Evidence map›Paper›PMID 27688996›Full record

ArticleMolecular metabolism2016

Estrogens modulate ventrolateral ventromedial hypothalamic glucose-inhibited neurons.

Ammy M Santiago, Deborah J Clegg, Vanessa H Routh

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Susceptibility of Glucose Regulation to Social Isolation.bioRxiv : the preprint server for biology · 2025
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  20. Essential and sex-specific effects of mGluR5 in ventromedial hypothalamus regulating estrogen signaling and glucose balance.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
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.

Ammy M SantiagoNew Jersey Medical School, Rutgers University, 185 South Orange Ave, Newark, NJ 07103, United States. Electronic address: santiaa1@njms.rutgers.edu.
Deborah J CleggCedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048, United States. Electronic address: Deborah.Clegg@cshs.org.
Vanessa H RouthNew Jersey Medical School, Rutgers University, 185 South Orange Ave, Newark, NJ 07103, United States. Electronic address: routhvh@njms.rutgers.edu.
Rutgers, The State University of New Jersey · USCedars-Sinai Medical Center · US

Funding

Hypoglycemia-induced NO in glucose sensing neurons and counterregulationR01DK081538 · NIDDK · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ROUTH, VANESSA H · 2009 to 2013
$1.7M
Characterization of Estrogen Sensitive Ventromedial Hypothalamic Glucose SensingF31DK093331 · NIDDK · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI SANTIAGO, AMMY MARIE · 2011 to 2014
$115k
NIDDK NIH HHS F31 DK093331NIDDK NIH HHS R01 DK081538
6 · The paper itself

Abstract

objectiveBrain regulation of glucose homeostasis is sexually dimorphic; however, the impact sex hormones have on specific neuronal populations within the ventromedial hypothalamic nucleus (VMN), a metabolically sensitive brain region, has yet to be fully characterized. Glucose-excited (GE) and -inhibited (GI) neurons are located throughout the VMN and may play a critical role in glucose and energy homeostasis. Within the ventrolateral portion of the VMN (VL-VMN), glucose sensing neurons and estrogen receptor (ER) distributions overlap. We therefore tested the hypothesis that VL-VMN glucose sensing neurons were sexually dimorphic and regulated by 17β-estradiol (17βE).

methodsElectrophysiological recordings of VL-VMN glucose sensing neurons in brain slices isolated from age- and weight-matched female and male mice were performed in the presence and absence of 17βE.

resultsWe found a new class of VL-VMN GI neurons whose response to low glucose was transient despite continued exposure to low glucose. Heretofore, we refer to these newly identified VL-VMN GI neurons as 'adapting' or AdGI neurons. We found a sexual dimorphic response to low glucose, with male nonadapting GI neurons, but not AdGI neurons, responding more robustly to low glucose than those from females. 17βE blunted the response of both nonadapting GI and AdGI neurons to low glucose in both males and females, which was mediated by activation of estrogen receptor β and inhibition of AMP-activated kinase. In contrast, 17βE had no impact on GE or non-glucose sensing neurons in either sex.

conclusionThese data suggest sex differences and estrogenic regulation of VMN hypothalamic glucose sensing may contribute to the sexual dimorphism in glucose homeostasis.

Indexed as

17βE, 17β-estradiol17β-estradiolAICAR, aminoimidazole-4-carboxamide-1-β-d-ribofuranosideAMP-activated kinaseAMPK, AMP-activated protein kinaseARC, arcuate nucleusBSA-17βE, bovine serum albumin-conjugated 17βECC, compound CER, estrogen receptorGABA, γ-aminobutyric acidGE, glucose-excitedGI, glucose-inhibitedGlucose excited neuronsGlucose inhibited neuronsHRP, horse radish peroxidaseIR, input resistanceMPP, methylphenolpyrazoleNGS, non-glucose sensingPHTPP, phenyltrifluoromethylpyrazolophenolPOMC, pro-opiomelanocortinPVDF, polyvinylidene difluorideSexual dimorphismSF-1, steroidogenic factorTTX, tetrodotoxinVentromedial hypothalamic nucleusVL-VMN, ventrolateral VMNVMH, ventromedial hypothalamusVm, membrane potentialVMN, ventromedial hypothalamic nucleus

Identifiers

PMID27688996
PMCPMC5034617
OpenAlexW2516084959

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.