Evidence map›Paper›PMID 21652728›Full record

ArticleEndocrinology2011

Fetal hypothalamic neuroprogenitor cell culture: preferential differentiation paths induced by leptin and insulin.

Mina Desai, Tie Li, Michael G Ross

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 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. D-Fructose Exposure Impairs Neuronal Development in Mouse Neural Stem Cells.International journal of molecular sciences · 2026
    Article
  3. Adipogenesis Under Leptin Control: Mechanisms and Model-Specific Effects.International journal of molecular sciences · 2026
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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

3 authors at 2 institutions in 1 country.

Mina DesaiPerinatal Research Laboratories, Department of Obstetrics and Gynecology, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California 90095, USA. mdesai@obgyn.humc.edu
Tie Li
Michael G Ross
Harbor–UCLA Medical Center · USUniversity of California, Los Angeles · US

Funding

Mechanisms of Programmed Gestational HyperphagiaR01HD054751 · NICHD · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI ROSS, MICHAEL GLENN · 2008 to 2012
$1.4M
Programmed Adipogenesis and Lipid DysregulationR01DK081756 · NIDDK · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI DESAI, MINA · 2010 to 2014
$1.4M
Adipocyte Renin-Angiotensin System and Programming of HypertensionR03HD060241 · NICHD · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI DESAI, MINA · 2009 to 2010
$138k
NICHD NIH HHS R01 HD054751NICHD NIH HHS R01HD054751NICHD NIH HHS R03 HD060241NICHD NIH HHS R03HD060241NIDDK NIH HHS R01 DK081756NIDDK NIH HHS R01DK081756
6 · The paper itself

Abstract

In response to temporally orchestrated growth factor stimulation, developing neural stem/progenitor cells undergo extensive self-renewal and then generate neurons and astrocytes. Fetal neonatal leptin and insulin deficiency results in reduced hypothalamic axonal pathways regulating appetite, which may predispose to offspring hyperphagia and obesity. Neural development of the arcuate nucleus, a key target of adiposity signals, leptin and insulin, is immature at birth. Hence, to explore proximate effects of leptin/insulin on hypothalamic development, we determined trophic and differentiation effects on neural stem/progenitor cells using a model of fetal hypothalamic neurospheres (NS). NS cultures were produced from embryonic d 20 fetal rats and passage 1 and passage 2 cells examined for proliferation and differentiation into neurons (neuronal nuclei, class IIIβ-tubulin, and doublecortin) and astrocytes (glial fibrillary acidic protein). Leptin-induced NS proliferation was significantly greater than that induced by insulin, although both effects were blocked by Notch, extracellular signal-regulated kinase, or signal transducer and activator of transcription 3 inhibition. Leptin preferentially induced neuronal, whereas insulin promoted astrocyte differentiation. Extracellular signal-regulated kinase inhibition suppressed both leptin and insulin-mediated differentiation, whereas signal transducer and activator of transcription inhibition only affected leptin-mediated responses. These findings demonstrate preferential and disparate differentiation paths induced by leptin and insulin. Altered fetal exposure to leptin or insulin, resulting from fetal growth restriction, macrosomia, or maternal diabetes, may potentially have marked effects on fetal brain development.

Indexed as

AnimalsArcuate Nucleus of HypothalamusCell DifferentiationDoublecortin ProteinExtracellular Signal-Regulated MAP KinasesFemaleInsulinLeptinNeural Stem CellsPregnancyRatsRats, Sprague-DawleySignal TransductionSTAT3 Transcription FactorDcx protein, ratDoublecortin ProteinExtracellular Signal-Regulated MAP KinasesInsulinLeptinSTAT3 Transcription Factor

Identifiers

PMID21652728
PMCPMC3138224
OpenAlexW2079615051

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.