Evidence map›Paper›PMID 32312898›Full record

ArticleDiabetes2020

Leptin: Less Is More.

Shangang Zhao, Christine M Kusminski, Joel K Elmquist, Philipp E Scherer

Open access · greenAbstract read
In one paragraph

Article in Diabetes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
6.7field-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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
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  10. Article
  11. Central leptin pathways in metabolic homeostasis.Clinical science (London, England : 1979) · 2025
    Review
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  14. Article
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14 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

4 authors at 1 institution in 1 country.

Shangang ZhaoTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.
Christine M KusminskiTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX.
Joel K ElmquistDivision of Hypothalamic Research, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX philipp.scherer@utsouthwestern.edu joel.elmquist@utsouthwestern.edu.
Philipp E SchererTouchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX philipp.scherer@utsouthwestern.edu joel.elmquist@utsouthwestern.edu.ORCID 0000-0003-0680-3392
The University of Texas Southwestern Medical Center · US

Funding

Novel Mechanisms Regulating the Adipocyte-Brain-Hepatocyte AxisP01DK088761 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI SCHERER, PHILIPP E · 2010 to 2019
$17.4M
Adiponectin, A Protein Secreted From Adipose TissueR01DK055758 · NIDDK · YESHIVA UNIVERSITY · PI SCHERER, PHILIPP E · 2000 to 2024
$10.9M
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
INTERACTIONS OF LEPTIN AND CENTRAL SEROTONIN SYSTEMSR01DK088423 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI ELMQUIST, JOEL K. · 2010 to 2019
$3.8M
Interactions of Leptin and the Melanocortin SystemR01DK118725 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST · 2018 to 2026
$3.5M
NIDDK NIH HHS P01 DK088761NIDDK NIH HHS R01 DK055758NIDDK NIH HHS R01 DK088423NIDDK NIH HHS R01 DK099110NIDDK NIH HHS R01 DK118725NIDDK NIH HHS RC2 DK118620
6 · The paper itself

Abstract

The successful use of leptin for the treatment of individuals with lipodystrophy and leptin deficiency is well established. However, pharmacological approaches of leptin therapy for the treatment of diet-induced obesity have been ineffective. There is ample room for a better understanding of the much famed "leptin resistance" phenomenon. Our recent data in this area prompt us to call for a conceptual shift. This shift entails a model in which a reduction of bioactive leptin levels in the context of obesity triggers a high degree of leptin sensitization and improved leptin action, both centrally and peripherally. Put another way, hyperleptinemia per se causes leptin resistance and associated metabolic disorders. In this perspective, we briefly discuss the underlying conceptual steps that led us to explore partial leptin reduction as a viable therapeutic avenue. We hope this discussion will contribute to potential future applications of partial leptin reduction therapy for the treatment of obesity and type 2 diabetes.

Indexed as

AnimalsBiological EvolutionHumansLeptinMiceObesityLeptin

Identifiers

PMID32312898
PMCPMC7171955
OpenAlexW3016618011

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.