Evidence map›Paper›PMID 20002964›Full record

ArticleJournal of neuroendocrinology2010

The response of glucose-excited neurones in the ventromedial hypothalamus to decreased glucose is enhanced in a murine model of type 2 diabetes mellitus.

V E Cotero, B B Zhang, V H Routh

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroendocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.5field-weighted citation impact, top 44% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  11. Glucosensing in the gastrointestinal tract: Impact on glucose metabolism.American journal of physiology. Gastrointestinal and liver physiology · 2016
    Review
  12. Hypothalamic glucose sensing: making ends meet.Frontiers in systems neuroscience · 2014
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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

3 authors at 3 institutions in 1 country.

V E CoteroDepartment of Pharmacology and Physiology, New Jersey Medical School (UMDNJ), Newark, NJ, USA.
B B Zhang
V H Routh
Merck & Co., Inc., Rahway, NJ, USA (United States) · USRutgers New Jersey Medical SchoolUniversity Hospital, Newark · US

Funding

THE ARCUATE K ATP CHANNEL IN HEALTH, OBESITY AND DIABETER01DK055619 · NIDDK · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ROUTH, VANESSA H · 2000 to 2008
$2.2M
Hormonal regulation of glucose sensing neurons in health and diabetesR56DK055619 · NIDDK · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ROUTH, VANESSA H · 2009 to 2009
$390k
NIDDK NIH HHS 2R01 DK55619NIDDK NIH HHS R01 DK055619NIDDK NIH HHS R56 DK055619NINDS NIH HHS 5F31NS05681
6 · The paper itself

Abstract

Obesity and type 2 diabetes mellitus (T2DM) are associated with dysfunctional insulin signalling and impaired central glucose sensing. Glucose sensing neurones reside in key areas of the brain involved in glucose and energy homeostasis (e.g. ventromedial hypothalamus; VMH). We have recently shown that insulin attenuates the ability of glucose-excited (GE) neurones to sense decreased glucose. We hypothesise that this effect of insulin on VMH GE neurones is impaired during T2DM when insulin signalling is dysfunctional. To test our hypotheses, we used whole cell patch clamp recording techniques to evaluate the effects of insulin on VMH GE neurones in brain slices from wild-type and diabetic (db/db) mice. The effects of decreasing glucose from 2.5 to 0.1 mM on VMH GE neurones were similar in wild-type and db/db mice. However, decreasing glucose from 2.5 to 0.5 mM decreased the action potential frequency, membrane potential and input resistance of VMH GE neurones to a significantly greater extent in db/db versus wild-type mice. Furthermore, insulin (5 nM) blunted the effects of decreased glucose in wild-type, but not db/db mice. These differences in both glucose and insulin sensitivity between wild-type and db/db mice were completely ameliorated by the insulin sensitiser, Compound 2 (300 nM). These data are consistent with our hypothesis that impaired insulin signalling in T2DM sensitises VMH GE neurones to decreased glucose.

Indexed as

ActinsAction PotentialsAnimalsBlotting, WesternCell MembraneDiabetes Mellitus, ExperimentalExtracellular SpaceGlucoseInsulinIn Vitro TechniquesMaleMembrane PotentialsMiceMice, TransgenicNeuronsPatch-Clamp TechniquesActinsGlucoseInsulin

Identifiers

PMID20002964
PMCPMC4270105
OpenAlexW2084891762

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.