Evidence map›Paper›PMID 24523344›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2014

Systemic leptin dose-dependently increases STAT3 phosphorylation within hypothalamic and hindbrain nuclei.

James W Maniscalco, Linda Rinaman

Abstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Leptin in the VMH contributes to the initial overconsumption of palatable diets by rats.American journal of physiology. Endocrinology and metabolism · 2025
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  9. Consuming sucrose solution promotes leptin resistance and site specifically modifies hypothalamic leptin signaling in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
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  12. Leptin Sensitizes NTS Neurons to Vagal Input by Increasing Postsynaptic NMDA Receptor Currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
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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

2 authors at 1 institution in 1 country.

James W ManiscalcoDepartment of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania.
Linda Rinaman
University of Pittsburgh · US

Funding

POSTNATAL DEVELOPMENT OF VAGAL-HYPOTHALAMIC CONNECTIONSR01MH059911 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI RINAMAN, LINDA M · 1999 to 2024
$7.3M
Brainstem Satiety Circuits and High Fat Diet HyperphagiaR01DK100685 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI RINAMAN, LINDA M · 2014 to 2018
$1.6M
NIDDK NIH HHS R01 DK100685NIMH NIH HHS MH59911
6 · The paper itself

Abstract

Leptin released peripherally acts within the central nervous system (CNS) to modulate numerous physiological and behavioral functions. Histochemical identification of leptin-responsive CNS cells can reveal the specific cellular phenotypes and neural circuits through which leptin signaling modulates these functions. Leptin signaling elicits phosphorylation of signal transducer and activator of transcription 3 (pSTAT3), making pSTAT3-immunoreactivity (ir) a useful proxy for identifying leptin-responsive cells. Relatively low systemic doses of leptin (i.e., 10-130 μg/kg body wt) are sufficient to decrease food intake, inhibit gastric emptying, and increase sympathetic activity, but there are no histological reports of central pSTAT3-ir following leptin doses within this range. Considering this, we quantified central pSTAT3-ir in rats after intraperitoneal injections of leptin at doses ranging from 50 to 800 μg/kg body wt. Tissue sections were processed to identify pSTAT3-ir alone or in combination with immunolabeling for cocaine- and amphetamine-regulated transcript (CART), glucagon-like peptide-1 (GLP-1), prolactin-releasing peptide (PrRP), or dopamine-β-hydroxylase (DβH). Leptin doses as low as 50, 100, and 200 μg/kg body wt significantly increased the number of pSTAT3-ir cells in the arcuate nucleus of the hypothalamus (ARC), nucleus of the solitary tract (NTS), and ventromedial nucleus of the hypothalamus, respectively, and also led to robust pSTAT3 labeling in neural processes. The differential dose-dependent increases in pSTAT3-ir across brain regions provide new information regarding central leptin sensitivity. Within the ARC, CART-ir and pSTAT3-ir were often colocalized, consistent with evidence of leptin sensitivity in this neural population. Conversely, within the NTS, pSTAT3 only rarely colocalized with PrRP and/or DβH, and never with GLP-1.

Indexed as

AnimalsArcuate Nucleus of HypothalamusGlucagon-Like Peptide 1HypothalamusLeptinMaleNeuronsPhosphorylationProto-Oncogene Proteins c-fosRatsRats, Sprague-DawleyRhombencephalonSignal TransductionSolitary NucleusSTAT3 Transcription FactorGlucagon-Like Peptide 1LeptinProto-Oncogene Proteins c-fosStat3 protein, ratSTAT3 Transcription Factorarcuate nucleus of the hypothalamuscocaine- and amphetamine-regulated transcriptglucagon-like peptide-1leptinnoradrenergicnucleus of the solitary tractprolactin-releasing peptidesignal transducer and activator of transcription 3ventromedial nucleus of the hypothalamus

Identifiers

PMID24523344
PMCPMC4120405
OpenAlexW1964016978

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.