Evidence map›Paper›PMID 21617180›Full record

ArticleDiabetes2011

Genetic defect in phospholipase Cδ1 protects mice from obesity by regulating thermogenesis and adipogenesis.

Masayuki Hirata, Mutsumi Suzuki, Rika Ishii, Reiko Satow, Takafumi Uchida, Tomoya Kitazumi, Tsutomu Sasaki, Tadahiro Kitamura, Hideki Yamaguchi, Yoshikazu Nakamura and 1 more

Open access · greenAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Spinophilin-deficient mice are protected from diet-induced obesity and insulin resistance.American journal of physiology. Endocrinology and metabolism · 2020
    Article
  5. Review
  6. Effects of exercise on brown and beige adipocytes.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019
    Review
  7. Foxn1 in Skin Development, Homeostasis and Wound Healing.International journal of molecular sciences · 2018
    Review
  8. Warming the mouse to model human diseases.Nature reviews. Endocrinology · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. 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

11 authors at 2 institutions in 1 country.

Masayuki HirataLaboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, Japan.
Mutsumi Suzuki
Rika Ishii
Reiko Satow
Takafumi Uchida
Tomoya Kitazumi
Tsutomu Sasaki
Tadahiro Kitamura
Hideki Yamaguchi
Yoshikazu Nakamura
Kiyoko Fukami
Tokyo University of Pharmacy and Life Sciences · JPJapan Science and Technology Agency · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRegulation of obesity development is an important issue to prevent metabolic syndromes. Gene-disrupted mice of phospholipase Cδ1 (PLCδ1), a key enzyme of phosphoinositide turnover, seemed to show leanness. Here we examined whether and how PLCδ1 is involved in obesity. RESEARCH DESIGN AND

methodsWeight gain, insulin sensitivity, and metabolic rate in PLCδ1(-/-) mice were compared with PLCδ1(+/-) littermate mice on a high-fat diet. Thermogenic and adipogenetic potentials of PLCδ1(-/-) immortalized brown adipocytes and adipogenesis of PLCδ1-knockdown (KD) 3T3L1 cells, or PLCδ1(-/-) white adipose tissue (WAT) stromal-vascular fraction (SVF) cells, were also investigated.

resultsPLCδ1(-/-) mice showed marked decreases in weight gain and mass of epididymal WAT and preserved insulin sensitivity compared with PLCδ1(+/-) mice on a high-fat diet. In addition, PLCδ1(-/-) mice have a higher metabolic rate such as higher oxygen consumption and heat production. When control immortalized brown adipocytes were treated with thermogenic inducers, expression of PLCδ1 was decreased and thermogenic gene uncoupling protein 1 (UCP1) was upregulated to a greater extent in PLCδ1(-/-) immortalized brown adipocytes. In contrast, ectopic expression of PLCδ1 in PLCδ1(-/-) brown adipocytes induced a decrease in UCP expression, indicating that PLCδ1 negatively regulates thermogenesis. Importantly, accumulation of lipid droplets was severely decreased when PLCδ1-KD 3T3L1 cells, or PLCδ1(-/-) WAT SVF cells, were differentiated, whereas differentiation of PLCδ1(-/-) brown preadipocytes was promoted.

conclusionsPLCδ1 has essential roles in thermogenesis and adipogenesis and thereby contributes to the development of obesity.

Indexed as

3T3-L1 CellsAdipocytes, BrownAdipogenesisAdipose Tissue, WhiteAnimalsCell DifferentiationCells, CulturedDietary FatsGene Expression ProfilingInsulinIon ChannelsMiceMice, NudeMitochondrial ProteinsNFATC Transcription FactorsObesityDietary FatsInsulinIon ChannelsMitochondrial ProteinsNfatc4 protein, mouseNFATC Transcription FactorsPhospholipase C deltaPlcd1 protein, mouseProtein Kinase CProtein Kinase C-epsilonUcp1 protein, mouseUncoupling Protein 1

Identifiers

PMID21617180
PMCPMC3121440
OpenAlexW2131696379

What OpenQuestion 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 OpenQuestion graph.