Evidence map›Paper›PMID 19535676›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2009

Characteristics and mechanisms of hypothalamic neuronal fatty acid sensing.

Christelle Le Foll, Boman G Irani, Christophe Magnan, Ambrose A Dunn-Meynell, Barry E Levin

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

62 citing papers in PubMed, 151 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Pathophysiology of Lipid Droplets in Neuroglia.Antioxidants (Basel, Switzerland) · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Oleic Acid in the Ventral Tegmental Area Inhibits Feeding, Food Reward, and Dopamine Tone.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Oleate induces KNeuroscience · 2017
    Article
  19. Review
  20. Review

2 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Christelle Le FollNeurology Service, VA Medical Center, 385 Tremont Ave., East Orange, NJ 07018-1095, USA.
Boman G Irani
Christophe Magnan
Ambrose A Dunn-Meynell
Barry E Levin
East Orange VA Medical Center · US

Funding

BRAIN GLUCOSENSING NEURONS IN HEALTH AND DIABETESR01DK053181 · NIDDK · VETERANS BIOMEDICAL RESEARCH INSTITUTE · PI LEVIN, BARRY E · 1998 to 2014
$5.6M
NIDDK NIH HHS DK-53181
6 · The paper itself

Abstract

We assessed the mechanisms by which specialized hypothalamic ventromedial nucleus (VMN) neurons utilize both glucose and long-chain fatty acids as signaling molecules to alter their activity as a potential means of regulating energy homeostasis. Fura-2 calcium (Ca(2+)) and membrane potential dye imaging, together with pharmacological agents, were used to assess the mechanisms by which oleic acid (OA) alters the activity of dissociated VMN neurons from 3- to 4-wk-old rats. OA excited up to 43% and inhibited up to 29% of all VMN neurons independently of glucose concentrations. In those neurons excited by both 2.5 mM glucose and OA, OA had a concentration-dependent effective excitatory concentration (EC(50)) of 13.1 nM. Neurons inhibited by both 2.5 mM glucose and OA had an effective inhibitory concentration (IC(50)) of 93 nM. At 0.5 mM glucose, OA had markedly different effects on these same neurons. Inhibition of carnitine palmitoyltransferase, reactive oxygen species formation, long-chain acetyl-CoA synthetase and ATP-sensitive K(+) channel activity or activation of uncoupling protein 2 (UCP2) accounted for only approximately 20% of OA's excitatory effects and approximately 40% of its inhibitory effects. Inhibition of CD36, a fatty acid transporter that can alter cell function independently of intracellular fatty acid metabolism, reduced the effects of OA by up to 45%. Thus OA affects VMN neuronal activity through multiple pathways. In glucosensing neurons, its effects are glucose dependent. This glucose-OA interaction provides a potential mechanism whereby such "metabolic sensing" neurons can respond to differences in the metabolic states associated with fasting and feeding.

Indexed as

Calcium SignalingEnergy MetabolismAnimalsCarnitine O-PalmitoyltransferaseCD36 AntigensCoenzyme A LigasesEnzyme InhibitorsFree Radical ScavengersGlucoseHomeostasisIon ChannelsKATP ChannelsMaleMembrane PotentialsMicroscopy, FluorescenceMitochondrial ProteinsCarnitine O-PalmitoyltransferaseCD36 AntigensCoenzyme A LigasesEnzyme InhibitorsFree Radical ScavengersGlucoseIon ChannelsKATP ChannelsMitochondrial ProteinsOleic AcidPotassium Channel BlockersReactive Oxygen SpeciesUcp2 protein, ratUncoupling Protein 2

Identifiers

PMID19535676
PMCPMC2739790
OpenAlexW2067285665

What OpenQuestion holds

Textmetadata
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.