Evidence map›Paper›PMID 26628639›Full record

ArticleJournal of lipid research2016

Suppression of NLRP3 inflammasome by γ-tocotrienol ameliorates type 2 diabetes.

Yongeun Kim, Wei Wang, Meshail Okla, Inhae Kang, Regis Moreau, Soonkyu Chung

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
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  8. A20 as a Potential Therapeutic Target for COVID-19.Immunity, inflammation and disease · 2025
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  19. Revisiting the therapeutic potential of tocotrienol.BioFactors (Oxford, England) · 2022
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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

6 authors at 1 institution in 1 country.

Yongeun KimDepartment of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE 68583.
Wei WangDepartment of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE 68583.
Meshail OklaDepartment of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE 68583.
Inhae KangDepartment of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE 68583.
Regis MoreauDepartment of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE 68583.
Soonkyu ChungDepartment of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE 68583 schung4@unl.edu.
University of Nebraska–Lincoln · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Nod-like receptor 3 (NLRP3) inflammasome is an intracellular sensor that sets off the innate immune system in response to microbial-derived and endogenous metabolic danger signals. We previously reported that γ-tocotrienol (γT3) attenuated adipose tissue inflammation and insulin resistance in diet-induced obesity, but the underlying mechanism remained elusive. Here, we investigated the effects of γT3 on NLRP3 inflammasome activation and attendant consequences on type 2 diabetes. γT3 repressed inflammasome activation, caspase-1 cleavage, and interleukin (IL) 1β secretion in murine macrophages, implicating the inhibition of NLRP3 inflammasome in the anti-inflammatory and antipyroptotic properties of γT3. Furthermore, supplementation of leptin-receptor KO mice with γT3 attenuated immune cell infiltration into adipose tissue, decreased circulating IL-18 levels, preserved pancreatic β-cells, and improved insulin sensitivity. Mechanistically, γT3 regulated the NLRP3 inflammasome via a two-pronged mechanism: 1) the induction of A20/TNF-α interacting protein 3 leading to the inhibition of the TNF receptor-associated factor 6/nuclear factor κB pathway and 2) the activation of AMP-activated protein kinase/autophagy axis leading to the attenuation of caspase-1 cleavage. Collectively, we demonstrated, for the first time, that γT3 inhibits the NLRP3 inflammasome thereby delaying the progression of type 2 diabetes. This study also provides an insight into the novel therapeutic values of γT3 for treating NLRP3 inflammasome-associated chronic diseases.

Indexed as

Adipose TissueAMP-Activated Protein KinasesAnimalsCarrier ProteinsCaspase 1ChromansDiabetes Mellitus, Type 2InflammasomesInflammationInsulin ResistanceInterleukin-1betaLipopolysaccharidesMacrophages, PeritonealMaleMiceMice, Inbred NODAMP-Activated Protein KinasesCarrier ProteinsCaspase 1ChromansInflammasomesInterleukin-1betaLipopolysaccharidesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseplastochromanol 8Tumor Necrosis Factor-alphaVitamin EA20caspase 1diet and dietary lipidsinflammationinsulin signalingNOD-like receptor protein 3obesityvitamin E

Identifiers

PMID26628639
PMCPMC4689338
OpenAlexW2187931582

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.