Evidence map›Paper›PMID 36889283›Full record

ArticleCell metabolism2023

Estradiol regulates leptin sensitivity to control feeding via hypothalamic Cited1.

Ismael González-García, Elena García-Clavé, Alberto Cebrian-Serrano, Ophélia Le Thuc, Raian E Contreras, Yanjun Xu, Tim Gruber, Sonja C Schriever, Beata Legutko, Jutta Lintelmann and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Cell metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
7.7field-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

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

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Hypothalamic regulation of energy homeostasis: Quo vadis.Reviews in endocrine & metabolic disorders · 2026
    Review
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  10. TonEBP as a key regulator of hypothalamic leptin signaling and resistance.Cellular and molecular life sciences : CMLS · 2026
    Article
  11. Review
  12. Sex-specific systemic metabolic predictors of resistance to calorie restriction-induced weight loss in obese diversity outbred mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 4 institutions in 4 countries.

Ismael González-GarcíaInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany.
Elena García-ClavéInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany.
Alberto Cebrian-SerranoInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany.
Ophélia Le ThucInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany.
Raian E ContrerasInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany; Research Unit NeuroBiology of Diabetes, Helmholtz Zentrum München, 85764 Neuherberg, Germany.
Yanjun XuInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany.
Tim GruberInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany.
Sonja C SchrieverInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany; Research Unit NeuroBiology of Diabetes, Helmholtz Zentrum München, 85764 Neuherberg, Germany.
Beata LegutkoInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany.
Jutta LintelmannInstitute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstraße 1, 85764 Neuherberg, Germany.
Jerzy AdamskiInstitute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstraße 1, 85764 Neuherberg, Germany; Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Medical Drive 8, Singapore 117597, Singapore; Institute of Biochemistry, Faculty of Medicine, University of Ljubljana, Vrazov trg 2, 1000 Ljubljana, Slovenia.
Wolfgang WurstInstitute of Developmental Genetics, Helmholtz Zentrum München, 85764 Neuherberg, Germany; Developmental Genetics, TUM School of Life Sciences, Technische Universität München, Freising-Weihenstephan, Germany; Deutsches Institut für Neurodegenerative Erkrankungen (DZNE) Site Munich, Feodor-Lynen-Str. 17, 81377 Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Adolf-Butenandt-Institut, LudwigMaximilians Universität München, Feodor-Lynen-Str. 17, 81377 Munich, Germany.
Timo D MüllerInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany.
Stephen C WoodsDepartment of Psychiatry and Behavioral Neuroscience, University of Cincinnati, Cincinnati, OH, USA.
Paul T PflugerInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany; Research Unit NeuroBiology of Diabetes, Helmholtz Zentrum München, 85764 Neuherberg, Germany; Division of Neurobiology of Diabetes, TUM School of Medicine, Technical University of Munich, 80333 Munich, Germany.
Matthias H TschöpInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany; Division of Metabolic Diseases, Technische Universität München, 80333 Munich, Germany.
Alexandre FisetteInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany. Electronic address: alexandre.fisette@uqtr.ca.
Cristina García-CáceresInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764 Neuherberg, Germany; German Center for Diabetes Research (DZD), 85764 Neuherberg, Germany; Medizinische Klinik und Poliklinik IV, Klinikum der Universität, Ludwig-Maximilians-Universität München, 80336 Munich, Germany. Electronic address: garcia-caceres@helmholtz-muenchen.de.
Helmholtz Zentrum München · DEGerman Center for Neurodegenerative Diseases · DEUniversity of Cincinnati · USUniversity of Ljubljana · SI

Funding

CIHR 152588
6 · The paper itself

Abstract

Until menopause, women have a lower propensity to develop metabolic diseases than men, suggestive of a protective role for sex hormones. Although a functional synergy between central actions of estrogens and leptin has been demonstrated to protect against metabolic disturbances, the underlying cellular and molecular mechanisms mediating this crosstalk have remained elusive. By using a series of embryonic, adult-onset, and tissue/cell-specific loss-of-function mouse models, we document an unprecedented role of hypothalamic Cbp/P300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 1 (Cited1) in mediating estradiol (E2)-dependent leptin actions that control feeding specifically in pro-opiomelanocortin (Pomc) neurons. We reveal that within arcuate Pomc neurons, Cited1 drives leptin's anorectic effects by acting as a co-factor converging E2 and leptin signaling via direct Cited1-ERα-Stat3 interactions. Together, these results provide new insights on how melanocortin neurons integrate endocrine inputs from gonadal and adipose axes via Cited1, thereby contributing to the sexual dimorphism in diet-induced obesity.

Indexed as

Arcuate Nucleus of HypothalamusLeptinAnimalsEstradiolFemaleHypothalamusMiceObesityPro-OpiomelanocortinEstradiolLeptinPro-OpiomelanocortinARCdiet-induced obesityestradiolhypothalamusleptinPomc

Identifiers

PMID36889283
PMCPMC10028007
OpenAlexW4323530529

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.