Evidence map›Paper›PMID 24011078›Full record

ArticleCell metabolism2013

K(ATP)-channel-dependent regulation of catecholaminergic neurons controls BAT sympathetic nerve activity and energy homeostasis.

Sulay Tovar, Lars Paeger, Simon Hess, Donald A Morgan, A Christine Hausen, Hella S Brönneke, Brigitte Hampel, P Justus Ackermann, Nadine Evers, Hildegard Büning and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.3field-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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Central noradrenaline transporter availability in highly obese, non-depressed individuals.European journal of nuclear medicine and molecular imaging · 2017
    Trial
  2. FGF21 acting on the noradrenergic nervous system protects against influenza virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Integrating causal human genetics andFrontiers in molecular biosciences · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Energy metabolism and syncope.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
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

14 authors at 4 institutions in 2 countries.

Sulay TovarDepartment of Mouse Genetics and Metabolism, Institute for Genetics and Center for Molecular Medicine (CMMC), University of Cologne, Zülpicher Strasse 47b, 50674 Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Zülpicher Strasse 47b, 50674 Cologne, Germany; Max Planck Institute for Neurological Research, Gleueler Strasse 50, 50931 Cologne, Germany.
Lars Paeger
Simon Hess
Donald A Morgan
A Christine Hausen
Hella S Brönneke
Brigitte Hampel
P Justus Ackermann
Nadine Evers
Hildegard Büning
F Thomas Wunderlich
Kamal Rahmouni
Peter Kloppenburg
Jens C Brüning
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DEMax Planck Institute for Metabolism Research · DEUniversity of Iowa · US

Funding

Role of the brain Renin-Angiotensin Sys. in Cardiovas and Metabolic RegulationP01HL084207 · NHLBI · UNIVERSITY OF IOWA · PI GROBE, JUSTIN L · 2007 to 2022
$30.2M
NHLBI NIH HHS HL084207NHLBI NIH HHS P01 HL084207
6 · The paper itself

Abstract

Brown adipose tissue (BAT) is a critical regulator of glucose, lipid, and energy homeostasis, and its activity is tightly controlled by the sympathetic nervous system. However, the mechanisms underlying CNS-dependent control of BAT sympathetic nerve activity (SNA) are only partly understood. Here, we demonstrate that catecholaminergic neurons in the locus coeruleus (LC) adapt their firing frequency to extracellular glucose concentrations in a K(ATP)-channel-dependent manner. Inhibiting K(ATP)-channel-dependent control of neuronal activity via the expression of a variant K(ATP) channel in tyrosine-hydroxylase-expressing neurons and in neurons of the LC enhances diet-induced obesity in mice. Obesity results from decreased energy expenditure, lower steady-state BAT SNA, and an attenuated ability of centrally applied glucose to activate BAT SNA. This impairs the thermogenic transcriptional program of BAT. Collectively, our data reveal a role of K(ATP)-channel-dependent neuronal excitability in catecholaminergic neurons in maintaining thermogenic BAT sympathetic tone and energy homeostasis.

Indexed as

Adipose Tissue, BrownAnimalsCholinergic NeuronsDiet, High-FatEnergy MetabolismGlucoseKcnj11 ChannelLocus CoeruleusMaleMiceMice, Inbred C57BLMice, TransgenicMutationObesityPotassium Channels, Inwardly RectifyingSympathetic Nervous SystemGlucoseKcnj11 ChannelPotassium Channels, Inwardly RectifyingTyrosine 3-Monooxygenase

Identifiers

PMID24011078
PMCPMC5684875
OpenAlexW2008967906

What OpenQuestion holds

Textmetadata
LicenceTDM
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.