Evidence map›Paper›PMID 22228714›Full record

ArticleDiabetes2012

CGI-58/ABHD5-derived signaling lipids regulate systemic inflammation and insulin action.

Caleb C Lord, Jenna L Betters, Pavlina T Ivanova, Stephen B Milne, David S Myers, Jennifer Madenspacher, Gwynneth Thomas, Soonkyu Chung, Mingxia Liu, Matthew A Davis and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Syndromic Conundrums in Diabetes: Seek and Ye Shall Find: The Dorfman-Chanarin Syndrome.Clinical diabetes : a publication of the American Diabetes Association · 2021
    Article
  10. CGI-58: Versatile Regulator of Intracellular Lipid Droplet Homeostasis.Advances in experimental medicine and biology · 2020
    Review
  11. Article
  12. Article
  13. Genetically modified mouse models to study hepatic neutral lipid mobilization.Biochimica et biophysica acta. Molecular basis of disease · 2019
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

18 authors at 5 institutions in 1 country.

Caleb C LordDepartment of Pathology, Section on Lipid Sciences, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.
Jenna L Betters
Pavlina T Ivanova
Stephen B Milne
David S Myers
Jennifer Madenspacher
Gwynneth Thomas
Soonkyu Chung
Mingxia Liu
Matthew A Davis
Richard G Lee
Rosanne M Crooke
Mark J Graham
John S Parks
Dawn L Brasaemle
Michael B Fessler
H Alex Brown
J Mark Brown
Wake Forest University · USVanderbilt University · USIonis Pharmaceuticals (United States) · USTriangle · USRutgers, The State University of New Jersey · US

Funding

STEROL LIPIDSU54GM069338 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DENNIS, EDWARD A · 2003 to 2013
$72.2M
Cell Signaling of Host DefenseZIAES102005 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI FESSLER, MICHAEL B · 2009 to 2025
$41.7M
TISSUE CULTURE COREP01HL049373 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RUDEL, LAWRENCE L · 1993 to 2012
$23.8M
Cell Signaling of Host DefenseZ01ES102005 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI FESSLER, MICHAEL B · 2006 to 2008
$3.3M
Integrative Lipid Metabolism, Inflammation, and Chronic DiseasesT32HL091797 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI PARKS, JOHN S · 2008 to 2017
$1.8M
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
CGI-58 Regulation of Triglyceride Metabolism and InflammationF32DK084582 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BETTERS, JENNA · 2009 to 2010
$108k
Intramural NIH HHS Z01 ES102005NHLBI NIH HHS 1-K99-HL-096166NHLBI NIH HHS 5-P01-HL-049373NHLBI NIH HHS 5-T32-HL-091796NHLBI NIH HHS K99 HL096166NHLBI NIH HHS P01 HL049373NHLBI NIH HHS R00 HL096166NHLBI NIH HHS T32 HL091797NIDDK NIH HHS 1-F32-DK-084582NIDDK NIH HHS F32 DK084582NIGMS NIH HHS U54 GM069338NIGMS NIH HHS U54-GM-069338PHS HHS 1-R01-054797
6 · The paper itself

Abstract

Mutations of comparative gene identification 58 (CGI-58) in humans cause Chanarin-Dorfman syndrome, a rare autosomal recessive disease in which excess triacylglycerol (TAG) accumulates in multiple tissues. CGI-58 recently has been ascribed two distinct biochemical activities, including coactivation of adipose triglyceride lipase and acylation of lysophosphatidic acid (LPA). It is noteworthy that both the substrate (LPA) and the product (phosphatidic acid) of the LPA acyltransferase reaction are well-known signaling lipids. Therefore, we hypothesized that CGI-58 is involved in generating lipid mediators that regulate TAG metabolism and insulin sensitivity. Here, we show that CGI-58 is required for the generation of signaling lipids in response to inflammatory stimuli and that lipid second messengers generated by CGI-58 play a critical role in maintaining the balance between inflammation and insulin action. Furthermore, we show that CGI-58 is necessary for maximal TH1 cytokine signaling in the liver. This novel role for CGI-58 in cytokine signaling may explain why diminished CGI-58 expression causes severe hepatic lipid accumulation yet paradoxically improves hepatic insulin action. Collectively, these findings establish that CGI-58 provides a novel source of signaling lipids. These findings contribute insight into the basic mechanisms linking TH1 cytokine signaling to nutrient metabolism.

Indexed as

Insulin ResistanceSignal Transduction1-Acylglycerol-3-Phosphate O-AcyltransferaseAcyltransferasesAnimalsDiet, High-FatEndotoxinsInflammationLipolysisLiverMaleMiceMice, Inbred C57BLTriglyceridesTumor Necrosis Factor-alpha1-Acylglycerol-3-Phosphate O-Acyltransferase2-acylglycerophosphate acyltransferaseAbhd5 protein, mouseAcyltransferasesEndotoxinsTriglyceridesTumor Necrosis Factor-alpha

Identifiers

PMID22228714
PMCPMC3266405
OpenAlexW2107193895

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.