventricularLeptinMaleQa-SNARE ProteinsRatsGlial Fibrillary Acidic ProteinLeptinQa-SNARE ProteinsSynapsinsVimentin

Identifiers

PMID21343257
PMCPMC3860256
OpenAlexW2157077335

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.