Evidence map›Paper›PMID 34959926›Full record

ArticleNutrients2021

Astaxanthin, a Marine Carotenoid, Maintains the Tolerance and Integrity of Adipose Tissue and Contributes to Its Healthy Functions.

Allah Nawaz, Yasuhiro Nishida, Akiko Takikawa, Shiho Fujisaka, Tomonobu Kado, Aminuddin Aminuddin, Muhammad Bilal, Ishtiaq Jeelani, Muhammad Rahil Aslam, Ayumi Nishimura and 10 more

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Effect of StandardizedNutrients · 2022
    Trial
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Editorial: Recent advances in immunometabolism.Frontiers in pharmacology · 2024
    Article
  10. Review
  11. 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

20 authors at 6 institutions in 3 countries.

Allah NawazDepartment of Molecular and Medical Pharmacology, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Yasuhiro NishidaFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.ORCID 0000-0002-6169-9930
Akiko TakikawaFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Shiho FujisakaFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Tomonobu KadoFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Aminuddin AminuddinFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.ORCID 0000-0001-8564-7847
Muhammad BilalFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.ORCID 0000-0003-3623-2914
Ishtiaq JeelaniDepartment of Molecular and Medical Pharmacology, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.ORCID 0000-0001-9903-6326
Muhammad Rahil AslamFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Ayumi NishimuraFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Takahide KuwanoFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Yoshiyuki WatanabeFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Yoshiko IgarashiFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Keisuke OkabeDepartment of Molecular and Medical Pharmacology, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Saeed AhmedDepartment of Medicine and Surgery, Rawalpindi Medical University, Rawalpindi 46000, Pakistan.
Azhar ManzoorIndus Hospital Bhong, Sadiqabad 64350, Pakistan.
Isao UsuiDepartment of Endocrinology and Metabolism, Dokkyo Medical University, Mibu 321-0293, Japan.
Kunimasa YagiFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Takashi NakagawaDepartment of Molecular and Medical Pharmacology, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.ORCID 0000-0001-5539-7605
Kazuyuki TobeFirst Department of Internal Medicine, Faculty of Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
University of Toyama · JPDokkyo Medical University · JPFuji Chemical Industries (Japan) · JPIndus Hospital · PKRawalpindi Medical University · PKToyama University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, obesity-induced insulin resistance, type 2 diabetes, and cardiovascular disease have become major social problems. We have previously shown that Astaxanthin (AX), which is a natural antioxidant, significantly ameliorates obesity-induced glucose intolerance and insulin resistance. It is well known that AX is a strong lipophilic antioxidant and has been shown to be beneficial for acute inflammation. However, the actual effects of AX on chronic inflammation in adipose tissue (AT) remain unclear. To observe the effects of AX on AT functions in obese mice, we fed six-week-old male C57BL/6J on high-fat-diet (HFD) supplemented with or without 0.02% of AX for 24 weeks. We determined the effect of AX at 10 and 24 weeks of HFD with or without AX on various parameters including insulin sensitivity, glucose tolerance, inflammation, and mitochondrial function in AT. We found that AX significantly reduced oxidative stress and macrophage infiltration into AT, as well as maintaining healthy AT function. Furthermore, AX prevented pathological AT remodeling probably caused by hypoxia in AT. Collectively, AX treatment exerted anti-inflammatory effects via its antioxidant activity in AT, maintained the vascular structure of AT and preserved the stem cells and progenitor's niche, and enhanced anti-inflammatory hypoxia induction factor-2α-dominant hypoxic response. Through these mechanisms of action, it prevented the pathological remodeling of AT and maintained its integrity.

Indexed as

Anti-Inflammatory AgentsAntioxidantsDietary SupplementsAdipose TissueAnimalsCytokinesGlucoseInflammationInflammation MediatorsInsulin ResistanceMacrophagesMaleMiceMice, Inbred C57BLMitochondriaOxidative StressAnti-Inflammatory AgentsAntioxidantsastaxanthineCytokinesGlucoseInflammation MediatorsXanthophyllsadipose tissue macrophagesadipose tissue remodelingAstaxanthininsulin resistancenatural antioxidantobesity

Identifiers

PMID34959926
PMCPMC8703397
OpenAlexW4200596974

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.