Evidence map›Paper›PMID 27128935›Full record

ReviewNutrients2016

Metabolic Inflammation-Differential Modulation by Dietary Constituents.

Claire L Lyons, Elaine B Kennedy, Helen M Roche

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
13.3field-weighted citation impact, top 1% 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

52 citing papers in PubMed, 102 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. The cause-effect relation of tuberculosis on incidence of diabetes mellitus.Frontiers in cellular and infection microbiology · 2023
    Review
  9. Polyphenols in Metabolic Diseases.Molecules (Basel, Switzerland) · 2022
    Review
  10. Review
  11. Modulation of endothelium function by fatty acids.Molecular and cellular biochemistry · 2022
    Review
  12. Article
  13. Article
  14. Nutrigenomics of Dietary Lipids.Antioxidants (Basel, Switzerland) · 2021
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. 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.

Claire L LyonsNutrigenomics Research Group, UCD Conway Institute of Biomolecular and Biomedical Research and UCD Institute of Food and Health, University College Dublin, Belfield, Dublin 4, Ireland. claire.lyons.2@ucdconnect.ie.
Elaine B KennedyNutrigenomics Research Group, UCD Conway Institute of Biomolecular and Biomedical Research and UCD Institute of Food and Health, University College Dublin, Belfield, Dublin 4, Ireland. elaine.kennedy.1@ucdconnect.ie.
Helen M RocheNutrigenomics Research Group, UCD Conway Institute of Biomolecular and Biomedical Research and UCD Institute of Food and Health, University College Dublin, Belfield, Dublin 4, Ireland. helen.roche@ucd.ie.
University College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity arises from a sustained positive energy balance which triggers a pro-inflammatory response, a key contributor to metabolic diseases such as T2D. Recent studies, focused on the emerging area of metabolic-inflammation, highlight that specific metabolites can modulate the functional nature and inflammatory phenotype of immune cells. In obesity, expanding adipose tissue attracts immune cells, creating an inflammatory environment within this fatty acid storage organ. Resident immune cells undergo both a pro-inflammatory and metabolic switch in their function. Inflammatory mediators, such as TNF-α and IL-1β, are induced by saturated fatty acids and disrupt insulin signaling. Conversely, monounsaturated and polyunsaturated fatty acids do not interrupt metabolism and inflammation to the same extent. AMPK links inflammation, metabolism and T2D, with roles to play in all and is influenced negatively by obesity. Lipid spillover results in hepatic lipotoxicity and steatosis. Also in skeletal muscle, excessive FFA can impede insulin's action and promote inflammation. Ectopic fat can also affect pancreatic β-cell function, thereby contributing to insulin resistance. Therapeutics, lifestyle changes, supplements and dietary manipulation are all possible avenues to combat metabolic inflammation and the subsequent insulin resistant state which will be explored in the current review.

Indexed as

Adipose TissueCytokinesDietGene Expression RegulationHumansInflammationObesityCytokinesadipose tissuedietfatty acidsinsulin resistancelivermetabolic-inflammationmusclenutritionpancreas

Identifiers

PMID27128935
PMCPMC4882660
OpenAlexW2342689171

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.