Evidence map›Paper›PMID 25576054›Full record

ArticleDiabetes2015

Overweight in mice and enhanced adipogenesis in vitro are associated with lack of the hedgehog coreceptor boc.

Hye-Jin Lee, Shin-Bum Jo, Anthony I Romer, Hyo-Jeong Lim, Min-Jung Kim, Seung-Hoi Koo, Robert S Krauss, Jong-Sun Kang

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Systemic Sonic Hedgehog Signaling Links Intestinal Nutrient Sensing With Sex-Specific Type 2 Diabetes Progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  7. Review
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  11. Cdon deficiency causes cardiac remodeling through hyperactivation of WNT/β-catenin signaling.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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

8 authors at 4 institutions in 2 countries.

Hye-Jin LeeDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, Republic of Korea.
Shin-Bum JoDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, Republic of Korea.
Anthony I RomerDepartment of Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY.
Hyo-Jeong LimDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, Republic of Korea.
Min-Jung KimDivision of Life Sciences, Korea University, Seoul, Republic of Korea.
Seung-Hoi KooDivision of Life Sciences, Korea University, Seoul, Republic of Korea.
Robert S KraussDepartment of Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY kangj01@skku.edu robert.krauss@mssm.edu.
Jong-Sun KangDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, Republic of Korea kangj01@skku.edu robert.krauss@mssm.edu.
Sungkyunkwan University · KRIcahn School of Medicine at Mount Sinai · USKorea University · KRSamsung (South Korea) · KR

Funding

THE ROLE OF CDO IN MYOGENIC DIFFERENTIATIONR01AR046207 · NIAMS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI KRAUSS, ROBERT S. · 2000 to 2015
$5.1M
NIAMS NIH HHS AR-46207NIAMS NIH HHS R01 AR046207
6 · The paper itself

Abstract

Obesity arises from a combination of genetic, environmental, and behavioral factors. However, the processes that regulate white adipose tissue (WAT) expansion at the level of the adipocyte are not well understood. The Hedgehog (HH) pathway plays a conserved role in adipogenesis, inhibiting fat formation in vivo and in vitro, but it has not been shown that mice with reduced HH pathway activity have enhanced adiposity. We report that mice lacking the HH coreceptor BOC displayed age-related overweight and excess WAT. They also displayed alterations in some metabolic parameters but normal food intake. Furthermore, they had an exacerbated response to a high-fat diet, including enhanced weight gain and adipocyte hypertrophy, livers with greater fat accumulation, and elevated expression of genes related to adipogenesis, lipid metabolism, and adipokine production. Cultured Boc(-/-) mouse embryo fibroblasts showed enhanced adipogenesis relative to Boc(+/+) cells, and they expressed reduced levels of HH pathway target genes. Therefore, a loss-of-function mutation in an HH pathway component is associated with WAT accumulation and overweight in mice. Variant alleles of such HH regulators may contribute to WAT accumulation in human individuals with additional genetic or lifestyle-based predisposition to obesity.

Indexed as

AdipogenesisAnimalsCells, CulturedImmunoglobulin GIn Vitro TechniquesMaleMiceMice, Mutant StrainsOverweightReceptors, Cell SurfaceReverse Transcriptase Polymerase Chain ReactionBoc protein, mouseImmunoglobulin GReceptors, Cell Surface

Identifiers

PMID25576054
PMCPMC4439556
OpenAlexW2151167953

What OpenQuestion holds

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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.