Evidence map›Paper›PMID 28445389›Full record

ReviewNutrients2017

Fructose, Glucocorticoids and Adipose Tissue: Implications for the Metabolic Syndrome.

Balázs Legeza, Paola Marcolongo, Alessandra Gamberucci, Viola Varga, Gábor Bánhegyi, Angiolo Benedetti, Alex Odermatt

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
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  6. Review
  7. Chronic kidney disease combined with metabolic syndrome is a non-negligible risk factor.Therapeutic advances in endocrinology and metabolism · 2024
    Review
  8. Article
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  15. MH-76, a Novel Non-Quinazoline αPharmaceuticals (Basel, Switzerland) · 2021
    Article
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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

7 authors at 3 institutions in 3 countries.

Balázs LegezaDivision of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Klingelbergstrasse 50, 4056 Basel, Switzerland. balazs.legeza@dkf.unibe.ch.
Paola MarcolongoDepartment of Molecular and Developmental Medicine, University of Siena, 53100 Siena, Italy. paola.marcolongo@unisi.it.
Alessandra GamberucciDepartment of Molecular and Developmental Medicine, University of Siena, 53100 Siena, Italy. alessandra.gamberucci@unisi.it.
Viola VargaDepartment of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest 1085, Hungary. varviola@gmail.com.
Gábor BánhegyiDepartment of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest 1085, Hungary. banhegyi.gabor@med.semmelweis-univ.hu.
Angiolo BenedettiDepartment of Molecular and Developmental Medicine, University of Siena, 53100 Siena, Italy. benedetti@unisi.it.
Alex OdermattDivision of Molecular and Systems Toxicology, Department of Pharmaceutical Sciences, University of Basel, Klingelbergstrasse 50, 4056 Basel, Switzerland. alex.odermatt@unibas.ch.
Semmelweis University · HUUniversity of Siena · ITUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The modern Western society lifestyle is characterized by a hyperenergetic, high sugar containing food intake. Sugar intake increased dramatically during the last few decades, due to the excessive consumption of high-sugar drinks and high-fructose corn syrup. Current evidence suggests that high fructose intake when combined with overeating and adiposity promotes adverse metabolic health effects including dyslipidemia, insulin resistance, type II diabetes, and inflammation. Similarly, elevated glucocorticoid levels, especially the enhanced generation of active glucocorticoids in the adipose tissue due to increased 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) activity, have been associated with metabolic diseases. Moreover, recent evidence suggests that fructose stimulates the 11β-HSD1-mediated glucocorticoid activation by enhancing the availability of its cofactor NADPH. In adipocytes, fructose was found to stimulate 11β-HSD1 expression and activity, thereby promoting the adipogenic effects of glucocorticoids. This article aims to highlight the interconnections between overwhelmed fructose metabolism, intracellular glucocorticoid activation in adipose tissue, and their metabolic effects on the progression of the metabolic syndrome.

Indexed as

11-beta-Hydroxysteroid Dehydrogenase Type 1Adipose TissueFructoseGene Expression Regulation, EnzymologicGlucocorticoidsHumansMetabolic Syndrome11-beta-Hydroxysteroid Dehydrogenase Type 1FructoseGlucocorticoidsHSD11B1 protein, humanadipogenesisfructoseglucocorticoidmetabolic syndromeobesity

Identifiers

PMID28445389
PMCPMC5452156
OpenAlexW2608881682

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.