Evidence map›Paper›PMID 18508097›Full record

ReviewPhysiology & behavior2008

Leptin resistance and the response to positive energy balance.

Christopher D Morrison

Open access · greenAbstract readReview
In one paragraph

Review in Physiology & behavior, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Luciferase Reporter Mice forJournal of the Endocrine Society · 2019
    Article
  10. Review
  11. Life in the fat lane: seasonal regulation of insulin sensitivity, food intake, and adipose biology in brown bears.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2017
    Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Leptin resistance does not induce hyperphagia in the rat.The journal of physiological sciences : JPS · 2012
    Article
  17. Bidirectional metabolic regulation of neurocognitive function.Neurobiology of learning and memory · 2011
    Review
  18. Article
  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

1 author at 1 institution in 1 country.

Christopher D MorrisonPennington Biomedical Research Center, Baton Rouge, LA 70808, USA. morriscd@pbrc.edu
Pennington Biomedical Research Center · US

Funding

Research BaseP30DK072476 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI ROBERT A KESTERSON · 2005 to 2026
$26.5M
THE ROLE OF PROTEIN MALNUTRITION ON CIRCADIAN PHYSIOLOGY OF C57BL/6J MOUSE DAMSP20RR021945 · NCRR · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI GETTYS, THOMAS W · 2006 to 2011
$9.5M
Hypothalamic Leptin and Insulin SignalingR03NS051570 · NINDS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI MORRISON, CHRISTOPHER D · 2006 to 2007
$145k
NCRR NIH HHS P20 RR021945NIDDK NIH HHS P30 DK072476NINDS NIH HHS R03 NS051570
6 · The paper itself

Abstract

Animals readily reduce food intake and normalize body weight following a period of involuntary overfeeding, suggesting that regulatory systems are engaged to defend against excess weight gain. However, these data exist in the background of an ongoing obesity epidemic, where the ready availability of palatable, energy dense foods often leads to obesity. Currently we know very little about the mechanisms underlying the normalization of body weight following involuntary overfeeding, nor do we fully understand why select individuals successfully remain lean despite living in an obesigenic environment. Recent progress in the study of leptin signaling indicates that manipulations which enhance leptin sensitivity reduce food intake and attenuate diet-induced obesity, while reductions in leptin signaling predispose to obesity. While it remains unclear whether a failure or insufficiency in the weight regulatory system contributes to obesity, this work highlights the importance of this system for the regulation of body weight and its potential value for the treatment of obesity. Nonetheless, it is necessary to more clearly identify those mechanisms that protect lean individuals from weight gain and mediate the normalization of body weight that follows involuntary overfeeding, because it is only with this knowledge that we can clearly determine whether obesity is dependent on, or independent of, a failure in the weight regulatory system.

Indexed as

Adaptation, PhysiologicalAdipose TissueAnimalsArcuate Nucleus of HypothalamusEnergy MetabolismHumansLeptinNeuronsOvernutritionReceptors, LeptinLeptinReceptors, Leptin

Identifiers

PMID18508097
PMCPMC2517010
OpenAlexW1994069460

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.