Evidence map›Paper›PMID 30323174›Full record

ReviewEuropean journal of clinical nutrition2019

Determinants of ectopic liver fat in metabolic disease.

Anja Bosy-Westphal, Wiebke Braun, Viktoria Albrecht, Manfred J Müller

Abstract readReview
PubMed Publisher
In one paragraph

Review in European journal of clinical nutrition, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

26 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Advances in body composition: a 100-year journey.International journal of obesity (2005) · 2025
    Review
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  9. Metabolic syndrome.Nature reviews. Disease primers · 2024
    Review
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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

4 authors.

Anja Bosy-WestphalInstitute for Human Nutrition and Food Science, Christian-Albrechts-University Kiel, Kiel, Germany. abosyw@nutrition.uni-kiel.de.
Wiebke BraunInstitute for Human Nutrition and Food Science, Christian-Albrechts-University Kiel, Kiel, Germany.
Viktoria AlbrechtInstitute for Human Nutrition and Food Science, Christian-Albrechts-University Kiel, Kiel, Germany.
Manfred J MüllerInstitute for Human Nutrition and Food Science, Christian-Albrechts-University Kiel, Kiel, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Common obesity-associated hepatic steatosis (nonalcoholic fatty liver disease (NAFLD)) and insulin resistance are mainly caused by dysfunctional adipose tissue. This adipose tissue dysfunction leads to increased delivery of NEFA and glycerol to the liver that (i) drives hepatic gluconeogenesis and (ii) facilitates the accumulation of lipids and insulin signaling inhibiting lipid intermediates. Dysfunctional adipose tissue can be caused by impaired lipid storage (overflow hypothesis, characterized by large visceral adipocytes) or increased lipolysis (due to impaired postprandial suppression of lipolysis in inflamed, insulin-resistant adipocytes). In line with the adipose tissue expandability hypothesis the amount and distribution of adipose tissue correlate with its dysfunction and thus with liver fat. This relationship is however modified by endocrine effects on lipid storage and lipolysis as well as dietary effects on hepatic lipogenesis and lipid oxidation. The association between body composition characteristics like visceral obesity or fat cell size and ectopic liver fat is modified by these influences. Phenotyping obesity according to metabolic risk should integrate body composition characteristics, endocrine parameters and information on diet.

Indexed as

Adipose TissueHumansNon-alcoholic Fatty Liver Disease

Identifiers

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.