Evidence map›Paper›PMID 33188191›Full record

ArticleNature communications2020

Primary cilia mediate early life programming of adiposity through lysosomal regulation in the developing mouse hypothalamus.

Chan Hee Lee, Do Kyeong Song, Chae Beom Park, Jeewon Choi, Gil Myoung Kang, Sung Hoon Shin, Ijoo Kwon, Soyoung Park, Seongjun Kim, Ji Ye Kim and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Primary cilia dysfunction: A critical driver of metabolic diseases (Review).International journal of molecular medicine · 2026
    Review
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  7. Disulfide-Bridged Ru Complex-Mediated Photo-Disulfidptosis for Colorectal Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

16 authors at 3 institutions in 2 countries.

Chan Hee LeeAsan Institute for Life Science, University of Ulsan College of Medicine, Seoul, 05505, Korea.ORCID 0000-0001-8791-817X
Do Kyeong SongDivision of Endocrinology and Metabolism, Department of Internal Medicine, Asan Medical Center and University of Ulsan College of Medicine, Seoul, 05505, Korea.ORCID 0000-0003-2101-6661
Chae Beom ParkDepartment of Biomedical Science, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center and University of Ulsan College of Medicine, Seoul, 05505, Korea.ORCID 0000-0002-8384-617X
Jeewon ChoiDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, 34141, Korea.
Gil Myoung KangAsan Institute for Life Science, University of Ulsan College of Medicine, Seoul, 05505, Korea.
Sung Hoon ShinDepartment of Biomedical Science, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center and University of Ulsan College of Medicine, Seoul, 05505, Korea.ORCID 0000-0002-0349-1920
Ijoo KwonAsan Institute for Life Science, University of Ulsan College of Medicine, Seoul, 05505, Korea.ORCID 0000-0002-9134-0988
Soyoung ParkDevelopmental Neuroscience & Diabetes and Obesity Programs, Children's Hospital Los Angeles, University of Southern California, Los Angeles, CA, 90027, USA.
Seongjun KimDepartment of Biomedical Science, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center and University of Ulsan College of Medicine, Seoul, 05505, Korea.
Ji Ye KimAsan Institute for Life Science, University of Ulsan College of Medicine, Seoul, 05505, Korea.
Hong DuguDepartment of Biomedical Science, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center and University of Ulsan College of Medicine, Seoul, 05505, Korea.ORCID 0000-0002-7491-7589
Jae Woo ParkDepartment of Biomedical Science, Asan Medical Institute of Convergence Science and Technology, Asan Medical Center and University of Ulsan College of Medicine, Seoul, 05505, Korea.ORCID 0000-0002-6306-7443
Jong Han ChoiDivision of Endocrinology and Metabolism, Department of Internal Medicine, Asan Medical Center and University of Ulsan College of Medicine, Seoul, 05505, Korea.ORCID 0000-0002-2667-4332
Se Hee MinDivision of Endocrinology and Metabolism, Department of Internal Medicine, Asan Medical Center and University of Ulsan College of Medicine, Seoul, 05505, Korea.ORCID 0000-0001-9423-3937
Jong-Woo SohnDepartment of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon, 34141, Korea. jwsohn@kaist.ac.kr.ORCID 0000-0002-2840-4176
Min-Seon KimAsan Institute for Life Science, University of Ulsan College of Medicine, Seoul, 05505, Korea. mskim@amc.seoul.kr.ORCID 0000-0002-4881-0390
Ulsan College · KRKorea Advanced Institute of Science and Technology · KRUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypothalamic neurons including proopiomelanocortin (POMC)-producing neurons regulate body weights. The non-motile primary cilium is a critical sensory organelle on the cell surface. An association between ciliary defects and obesity has been suggested, but the underlying mechanisms are not fully understood. Here we show that inhibition of ciliogenesis in POMC-expressing developing hypothalamic neurons, by depleting ciliogenic genes IFT88 and KIF3A, leads to adulthood obesity in mice. In contrast, adult-onset ciliary dysgenesis in POMC neurons causes no significant change in adiposity. In developing POMC neurons, abnormal cilia formation disrupts axonal projections through impaired lysosomal protein degradation. Notably, maternal nutrition and postnatal leptin surge have a profound impact on ciliogenesis in the hypothalamus of neonatal mice; through these effects they critically modulate the organization of hypothalamic feeding circuits. Our findings reveal a mechanism of early life programming of adult adiposity, which is mediated by primary cilia in developing hypothalamic neurons.

Indexed as

AdiposityAnimalsAnimals, NewbornArcuate Nucleus of HypothalamusAxonsCiliaEnergy MetabolismFemaleGlucoseHypothalamusLeptinLysosomesMalnutritionMice, Inbred C57BLMicrotubule-Associated ProteinsNeurogenesisGlucoseLeptinMap1lc3b protein, mouseMicrotubule-Associated ProteinsPro-Opiomelanocortin

Identifiers

PMID33188191
PMCPMC7666216
OpenAlexW3102447865

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.