Evidence map›Paper›PMID 27329323›Full record

ArticleScientific reports2016

Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice.

Masashi Satoh, Miyuki Hoshino, Koki Fujita, Misao Iizuka, Satoshi Fujii, Christopher S Clingan, Luc Van Kaer, Kazuya Iwabuchi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 67 citations in OpenAlex.

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  8. Macrophage and T cell networks in adipose tissue.Nature reviews. Endocrinology · 2024
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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

8 authors at 4 institutions in 2 countries.

Masashi SatohDepartment of Immunology, Kitasato University School of Medicine, Sagamihara, Japan.
Miyuki HoshinoDepartment of Immunology, Kitasato University School of Medicine, Sagamihara, Japan.
Koki FujitaDepartment of Immunology, Kitasato University School of Medicine, Sagamihara, Japan.
Misao IizukaDepartment of Immunology, Kitasato University School of Medicine, Sagamihara, Japan.
Satoshi FujiiDepartment of Laboratory Medicine, Asahikawa Medical University, Asahikawa, Japan.
Christopher S ClinganDepartment of Emergency Medicine, Tufts Medical Center, Lowell General Hospital, Boston, MA 02111, USA.
Luc Van KaerDepartment of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN, USA.
Kazuya IwabuchiDepartment of Immunology, Kitasato University School of Medicine, Sagamihara, Japan.
Kitasato University · JPAsahikawa Medical University · JPLowell General Hospital · USVanderbilt University · US

Funding

NIAID NIH HHS HHSN272201300006C
6 · The paper itself

Abstract

It has been shown that CD1d expression and glycolipid-reactive, CD1d-restricted NKT cells exacerbate the development of obesity and insulin resistance in mice. However, the relevant CD1d-expressing cells that influence the effects of NKT cells on the progression of obesity remain incompletely defined. In this study, we have demonstrated that 3T3-L1 adipocytes can present endogenous ligands to NKT cells, leading to IFN-γ production, which in turn, stimulated 3T3-L1 adipocytes to enhance expression of CD1d and CCL2, and decrease expression of adiponectin. Furthermore, adipocyte-specific CD1d deletion decreased the size of the visceral adipose tissue mass and enhanced insulin sensitivity in mice fed a high-fat diet (HFD). Accordingly, NKT cells were less activated, IFN-γ production was significantly reduced, and levels of adiponectin were increased in these animals as compared with control mice on HFD. Importantly, macrophage recruitment into the adipose tissue of adipocyte-specific CD1d-deficient mice was significantly blunted. These findings indicate that interactions between NKT cells and CD1d-expressing adipocytes producing endogenous NKT cell ligands play a critical role in the induction of inflammation and functional modulation of adipose tissue that leads to obesity.

Indexed as

3T3-L1 CellsAdipocytesAdiponectinAnimalsAntigen PresentationAntigens, CD1dB7-1 AntigenDiet, High-FatDisease Models, AnimalDisease ProgressionGalactosylceramidesInsulin ResistanceInterferon-gammaLymphocyte ActivationMacrophage ActivationMiceAdiponectinAdipoq protein, mousealpha-galactosylceramideAntigens, CD1dB7-1 AntigenCD1d antigen, mouseGalactosylceramidesInterferon-gamma

Identifiers

PMID27329323
PMCPMC4916414
OpenAlexW2467799705

What OpenQuestion holds

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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.