Evidence map›Paper›PMID 30582777›Full record

ArticleJournal of diabetes investigation2019

Kbtbd11 gene expression in adipose tissue increases in response to feeding and affects adipocyte differentiation.

Kazuhisa Watanabe, Ken Yoshida, Sadahiko Iwamoto

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Epigenetics of Muscle- and Brain-Specific Expression of KLHL Family Genes.International journal of molecular sciences · 2020
    Article
  7. A novel upstream transcription factor 1 target geneBiochemistry and biophysics reports · 2019
    Article
  8. Heliyon · 2019
    Article
  9. 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

3 authors at 1 institution in 1 country.

Kazuhisa WatanabeDivision of Human Genetics, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.ORCID https://orcid.org/0000-0002-5640-0818
Ken YoshidaDivision of Human Genetics, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.
Sadahiko IwamotoDivision of Human Genetics, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Japan.
Jichi Medical University · JP

Funding

Japan Society for the Promotion of Science 15K19523Japan Society for the Promotion of Science 17K09864Japan Society for the Promotion of Science 17K16153Jichi Medical UniversityMEXT
6 · The paper itself

Abstract

AIMS/

introductionThe putative tumor suppressor gene, KBTBD11, might play a role in tumorigenesis, and is associated with cellular apoptosis and proliferation in colorectal cancer cells. However, the function of Kbtbd11 during adipogenesis is unknown. The aim of the present study was to investigate the role of Kbtbd11 in the differentiation of 3T3-L1 preadipocytes. MATERIALS AND

methodsFor the fasting-refeeding protocol, mice were subjected to fasting for 24 h, followed by a chow diet for 12 h. Adenovirus infection methods were used to examine the effect of Kbtbd11, and 3T3-L1 cells were analyzed with Oil Red O staining and real-time polymerase chain reaction.

resultsThe white adipose tissue expression of Kbtbd11 messenger ribonucleic acid (mRNA) was significantly higher in the re-fed state than in the fasted state. Kbtbd11 mRNA levels were markedly increased in epididymal white adipose tissue of diet-induced obesity mice compared with those in the mice fed a chow diet. In addition, Kbtbd11 mRNA expression was increased in a differentiation-dependent manner in 3T3-L1 cells. Knockdown of Kbtbd11 mRNA through the infection with adenoviral vectors remarkably inhibited triglyceride accumulation and adipocyte differentiation in 3T3-L1 cells. In contrast, the overexpression of Kbtbd11 promoted the differentiation of 3T3-L1 adipocytes.

conclusionsThe present findings show that Kbtbd11 expression might be involved in nutritional regulation and is increased in obese adipose tissue. In addition, Kbtbd11 appears to be required for the differentiation of adipocytes in 3T3-L1 cells. Collectively, these results show a novel link between the expression of Kbtbd11 and fat accumulation, and suggest that Kbtbd11 is a new therapeutic target for obesity.

Indexed as

AdipogenesisCell DifferentiationFeeding BehaviorGene Expression RegulationAdipose TissueAnimalsDiet, High-FatMaleMiceMice, Inbred C57BLMice, ObeseObesityTumor Suppressor ProteinsKbtbd11 protein, mouseTumor Suppressor Proteins3T3-L1 preadipocytesDifferentiationKbtbd11

Identifiers

PMID30582777
PMCPMC6626956
OpenAlexW2905745820

What OpenQuestion holds

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LicenceCC BY-NC
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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.