Evidence map›Paper›PMID 31495688›Full record

ArticleCell metabolism2019

Partial Leptin Reduction as an Insulin Sensitization and Weight Loss Strategy.

Shangang Zhao, Yi Zhu, Robbie D Schultz, Na Li, Zhenyan He, Zhuzhen Zhang, Alexandre Caron, Qingzhang Zhu, Kai Sun, Wei Xiong and 15 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
167citing papers in PubMed, 2 pooled it
16.8field-weighted citation impact, top 1% 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

167 citing papers in PubMed, 2 syntheses or guidelines pooled it, 300 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Trial
  6. Effects ofNutrients · 2022
    Trial
  7. Trial
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Leptin antagonism improves Rett syndrome phenotype in symptomatic Mecp2-deficient mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  14. TonEBP as a key regulator of hypothalamic leptin signaling and resistance.Cellular and molecular life sciences : CMLS · 2026
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors at 7 institutions in 3 countries.

Shangang ZhaoTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Yi ZhuTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Robbie D SchultzTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Na LiTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Endocrinology and Metabolism, Tianjin Medical University General Hospital, Tianjin 300052, China.
Zhenyan HeDivision of Hypothalamic Research, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Neurosurgery and Endocrinology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
Zhuzhen ZhangTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Alexandre CaronDivision of Hypothalamic Research, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Qingzhang ZhuTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Kai SunTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA; Center for Metabolic and Degenerative Diseases, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Wei XiongTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Hui DengTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Jia SunDivision of Hypothalamic Research, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Neurosurgery and Endocrinology, Zhujiang Hospital, Southern Medical University, Guangzhou 510282, China.
Yingfeng DengTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Min KimTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Biological Sciences, School of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, South Korea.
Charlotte E LeeDivision of Hypothalamic Research, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Ruth GordilloTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Tiemin LiuDivision of Hypothalamic Research, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Angela K OdleNeurobiology & Developmental Sciences, College of Medicine, University of Arkansas for Medical Sciences.
Gwen V ChildsNeurobiology & Developmental Sciences, College of Medicine, University of Arkansas for Medical Sciences.
Ningyan ZhangTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Christine M KusminskiTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Joel K ElmquistDivision of Hypothalamic Research, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Kevin W WilliamsDivision of Hypothalamic Research, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
Zhiqiang AnTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, TX, USA.
Philipp E SchererTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: philipp.scherer@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USBrown Foundation · USUniversity of Arkansas for Medical Sciences · USZhujiang Hospital · CNSouthwestern Medical Center · USTianjin Medical University General Hospital · CNUniversity of Ulsan · KR

Funding

Novel Mechanisms Regulating the Adipocyte-Brain-Hepatocyte AxisP01DK088761 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI GORDILLO, RUTH · 2010 to 2019
$17.4M
Adiponectin, A Protein Secreted From Adipose TissueR01DK055758 · NIDDK · YESHIVA UNIVERSITY · PI SCHERER, PHILIPP E · 2000 to 2024
$10.9M
Ventromedial Hypothalamic Regulation of Metabolic Changes Induced by ExerciseP01DK119130 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI ELMQUIST, JOEL K. · 2019 to 2023
$10.0M
Generation of Novel Genetic Tools to Study Cellular Heterogeneity in Adipose TissuesRC2DK118620 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI GUPTA, RANA K, SCHERER, PHILIPP E · 2019 to 2023
$7.0M
White Adipose Tissue Physiology, Mitochondrial Function and AdiponectinR01DK099110 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI PHILIPP E SCHERER · 2013 to 2026
$6.7M
Center for Translational NeuroscienceP20GM103425 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI GARCIA-RILL, EDGAR E. · 2012 to 2013
$4.1M
Interactions of Leptin and the Melanocortin SystemR01DK118725 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST · 2018 to 2026
$3.5M
Post-transcriptional Pathways that Signal Leptin Regulation of GonadotropesR01HD087057 · NICHD · UNIV OF ARKANSAS FOR MED SCIS · PI CHILDS, GWEN V, MACNICOL, ANGUS M · 2016 to 2020
$2.3M
Central Mechanisms Regulating Acute Leptin and Insulin SignalingR01DK100699 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI WILLIAMS, KEVIN W · 2014 to 2018
$1.8M
Tropic Roles for Leptin in the Maturation of SomatotropesR01DK113776 · NIDDK · UNIV OF ARKANSAS FOR MED SCIS · PI CHILDS, GWEN V, MACNICOL, ANGUS M · 2017 to 2020
$1.8M
Cellular and Synaptic Reorganization after Exercise TrainingR01DK119169 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI WILLIAMS, KEVIN W · 2018 to 2021
$1.6M
The Significance of Leptin Signals to Neonatal Somatotropes and GonadotropesR01HD059056 · NICHD · UNIV OF ARKANSAS FOR MED SCIS · PI CHILDS, GWEN V · 2009 to 2013
$1.4M
NICHD NIH HHS R01 HD059056NICHD NIH HHS R01 HD087057NICHD NIH HHS R03 HD059066NIDDK NIH HHS K99 DK114498NIDDK NIH HHS K99 DK120894NIDDK NIH HHS P01 DK088761NIDDK NIH HHS P01 DK119130NIDDK NIH HHS R00 DK114498NIDDK NIH HHS R01 DK055758NIDDK NIH HHS R01 DK099110NIDDK NIH HHS R01 DK100699NIDDK NIH HHS R01 DK113776NIDDK NIH HHS R01 DK118725NIDDK NIH HHS R01 DK119169NIDDK NIH HHS RC1 DK086629NIDDK NIH HHS RC2 DK118620NIGMS NIH HHS P20 GM103425
6 · The paper itself

Abstract

The physiological role of leptin is thought to be a driving force to reduce food intake and increase energy expenditure. However, leptin therapies in the clinic have failed to effectively treat obesity, predominantly due to a phenomenon referred to as leptin resistance. The mechanisms linking obesity and the associated leptin resistance remain largely unclear. With various mouse models and a leptin neutralizing antibody, we demonstrated that hyperleptinemia is a driving force for metabolic disorders. A partial reduction of plasma leptin levels in the context of obesity restores hypothalamic leptin sensitivity and effectively reduces weight gain and enhances insulin sensitivity. These results highlight that a partial reduction in plasma leptin levels leads to improved leptin sensitivity, while pointing to a new avenue for therapeutic interventions in the treatment of obesity and its associated comorbidities.

Indexed as

Insulin ResistanceAnimalsAntibodies, NeutralizingEatingEnergy MetabolismInsulinLeptinMiceMice, Inbred StrainsObesityWeight LossWeight Reduction ProgramsAntibodies, NeutralizingInsulinLeptindiabeteshypothalamusleptinleptin resistanceobesity

Identifiers

PMID31495688
PMCPMC6774814
OpenAlexW2971451438

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.