Evidence map›Paper›PMID 23599282›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Leptin resistance is a secondary consequence of the obesity in ciliopathy mutant mice.

Nicolas F Berbari, Raymond C Pasek, Erik B Malarkey, S M Zaki Yazdi, Andrew D McNair, Wesley R Lewis, Tim R Nagy, Robert A Kesterson, Bradley K Yoder

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
9.0field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Treatment of Hypothalamic Obesity With GLP-1 Analogs.Journal of the Endocrine Society · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Hypothalamic primary cilium: A hub for metabolic homeostasis.Experimental & molecular medicine · 2021
    Review
  16. Article
  17. Artificial Intelligence Approaches to Assessing Primary Cilia.Journal of visualized experiments : JoVE · 2021
    Article
  18. Article
  19. Cilia signaling and obesity.Seminars in cell & developmental biology · 2021
    Review
  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

9 authors at 2 institutions in 2 countries.

Nicolas F BerbariDepartment of Cell, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Raymond C Pasek
Erik B Malarkey
S M Zaki Yazdi
Andrew D McNair
Wesley R Lewis
Tim R Nagy
Robert A Kesterson
Bradley K Yoder
Nutrition Sciences (Belgium) · BEUniversity of Alabama at Birmingham · US

Funding

Why is the prevalence of obesity so high in U.S. Southern States? Regional predictors of BMI and obesity treatment response.P30DK056336 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Gareth R Dutton · 2000 to 2026
$31.9M
ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
UAB Diabetes Research and Training CenterP60DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GARVEY, W TIMOTHY · 2008 to 2012
$8.4M
Training Program in Cell, Molecular, and Developmental BiologyT32GM008111 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YODER, BRADLEY K. · 1985 to 2022
$5.4M
Cilial dysfunction and pathogenesis of obesityR01DK075996 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YODER, BRADLEY K. · 2007 to 2010
$1.2M
Transcription Factor GATA-1 in Erythro-Megakaryocytic Development and LeukemiaR21DK075966 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI WEISS, MITCHELL J · 2006 to 2007
$448k
The Role of Primary Neuronal Cilia in Appetite and SatiationF32DK088404 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BERBARI, NICOLAS F · 2010 to 2011
$104k
TRAINING GRANT IN PULMONARY DISEASET32HL007578 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI WANNER, ADAM · 1985 to 1988
–
NHLBI NIH HHS T32 HL7578NIAMS NIH HHS P30 AR048311NIDDK NIH HHS F32 DK088404NIDDK NIH HHS P30 DK056336NIDDK NIH HHS P60 DK079626NIDDK NIH HHS R01DK075966-03S1NIDDK NIH HHS R01 DK075996NIDDK NIH HHS R21 DK075966NIGMS NIH HHS T32 GM008111
6 · The paper itself

Abstract

Although primary cilia are well established as important sensory and signaling structures, their function in most tissues remains unknown. Obesity is a feature associated with some syndromes of cilia dysfunction, such as Bardet-Biedl syndrome (BBS) and Alström syndrome, as well as in several cilia mutant mouse models. Recent data indicate that obesity in BBS mutant mice is due to defects in leptin receptor trafficking and leptin resistance. Furthermore, induction of cilia loss in leptin-responsive proopiomelanocortin neurons results in obesity, implicating cilia on hypothalamic neurons in regulating feeding behavior. Here, we directly test the importance of the cilium as a mediator of the leptin response. In contrast to the current dogma, a longitudinal study of conditional Ift88 cilia mutant mice under different states of adiposity indicates that leptin resistance is present only when mutants are obese. Our studies show that caloric restriction leads to an altered anticipatory feeding behavior that temporarily abrogates the anorectic actions of leptin despite normalized circulating leptin levels. Interestingly, preobese Bbs4 mutant mice responded to the anorectic effects of leptin and did not display other phenotypes associated with defective leptin signaling. Furthermore, thermoregulation and activity measurements in cilia mutant mice are inconsistent with phenotypes previously observed in leptin deficient ob/ob mice. Collectively, these data indicate that cilia are not directly involved in leptin responses and that a defect in the leptin signaling axis is not the initiating event leading to hyperphagia and obesity associated with cilia dysfunction.

Indexed as

AnimalsBardet-Biedl SyndromeBody CompositionCiliaDisease Models, AnimalFeeding BehaviorLeptinMiceMice, ObeseMice, TransgenicMotor ActivityMutationNeuronsObesityPhenotypeSignal TransductionLeptin

Identifiers

PMID23599282
PMCPMC3651481
OpenAlexW1998857508

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.