Evidence map›Paper›PMID 20216310›Full record

ReviewCurrent opinion in lipidology2010

Stearoyl-coenzyme A desaturase 1 inhibition and the metabolic syndrome: considerations for future drug discovery.

J Mark Brown, Lawrence L Rudel

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in lipidology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 105 citations in OpenAlex.

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  16. Exosome-mediated delivery of SCD-1 siRNA promoted the death of anaplastic thyroid carcinoma cells via regulating ROS level.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
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  19. Glycosaminoglycan fromFood science & nutrition · 2021
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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

2 authors at 1 institution in 1 country.

J Mark BrownDepartment of Pathology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1040, USA.
Lawrence L Rudel
Wake Forest University · US

Funding

TISSUE CULTURE COREP01HL049373 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RUDEL, LAWRENCE L · 1993 to 2012
$23.8M
The Wake Forest Center for Botanical Lipids and Inflammatory Disease PreventionP50AT002782 · NCCIH · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI CHILTON, FLOYD H · 2005 to 2014
$15.3M
Mechanisms Regulating Non-biliary Fecal Sterol LossR00HL096166 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BROWN, JONATHAN MARK · 2011 to 2013
$733k
Mechanisms Regulating Non-biliary Fecal Sterol LossK99HL096166 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BROWN, JONATHAN MARK · 2009 to 2010
$180k
NCCIH NIH HHS P50 AT002782NCCIH NIH HHS P50AT002782NHLBI NIH HHS 1K99HL096166-01NHLBI NIH HHS K99 HL096166NHLBI NIH HHS P01 HL049373NHLBI NIH HHS P01-HL49373NHLBI NIH HHS R00 HL096166
6 · The paper itself

Abstract

purpose of reviewThe metabolic syndrome has become a leading health concern in developed countries. In the search for strategies to combat this growing problem, stearoyl-CoA desaturase 1 (SCD1) inhibition has been proposed as an attractive therapeutic strategy. However, recent studies warn of potentially harmful consequences of SCD1 inhibition. The purpose of this review is to discuss recent insights into the potential for SCD1 inhibitors as viable metabolic syndrome therapeutics. RECENT

findingsSCD1 converts saturated fatty acids (SFAs) to monounsaturated fatty acids (MUFAs). Although SCD1 inhibition protects against diet-induced obesity, hepatic steatosis, and insulin resistance, recent studies have demonstrated that the accumulation of SCD1 substrates (SFA) can promote inflammation, atherosclerosis, steatohepatitis, and pancreatic beta cell dysfunction in preclinical rodent models. This suggests SCD1 may play a critical role in suppressing inflammatory diseases by shuttling proinflammatory SFAs into less biologically active MUFA-enriched neutral lipids. Given this, SCD1 inhibitors given in conjunction with anti-inflammatory agents may provide a useful strategy to prevent the metabolic syndrome without deleterious side-effects seen with SCD1 inhibition alone. SUMMARY: SCD1 inhibitors continue to hold promise as metabolic syndrome therapeutics; yet consideration must be taken to avoid the proinflammatory side-effects secondary to accumulation SCD1 substrates (SFAs).

Indexed as

Drug DiscoveryAnimalsEnzyme InhibitorsHumansInflammationMetabolic SyndromeStearoyl-CoA DesaturaseEnzyme InhibitorsStearoyl-CoA Desaturase

Identifiers

PMID20216310
PMCPMC3099527
OpenAlexW2048361679

What OpenQuestion holds

Textmetadata
LicenceTDM
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.