Evidence map›Paper›PMID 20357362›Full record

ArticleDiabetes2010

Pituitary adenylate cyclase-activating polypeptide stimulates glucose production via the hepatic sympathetic innervation in rats.

Chun-Xia Yi, Ning Sun, Mariette T Ackermans, Anneke Alkemade, Ewout Foppen, Jing Shi, Mireille J Serlie, Ruud M Buijs, Eric Fliers, Andries Kalsbeek

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. PACAP regulates neuroendocrine and behavioral stress responses via CRF-containing neurons of the rat hypothalamic paraventricular nucleus.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
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  11. Brain-liver connections: role of the preautonomic PVN neurons.American journal of physiology. Endocrinology and metabolism · 2016
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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

10 authors at 4 institutions in 2 countries.

Chun-Xia YiHypothalamic Integration Mechanisms, Netherlands Institute for Neuroscience, Amsterdam, the Netherlands. c.yi@nin.knaw.nl
Ning Sun
Mariette T Ackermans
Anneke Alkemade
Ewout Foppen
Jing Shi
Mireille J Serlie
Ruud M Buijs
Eric Fliers
Andries Kalsbeek
Academic Medical Center · NLHuazhong University of Science and Technology · CNUniversity of Amsterdam · NLNetherlands Institute for Neuroscience · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe unraveling of the elaborate brain networks that control glucose metabolism presents one of the current challenges in diabetes research. Within the central nervous system, the hypothalamus is regarded as the key brain area to regulate energy homeostasis. The aim of the present study was to investigate the hypothalamic mechanism involved in the hyperglycemic effects of the neuropeptide pituitary adenylyl cyclase-activating polypeptide (PACAP). RESEARCH DESIGN AND

methodsEndogenous glucose production (EGP) was determined during intracerebroventricular infusions of PACAP-38, vasoactive intestinal peptide (VIP), or their receptor agonists. The specificity of their receptors was examined by coinfusions of receptor antagonists. The possible neuronal pathway involved was investigated by 1) local injections in hypothalamic nuclei, 2) retrograde neuronal tracing from the thoracic spinal cord to hypothalamic preautonomic neurons together with Fos immunoreactivity, and 3) specific hepatic sympathetic or parasympathetic denervation to block the autonomic neuronal input to liver.

resultsIntracerebroventricular infusion of PACAP-38 increased EGP to a similar extent as a VIP/PACAP-2 (VPAC2) receptor agonist, and intracerebroventricular administration of VIP had significantly less influence on EGP. The PACAP-38 induced increase of EGP was significantly suppressed by preinfusion of a VPAC2 but not a PAC1 receptor antagonist, as well as by hepatic sympathetic but not parasympathetic denervation. In the hypothalamus, Fos immunoreactivity induced by PACAP-38 was colocalized within autonomic neurons in paraventricular nuclei projecting to preganglionic sympathetic neurons in the spinal cord. Local infusion of PACAP-38 directly into the PVN induced a significant increase of EGP.

conclusionsThis study demonstrates that PACAP-38 signaling via sympathetic preautonomic neurons located in the paraventricular nucleus is an important component in the hypothalamic control of hepatic glucose production.

Indexed as

Analysis of VarianceAnimalsGlucoseHomeostasisInjections, IntraventricularLiverMaleNeuronal Tract-TracersNeuronsParaventricular Hypothalamic NucleusPituitary Adenylate Cyclase-Activating PolypeptideProto-Oncogene Proteins c-fosRatsRats, WistarSympathetic Nervous SystemVasoactive Intestinal PeptideGlucoseNeuronal Tract-TracersPituitary Adenylate Cyclase-Activating PolypeptideProto-Oncogene Proteins c-fosVasoactive Intestinal Peptide

Identifiers

PMID20357362
PMCPMC2889757
OpenAlexW2106400751

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.