Evidence map›Paper›PMID 24500759›Full record

ArticleCellular and molecular life sciences : CMLS2014

BBS4 directly affects proliferation and differentiation of adipocytes.

Olga Aksanov, Pnina Green, Ruth Z Birk

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Follistatin like-1 (Adipocyte · 2024
    Article
  5. Adipocyte-specific disruption of the BBSome causes metabolic and autonomic dysfunction.American journal of physiology. Regulatory, integrative and comparative physiology · 2024
    Article
  6. Review
  7. Review
  8. Article
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  11. Article
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  14. Review
  15. Article
  16. The role of Rpgrip1l, a component of the primary cilium, in adipocyte development and function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  17. Article
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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

3 authors at 3 institutions in 1 country.

Olga AksanovNational Institute for Biotechnology in the Negev, Ben Gurion University, Beer-Sheva, Israel.
Pnina Green
Ruth Z Birk
Ariel University · ILBen-Gurion University of the Negev · ILTel Aviv University · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BBS4 is one of several proteins whose defects cause Bardet-Biedl syndrome (BBS), a multi-systemic disorder, manifesting with marked obesity. BBS4 polymorphisms have been associated with common non-syndromic morbid obesity. BBS4 obesity molecular mechanisms, and the role of the BBS4 gene in adipocyte differentiation and function are not entirely known. We now show that Bbs4 plays a direct and essential role in proliferation and adipogenesis: silencing of Bbs4 in 3T3F442A preadipocytes induced accelerated cell division and aberrant differentiation, evident through morphologic studies (light, scanning and transmission electron microscopy), metabolic analyses (fat accumulation, fatty acid profile and lipolysis) and adipogenic markers transcripts (Cebpα, Pparγ, aP2, ADRP, Perilipin). Throughout adipogenesis and when challenged with fat load, Bbs4 silenced cells accumulate significantly more triglycerides than control adipocytes, albeit in smaller (yet greater in number) droplets containing modified fatty acid profiles. Thus, greater fat accumulation in the silenced cells is a consequence of both a higher rate of adipocyte proliferation and of aberrant differentiation leading to augmented aberrant accumulation of fat per cell. Our findings suggest that the BBS obesity might be partly due to a direct role of BBS4 in physiological and pathophysiological mechanisms that underlie adipose tissue formation relevant to obesity.

Indexed as

3T3 CellsAdipocytesAdipogenesisAnimalsBiomarkersCell DivisionFatty AcidsGene Expression Regulation, DevelopmentalMiceMicrotubule-Associated ProteinsRecombinant Fusion ProteinsRNA InterferenceRNA, Small InterferingTriglyceridesBBS4 protein, mouseBiomarkersFatty AcidsMicrotubule-Associated ProteinsRecombinant Fusion ProteinsRNA, Small InterferingTriglycerides

Identifiers

PMID24500759
PMCPMC11113930
OpenAlexW1973897112

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.