Evidence map›Paper›PMID 21393446›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2011

Glucosensing by GnRH neurons: inhibition by androgens and involvement of AMP-activated protein kinase.

Alison V Roland, Suzanne M Moenter

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.0field-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

33 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Altered Electrophysiology and Transcriptome of GnRH Neurons in Middle-Aged Female Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  3. Article
  4. Review
  5. Neuromodulation or energy failure? Metabolic limitations silence network output in the hypoxic amphibian brainstem.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  6. Review
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  8. Article
  9. Review
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  11. Article
  12. Metabolic regulation of female puberty via hypothalamic AMPK-kisspeptin signaling.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  13. Review
  14. Remote control of glucose-sensing neurons to analyze glucose metabolism.American journal of physiology. Endocrinology and metabolism · 2018
    Review
  15. Article
  16. Article
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  20. 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

2 authors at 2 institutions in 1 country.

Alison V RolandDepartment of Pharmacology, University of Virginia, Charlottesville, Virginia 22908, USA.
Suzanne M Moenter
University of Michigan–Ann Arbor · USUniversity of Virginia · US

Funding

PROJECT 3 - Steroid-Metabolic Interactions In the Control of GnRH NeuronsU54HD028934 · NICHD · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI MARSHALL, JOHN C · 1998 to 2013
$16.5M
Interactions between metabolic cues and androgens in the control of GnRH neuronsF31NS062646 · NINDS · UNIVERSITY OF VIRGINIA · PI ROLAND, ALISON V · 2008 to 2010
$71k
NICHD NIH HHS U54 HD028934NICHD NIH HHS U54 HD28934NINDS NIH HHS F31 NS062646NINDS NIH HHS F31 NS62646
6 · The paper itself

Abstract

GnRH neurons integrate steroidal and metabolic cues to regulate fertility centrally. Central glucoprivation reduces LH secretion, which is governed by GnRH release, suggesting GnRH neuron activity is modulated by glucose availability. Here we tested whether GnRH neurons can sense changes in extracellular glucose, and whether glucosensing is altered by the steroids dihydrotestosterone (DHT) and/or estradiol (E). Extracellular recordings were made from GnRH neurons in brain slices from ovariectomized (OVX) mice ± DHT and/or E implants. Firing rate was reduced by a switch from 4.5 to 0.2 mm glucose in cells from OVX, OVX+E, and OVX+DHT+E mice, but not OVX+DHT mice. This suggests that androgens reduce the sensitivity of GnRH neurons to changes in extracellular glucose, but E mitigates this effect. Next we investigated potential mechanisms. In the presence of the ATP-sensitive potassium channel antagonist tolbutamide, glucosensing persisted. In contrast, glucosensing was attenuated in the presence of compound C, an antagonist of AMP-activated protein kinase (AMPK), suggesting a role for AMPK in glucosensing. The AMPK activator N1-(b-D-ribofuranosyl)-5-aminoimidazole-4-carboxamide (AICAR) mimicked the effect of low glucose and was less effective in cells from DHT-treated mice. The effect of DHT to diminish responses to low glucose and AICAR was abolished by blockade of fast synaptic transmission. Both AICAR and low glucose activated a current with a reversal potential near -50 mV, suggesting a nonspecific cation current. These studies indicate that glucosensing is one mechanism by which GnRH neurons sense fuel availability and point to a novel role for AMPK in the central regulation of fertility.

Indexed as

6-Cyano-7-nitroquinoxaline-2,3-dioneAminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsBrainDihydrotestosteroneEnzyme ActivationEstrogensFemaleGABA AntagonistsGlucoseGonadotropin-Releasing HormoneIn Vitro TechniquesMembrane PotentialsMiceMice, Transgenic2-amino-5-phosphopentanoic acid6-Cyano-7-nitroquinoxaline-2,3-dioneAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesDihydrotestosteroneEstrogensGABA AntagonistsGlucoseGonadotropin-Releasing HormoneN-MethylaspartateRibonucleotidesValine

Identifiers

PMID21393446
PMCPMC3082325
OpenAlexW1974898957

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.