Evidence map›Paper›PMID 41980928›Full record

ArticleNature communications2026

Thyrotropin-releasing hormone neurons of different hypothalamic nuclei increase energy expenditure.

Andreea Constantinescu, Akila Chandrasekar, Lena Kleindienst, Luca Höhne, Natalia Da Silva Lima, Marius Richter, Vanessa Neve, Frauke Spiecker, Ines Stölting, Wiebke Brandt and 9 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

19 authors.

Andreea Constantinescu *Institute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.ORCID 0000-0002-3081-0755
Akila Chandrasekar *Institute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.
Lena KleindienstInstitute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.
Luca HöhneInstitute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.
Natalia Da Silva LimaDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de, Compostela, Spain.ORCID 0000-0001-9448-4090
Marius RichterInstitute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.
Vanessa NeveInstitute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.
Frauke SpieckerInstitute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.
Ines StöltingInstitute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.
Wiebke BrandtInstitute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.
Urte MatschlDepartment Virus Immunology, Leibniz Institute of Experimental Virology (LIV), Hamburg, Germany.
Jan WenzelInstitute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.ORCID 0000-0001-6313-2439
Rebecca OelkrugInstitute of Experimental Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, Lübeck, Germany.
Vincent PrevotUniv. Lille, Inserm, CHU Lille, Laboratory of Development and Plasticity of the Neuroendocrine Brain, Lille Neuroscience & Cognition, UMR-S 1172, DISTALZ, EGID, Lille, France.ORCID 0000-0001-7185-3615
Heike HeuerDepartment of Endocrinology, Diabetes and Metabolism, University Hospital Essen, University Duisburg-Essen, Essen, Germany.ORCID 0000-0001-7094-6959
Jens MittagInstitute of Experimental Endocrinology, Center of Brain, Behavior and Metabolism, University of Lübeck, Lübeck, Germany.ORCID 0000-0001-7778-5158
Ruben NogueirasDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de, Compostela, Spain.ORCID 0000-0002-9976-9930
Markus SchwaningerInstitute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany.ORCID 0000-0002-4510-9718
Helge Müller-FielitzInstitute of Experimental and Clinical Pharmacology and Toxicology, Center of Brain, Behavior and Metabolism (CBBM), University of Lübeck, Lübeck, Germany. Helge.muellerfielitz@uni-luebeck.de.ORCID 0000-0003-2815-4426

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) GRK1957Deutsche Forschungsgemeinschaft (German Research Foundation) MU 3743/1-1Deutsche Forschungsgemeinschaft (German Research Foundation) Project-ID: 424957847 - CRC/TRR296Deutsche Forschungsgemeinschaft (German Research Foundation) Project-ID: 434396546
6 · The paper itself

Abstract

Several neuronal populations in the hypothalamus and brainstem express thyrotropin-releasing hormone (TRH). While TRH neurons in the paraventricular nucleus (PVN) regulate the thyroid axis, the roles of other TRH-producing neurons remain largely unknown. Here we investigate the role of TRH neurons in the PVN, the dorsomedial hypothalamus (DMH), the medial preoptic area (MPA), and the rostral raphe pallidus (RPa) for metabolism in mice. Selective activation of these populations using chemogenetics in mice revealed that TRH neurons of the hypothalamus increase food intake and influence energy homeostasis in different ways. Specifically, TRH neurons in the PVN and DMH enhance brown adipose tissue activity via a polysynaptic circuit, while MPA-located neurons increase locomotor activity and maintain cold tolerance. These effects were independent of the thyroid axis, demonstrating that TRH neurons have distinct, subtype-specific ways to increase energy expenditure beyond regulating the thyroid axis in mice.

Indexed as

Energy MetabolismHypothalamusNeuronsThyrotropin-Releasing HormoneAdipose Tissue, BrownAnimalsDorsomedial Hypothalamic NucleusEatingMaleMiceMice, Inbred C57BLParaventricular Hypothalamic NucleusPreoptic AreaThyrotropin-Releasing Hormone

Identifiers

PMID41980928
PMCPMC13083850

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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.