Evidence map›Paper›PMID 25268022›Full record

ArticleDiabetes & vascular disease research2015

Direct effects of recurrent hypoglycaemia on adrenal catecholamine release.

Branly O Orban, Vanessa H Routh, Barry E Levin, Joshua R Berlin

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes & vascular disease research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Insights into the role of neuronal glucokinase.American journal of physiology. Endocrinology and metabolism · 2016
    Review
  7. Article
  8. Fasting induces a form of autonomic synaptic plasticity that prevents hypoglycemia.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  9. Orexin signaling is necessary for hypoglycemia-induced prevention of conditioned place preference.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  10. 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

4 authors at 3 institutions in 1 country.

Branly O OrbanDepartment of Pharmacology & Physiology, New Jersey Medical School, Rutgers University, Newark, NJ, USA Actavis LLC, Elizabeth, NJ, USA.
Vanessa H RouthDepartment of Pharmacology & Physiology, New Jersey Medical School, Rutgers University, Newark, NJ, USA Department of Neurology & Neurosciences, New Jersey Medical School, Rutgers University, Newark, NJ, USA.
Barry E LevinDepartment of Neurology & Neurosciences, New Jersey Medical School, Rutgers University, Newark, NJ, USA Neurology Service, Veterans Affairs Medical Center, East Orange, NJ, USA.
Joshua R BerlinDepartment of Pharmacology & Physiology, New Jersey Medical School, Rutgers University, Newark, NJ, USA berlinjr@njms.rutgers.edu.
Rutgers, The State University of New Jersey · USAllergan (United States) · USVeterans Biomedical Research Institute · US

Funding

Mechanism for Reduced Adrenomedullary Epinephrine Release in Type 1 DiabetesF31DK086681 · NIDDK · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ORBAN, BRANLY OSVALDO · 2010 to 2012
$91k
NIDDK NIH HHS DK-086681NIDDK NIH HHS F31 DK086681
6 · The paper itself

Abstract

In Type 1 and advanced Type 2 diabetes mellitus, elevation of plasma epinephrine plays a key role in normalizing plasma glucose during hypoglycaemia. However, recurrent hypoglycaemia blunts this elevation of plasma epinephrine. To determine whether recurrent hypoglycaemia affects peripheral components of the sympatho-adrenal system responsible for epinephrine release, male rats were administered subcutaneous insulin daily for 3 days. These recurrent hypoglycaemic animals showed a smaller elevation of plasma epinephrine than saline-injected controls when subjected to insulin-induced hypoglycaemia. Electrical stimulation of an adrenal branch of the splanchnic nerve in recurrent hypoglycaemic animals elicited less release of epinephrine and norepinephrine than in controls, without a change in adrenal catecholamine content. Responsiveness of isolated, perfused adrenal glands to acetylcholine and other acetylcholine receptor agonists was also unchanged. These results indicate that recurrent hypoglycaemia compromised the efficacy with which peripheral neuronal activity stimulates adrenal catecholamine release and demonstrate that peripheral components of the sympatho-adrenal system were directly affected by recurrent hypoglycaemia.

Indexed as

Disease Models, AnimalDown-RegulationAcetylcholineAdrenal GlandsAnimalsBlood GlucoseCholinergic AgonistsElectric StimulationEpinephrineHypoglycemiaMaleMuscarinic AgonistsNicotineNorepinephrinePerfusionPilocarpineAcetylcholineBlood GlucoseCholinergic AgonistsEpinephrineMuscarinic AgonistsNicotineNorepinephrinePilocarpineReceptors, CholinergicAdrenal glandcatecholaminesdiabetesinsulinratrecurrent hypoglycaemiasplanchnic nerve

Identifiers

PMID25268022
PMCPMC8771481
OpenAlexW2111318745

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.