Evidence map›Paper›PMID 27666162›Full record

ArticlePhysiology & behavior2016

Ventromedial hypothalamic glucose sensing and glucose homeostasis vary throughout the estrous cycle.

Ammy M Santiago, Deborah J Clegg, Vanessa H Routh

Open access · greenAbstract read
In one paragraph

Article in Physiology & behavior, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Susceptibility of Glucose Regulation to Social Isolation.bioRxiv : the preprint server for biology · 2025
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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

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

objective17β-Estradiol (17βE) regulates glucose homeostasis in part by centrally mediated mechanisms. In female rodents, the influence of the ovarian cycle on hypoglycemia counterregulation and glucose tolerance is unclear. We found previously that in prepubertal females, 17βE modulates glucose sensing in nonadapting glucose-inhibited (GI) and adapting GI (AdGI) neurons within the ventrolateral portion of the ventromedial nucleus (VL-VMN). Nonadapting GI neurons persistently decrease their activity as glucose increases while AdGI neurons transiently respond to a glucose increase. To begin to understand if endogenous fluctuations in estrogen levels across the estrous cycle impact hypothalamic glucose sensing and glucose homeostasis, we assessed whether hypoglycemia counterregulation and glucose tolerance differed across the phases of the estrous cycle. We hypothesized that the response to insulin-induced hypoglycemia (IIH) and/or glucose tolerance would vary throughout the estrous cycle according to changes in 17βE availability. Moreover, that these changes would correlate with estrous-dependent changes in the glucose sensitivity of VL-VMN glucose-sensing neurons (GSNs).

methodsThese hypotheses were tested in female mice by measuring the response to IIH, glucose tolerance and the glucose sensitivity of VL-VMN GSNs during each phase of the estrous cycle. Furthermore, a physiological brain concentration of 17βE seen during proestrus was acutely applied to brain slices isolated on the day of diestrous and the response to low glucose in VL-VMN GSNs was assayed.

resultsThe response to IIH was strongest during diestrous. The response of nonadapting GI and AdGI neurons to a glucose decrease from 2.5 to 0.5mM also peaked during diestrous; an effect which was blunted by the addition of 17βE. In contrast, the glucose sensitivity of the subpopulation of GSNs which are excited by glucose (GE) was not affected by estrous phase or exogenous 17βE application.

conclusionThese data suggest that physiological fluctuations in circulating 17βE levels across the estrous cycle lead to changes in hypothalamic glucose sensing and the response to IIH.

Indexed as

Action PotentialsAnalysis of VarianceAnimalsBlood GlucoseEstradiolEstrous CycleFastingFemaleGlucoseGlucose Tolerance TestHomeostasisInsulinIn Vitro TechniquesMiceMice, Inbred C57BLNeuronsBlood GlucoseEstradiolGlucoseInsulinEstrogenGlucose-excited neuronsGlucose-inhibited neuronsGlucose toleranceHypoglycemia counterregulation

Identifiers

PMID27666162
PMCPMC5159237
OpenAlexW2523663299

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.