Evidence map›Paper›PMID 28420094›Full record

ReviewNutrients2017

Nonalcoholic Fatty Liver Disease and Insulin Resistance: New Insights and Potential New Treatments.

Hironori Kitade, Guanliang Chen, Yinhua Ni, Tsuguhito Ota

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 227 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
227citing papers in PubMed, 3 pooled it
30.5field-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

227 citing papers in PubMed, 3 syntheses or guidelines pooled it, 493 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Observational
  7. Article
  8. Article
  9. Disruption of Hepatic Insulin Signaling Causes Phospholipid Dysregulation in Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Gallstone disease as a clue for metabolic syndrome.Caspian journal of internal medicine · 2026
    Article
  16. Nutrients · 2025
    Article
  17. Article
  18. Article
  19. Article
  20. Article

167 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Hironori KitadeDepartment of Cell Metabolism and Nutrition, Brain/Liver Interface Medicine Research Center, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan. hiro.kitacchi@gmail.com.
Guanliang ChenDepartment of Cell Metabolism and Nutrition, Brain/Liver Interface Medicine Research Center, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan. guanliangc@gmail.com.
Yinhua NiDepartment of Cell Metabolism and Nutrition, Brain/Liver Interface Medicine Research Center, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan. shali0145@gmail.com.
Tsuguhito OtaDepartment of Cell Metabolism and Nutrition, Brain/Liver Interface Medicine Research Center, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan. tota@staff.kanazawa-u.ac.jp.
Kanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver disorders worldwide. It is associated with clinical states such as obesity, insulin resistance, and type 2 diabetes, and covers a wide range of liver changes, ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), liver cirrhosis, and hepatocellular carcinoma. Metabolic disorders, such as lipid accumulation, insulin resistance, and inflammation, have been implicated in the pathogenesis of NAFLD, but the underlying mechanisms, including those that drive disease progression, are not fully understood. Both innate and recruited immune cells mediate the development of insulin resistance and NASH. Therefore, modifying the polarization of resident and recruited macrophage/Kupffer cells is expected to lead to new therapeutic strategies in NAFLD. Oxidative stress is also pivotal for the progression of NASH, which has generated interest in carotenoids as potent micronutrient antioxidants in the treatment of NAFLD. In addition to their antioxidative function, carotenoids regulate macrophage/Kupffer cell polarization and thereby prevent NASH progression. In this review, we summarize the molecular mechanisms involved in the pathogenesis of NAFLD, including macrophage/Kupffer cell polarization, and disturbed hepatic function in NAFLD. We also discuss dietary antioxidants, such as β-cryptoxanthin and astaxanthin, that may be effective in the prevention or treatment of NAFLD.

Indexed as

Insulin ResistanceMacrophagesOxidative StressAntioxidantsCarotenoidsCryptoxanthinsHumansLiverNon-alcoholic Fatty Liver DiseaseXanthophyllsAntioxidantsastaxanthineCarotenoidsCryptoxanthinsXanthophyllsantioxidantsastaxanthinchemokinefibrosisinflammationinsulin resistancemacrophage/Kupffer cellsNAFLD/NASHβ-cryptoxanthin

Identifiers

PMID28420094
PMCPMC5409726
OpenAlexW2605866155

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.