Evidence map›Paper›PMID 25300978›Full record

ReviewJournal of inherited metabolic disease2015

Inborn errors of cytoplasmic triglyceride metabolism.

Jiang Wei Wu, Hao Yang, Shu Pei Wang, Krishnakant G Soni, Catherine Brunel-Guitton, Grant A Mitchell

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of inherited metabolic disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Disorders of fatty acid homeostasis.Journal of inherited metabolic disease · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Lipid Myopathies.Journal of clinical medicine · 2018
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Discovery of a stem-like multipotent cell fate.American journal of stem cells · 2018
    Article
  16. Lipid droplets and liver disease: from basic biology to clinical implications.Nature reviews. Gastroenterology & hepatology · 2017
    Review
  17. Review
  18. Article
  19. 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

6 authors at 4 institutions in 3 countries.

Jiang Wei WuDivision of Medical Genetics, Department of Pediatrics, Université de Montréal and CHU Sainte-Justine, 3175 Côte Sainte-Catherine, Montreal, QC, H3T 1C5, Canada.
Hao Yang
Shu Pei Wang
Krishnakant G Soni
Catherine Brunel-Guitton
Grant A Mitchell
Université de Montréal · CACentre Hospitalier Universitaire Sainte-Justine · CANorth West Agriculture and Forestry University · CNTexas A&M University · US

Funding

Canadian Institutes of Health Research 178978Canadian Institutes of Health Research 221920
6 · The paper itself

Abstract

Triglyceride (TG) synthesis, storage, and degradation together constitute cytoplasmic TG metabolism (CTGM). CTGM is mostly studied in adipocytes, where starting from glycerol-3-phosphate and fatty acyl (FA)-coenzyme A (CoA), TGs are synthesized then stored in cytoplasmic lipid droplets. TG hydrolysis proceeds sequentially, producing FAs and glycerol. Several reactions of CTGM can be catalyzed by more than one enzyme, creating great potential for complex tissue-specific physiology. In adipose tissue, CTGM provides FA as a systemic energy source during fasting and is related to obesity. Inborn errors and mouse models have demonstrated the importance of CTGM for non-adipose tissues, including skeletal muscle, myocardium and liver, because steatosis and dysfunction can occur. We discuss known inborn errors of CTGM, including deficiencies of: AGPAT2 (a form of generalized lipodystrophy), LPIN1 (childhood rhabdomyolysis), LPIN2 (an inflammatory condition, Majeed syndrome, described elsewhere in this issue), DGAT1 (protein loosing enteropathy), perilipin 1 (partial lipodystrophy), CGI-58 (gene ABHD5, neutral lipid storage disease (NLSD) with ichthyosis and "Jordan's anomaly" of vacuolated polymorphonuclear leukocytes), adipose triglyceride lipase (ATGL, gene PNPLA2, NLSD with myopathy, cardiomyopathy and Jordan's anomaly), hormone-sensitive lipase (HSL, gene LIPE, hypertriglyceridemia, and insulin resistance). Two inborn errors of glycerol metabolism are known: glycerol kinase (GK, causing pseudohypertriglyceridemia) and glycerol-3-phosphate dehydrogenase (GPD1, childhood hepatic steatosis). Mouse models often resemble human phenotypes but may diverge markedly. Inborn errors have been described for less than one-third of CTGM enzymes, and new phenotypes may yet be identified.

Indexed as

AdipocytesAdipose TissueAnimalsCatalysisCytoplasmDisease Models, AnimalGlycerol KinaseGlycerolphosphate DehydrogenaseGlycerophosphatesHumansHydrolysisLipidsLipolysisMetabolism, Inborn ErrorsMicePhenotypealpha-glycerophosphoric acidGlycerol KinaseGlycerolphosphate DehydrogenaseGlycerophosphatesLipidsTriglycerides

Identifiers

PMID25300978
OpenAlexW2092225219

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.