Evidence map›Paper›PMID 20179264›Full record

ArticleEndocrinology2010

Brain glucosamine boosts protective glucoprivic feeding.

Mayowa A Osundiji, Ligang Zhou, Jill Shaw, Stephen P Moore, Chen-Yu Yueh, Robert Sherwin, Lora K Heisler, Mark L Evans

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2010. 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
1.8field-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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Insights into the role of neuronal glucokinase.American journal of physiology. Endocrinology and metabolism · 2016
    Review
  5. Review
  6. Stimulation of feeding by three different glucose-sensing mechanisms requires hindbrain catecholamine neurons.American journal of physiology. Regulatory, integrative and comparative physiology · 2014
    Article
  7. Article
  8. Article
  9. Article
  10. 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

8 authors at 3 institutions in 3 countries.

Mayowa A OsundijiUniversity of Cambridge, Institute of Metabolic Science, IMS-MRL, Box 289 Addenbrookes Hospital, Hills Road, Cambridge CB2 0QQ United Kingdom.
Ligang Zhou
Jill Shaw
Stephen P Moore
Chen-Yu Yueh
Robert Sherwin
Lora K Heisler
Mark L Evans
Yale University · USChang Gung University · TWUniversity of Cambridge · GB

Funding

Central Serotonergic Pathways Regulating Energy BalanceR01DK065171 · NIDDK · UNIVERSITY OF CAMBRIDGE · PI HEISLER, LORA K · 2003 to 2007
$899k
Medical Research Council G0600717Medical Research Council G0600717(78464)NIDDK NIH HHS R01 DK065171NIDDK NIH HHS R01DK065171Wellcome Trust 081713
6 · The paper itself

Abstract

The risk of iatrogenic hypoglycemia is increased in diabetic patients who lose defensive glucoregulatory responses, including the important warning symptom of hunger. Protective hunger symptoms during hypoglycemia may be triggered by hypothalamic glucose-sensing neurons by monitoring changes downstream of glucose phosphorylation by the specialized glucose-sensing hexokinase, glucokinase (GK), during metabolism. Here we investigated the effects of intracerebroventricular (ICV) infusion of glucosamine (GSN), a GK inhibitor, on food intake at normoglycemia and protective feeding responses during glucoprivation and hypoglycemia in chronically catheterized rats. ICV infusion of either GSN or mannoheptulose, a structurally different GK inhibitor, dose-dependently stimulated feeding at normoglycemia. Consistent with an effect of GSN to inhibit competitively glucose metabolism, ICV coinfusion of d-glucose but not l-glucose abrogated the orexigenic effect of ICV GSN at normoglycemia. Importantly, ICV infusion of a low GSN dose (15 nmol/min) that was nonorexigenic at normoglycemia boosted feeding responses to glucoprivation in rats with impaired glucose counterregulation. ICV infusion of 15 nmol/min GSN also boosted feeding responses to threatened hypoglycemia in rats with defective glucose counterregulation. Altogether our findings suggest that GSN may be a potential therapeutic candidate for enhancing defensive hunger symptoms during hypoglycemia.

Indexed as

Analysis of VarianceAnimalsBlood GlucoseBrainBrain ChemistryDose-Response Relationship, DrugDrug Administration ScheduleEatingGlucokinaseGlucosamineGlucoseHomeostasisHungerHypoglycemiaMaleMannoheptuloseBlood GlucoseGlucokinaseGlucosamineGlucoseMannoheptuloseProto-Oncogene Proteins c-fos

Identifiers

PMID20179264
PMCPMC2850228
OpenAlexW2145473821

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.