Evidence map›Paper›PMID 19056818›Full record

ArticleEndocrinology2009

Hindbrain leptin stimulation induces anorexia and hyperthermia mediated by hindbrain melanocortin receptors.

Karolina P Skibicka, Harvey J Grill

Open access · greenAbstract read
In one paragraph

Article in Endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

53 citing papers in PubMed, 76 citations in OpenAlex.

  1. History and future of leptin: Discovery, regulation and signaling.Metabolism: clinical and experimental · 2024
    Review
  2. Article
  3. Consuming sucrose solution promotes leptin resistance and site specifically modifies hypothalamic leptin signaling in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  4. Loss of leptin receptor-expressing cells in the hindbrain decreases forebrain leptin sensitivity.American journal of physiology. Endocrinology and metabolism · 2020
    Article
  5. Article
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  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Structure, production and signaling of leptin.Metabolism: clinical and experimental · 2015
    Review
  18. Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Karolina P SkibickaGraduate Group of Psychology and Graduate Group of Neuroscience, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. skibicka@mail.med.upenn.edu
Harvey J Grill
University of Pennsylvania · US

Funding

NEURAL HIERARCHY IN THE MODULATION OF INGESTIVE BEHAVIORR01DK021397 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI GRILL, HARVEY J, HAYES, MATTHEW R · 1986 to 2021
$8.8M
Neural Hierarchy in the Modulation of Ingestive BehaviorR56DK021397 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI GRILL, HARVEY J · 2008 to 2008
$434k
Neurally distributed melanocortinergic control of energy expenditureF31NS059254 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI SKIBICKA, KAROLINA P · 2008 to 2009
$66k
NIDDK NIH HHS DK-21397NIDDK NIH HHS R01 DK021397NIDDK NIH HHS R56 DK021397NINDS NIH HHS F31 NS059254NINDS NIH HHS NS-059254
6 · The paper itself

Abstract

Of the central nervous system receptors that could mediate the energy balance effects of leptin, those of the hypothalamic arcuate nucleus receive the greatest attention. Melanocortin receptors (MC-Rs) contribute to the feeding and energetic effects of hypothalamically delivered leptin. Energy balance effects of leptin are also mediated by extrahypothalamic neurons including the hindbrain nucleus tractus solitarius. Hindbrain leptin receptors play a role in leptin's anorectic effects, but their contribution to its energetic effects and their functional interaction with melanocortin systems within the hindbrain remains unexplored. Here rats implanted with telemetric devices for recording energetic/cardiovascular responses were examined to determine whether: 1) hindbrain (fourth ventricular) leptin receptor stimulation triggers energetic and cardiovascular effects, 2) these effects are altered by a 6-wk high-fat diet maintenance, and 3) hindbrain MC-Rs mediate the thermogenic, cardiovascular, and anorexic effects of hindbrain leptin delivery. Results show that hindbrain leptin receptor stimulation produced long-lasting (>6 h) increases in core temperature and heart rate and also decreased food intake and body weight. These responses were not altered by high-fat maintenance, in contrast to what has been reported for forebrain leptin delivery. Fourth ventricular pretreatment with MC-R antagonist SHU 9119 completely abolished the hyperthermia, anorexia, and body weight loss seen with hindbrain-directed leptin but had no effects of its own. These data highlight a role for hindbrain leptin receptors in the initiation of energetic and anorexic responses and show that MCRs are part of the downstream mediation of hindbrain leptin-induced energy balance effects, paralleling effects observed for hypothalamic leptin receptors.

Indexed as

AnimalsAnorexiaBody TemperatureBody WeightDietary FatsEatingEnergy MetabolismFeverGlucose Tolerance TestHeart RateInjectionsLeptinMaleMelanocyte-Stimulating HormonesRatsRats, Sprague-DawleyDietary FatsLeptinMelanocyte-Stimulating HormonesReceptors, MelanocortinSHU 9119

Identifiers

PMID19056818
PMCPMC2659268
OpenAlexW2134520365

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.