Evidence map›Paper›PMID 32368109›Full record

ReviewDiabetes, metabolic syndrome and obesity : targets and therapy2020

Glucocorticoid-Induced Fatty Liver Disease.

Leili Rahimi, Aman Rajpal, Faramarz Ismail-Beigi

Open access · goldAbstract readReview
In one paragraph

Review in Diabetes, metabolic syndrome and obesity : targets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 4 pooled it
9.9field-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

75 citing papers in PubMed, 4 syntheses or guidelines pooled it, 130 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Prevalence of Nonalcoholic Fatty Liver Disease in Patients With Rheumatoid Arthritis: A Systematic Review and Meta-analysis.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2023
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15 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

3 authors at 1 institution in 1 country.

Leili RahimiDepartment of Medicine, Case Western Reserve University, University Hospitals Cleveland Medical Center, Cleveland, OH, USA.ORCID 0000-0002-3908-8324
Aman RajpalDepartment of Medicine, Case Western Reserve University, University Hospitals Cleveland Medical Center, Cleveland, OH, USA.ORCID 0000-0001-5277-4081
Faramarz Ismail-BeigiDepartment of Medicine, Case Western Reserve University, University Hospitals Cleveland Medical Center, Cleveland, OH, USA.
University Hospitals of Cleveland · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoids (GCs) are commonly used at high doses and for prolonged periods (weeks to months) in the treatment of a variety of diseases. Among the many side effects are increased insulin resistance with disturbances in glucose/insulin homeostasis and increased deposition of lipids (mostly triglycerides) in the liver. Here, we review the metabolic pathways of lipid deposition and removal from the liver that become altered by excess glucocorticoids. Pathways of lipid deposition stimulated by excess glucocorticoids include 1) increase in appetite and high caloric intake; 2) increased blood glucose levels due to GC-induced stimulation of gluconeogenesis; 3) stimulation of de novo lipogenesis that is augmented by the high glucose and insulin levels and by GC itself; and 4) increased release of free fatty acids from adipose stores and stimulation of their uptake by the liver. Pathways that decrease hepatic lipids affected by glucocorticoids include a modest stimulation of very-low-density lipoprotein synthesis and secretion into the circulation and inhibition of β-oxidation of fatty acids. Role of 11β-hydroxysteroid dehydrogenases-1 and -2 and the reversible conversion of cortisol to cortisone on intracellular levels of cortisol is examined. In addition, GC control of osteocalcin expression and the effect of this bone-derived hormone in increasing insulin sensitivity are discussed. Finally, research focused on gaining a better understanding of the dose and duration of treatment with glucocorticoids, which leads to increased triglyceride deposition in the liver, and the reversibility of the condition is highlighted.

Indexed as

Cushing’s diseasefatty liverhormone-sensitive lipasehyperphagiaLPLmetabolic syndromeobesity

Identifiers

PMID32368109
PMCPMC7171875
OpenAlexW3017076243

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.