Evidence map›Paper›PMID 21908646›Full record

ArticleJournal of lipid research2011

Group 1B phospholipase A₂ deficiency protects against diet-induced hyperlipidemia in mice.

Norris I Hollie, David Y Hui

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Hyperlipidemia in membranous nephropathy.Clinical kidney journal · 2026
    Review
  2. Article
  3. Article
  4. Inactivation of Group 1B Phospholipase AInternational journal of molecular sciences · 2023
    Article
  5. Review
  6. The interaction between brain and liver regulates lipid metabolism in the TBI pathology.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Cytotoxic, Antioxidant, and Metabolic Enzyme Inhibitory Activities ofOxidative medicine and cellular longevity · 2020
    Article
  13. Article
  14. Review
  15. Group 1B phospholipase ABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019
    Review
  16. Epithelial-Cell-Derived Phospholipase ACell host & microbe · 2017
    Article
  17. Article
  18. Article
  19. The Roles of the Secreted Phospholipase AAdvances in immunology · 2016
    Review
  20. A new era of secreted phospholipase A₂.Journal of lipid research · 2015
    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

2 authors at 1 institution in 1 country.

Norris I HollieDepartment of Pathology and Laboratory Medicine, Metabolic Diseases Institute, University of Cincinnati College of Medicine, Cincinnati, OH 45237, USA.
David Y Hui
University of Cincinnati Medical Center · US

Funding

Role of Group 1B Phospholipase A2 on Diet-induced Metabolic DiseasesR01DK069967 · NIDDK · UNIVERSITY OF CINCINNATI · PI HUI, DAVID YIU-KWAN · 2006 to 2014
$3.0M
NIDDK NIH HHS DK-069967NIDDK NIH HHS DK-069967-04S1NIDDK NIH HHS R01 DK069967
6 · The paper itself

Abstract

Excessive absorption of products of dietary fat digestion leads to type 2 diabetes and other obesity-related disorders. Mice deficient in the group 1B phospholipase A₂ (Pla2g1b), a gut digestive enzyme, are protected against diet-induced obesity and type 2 diabetes without displaying dietary lipid malabsorption. This study tested the hypothesis that inhibition of Pla2g1b protects against diet-induced hyperlipidemia. Results showed that the Pla2g1b(-/-) mice had decreased plasma triglyceride and cholesterol levels compared with Pla2g1b(+/+) mice subsequent to feeding a high-fat, high-carbohydrate (hypercaloric) diet. These differences were evident before differences in body weight gains were observed. Injection of Poloxamer 407 to inhibit lipolysis revealed decreased VLDL production in Pla2g1b(-/-) mice. Supplementation with lysophosphatidylcholine, the product of Pla2g1b hydrolysis, restored VLDL production rates in Pla2g1b(-/-) mice and further elevated VLDL production in Pla2g1b(+/+) mice. The Pla2g1b(-/-) mice also displayed decreased postprandial lipidemia compared with Pla2g1b(+/+) mice. These results show that, in addition to dietary fatty acids, gut-derived lysophospholipids derived from Pla2g1b hydrolysis of dietary and biliary phospholipids also promote hepatic VLDL production. Thus, the inhibition of lysophospholipid absorption via Pla2g1b inactivation may prove beneficial against diet-induced hyperlipidemia in addition to the protection against obesity and diabetes.

Indexed as

Animal FeedAnimalsDietDietary CarbohydratesDietary SupplementsDiet, High-FatGroup IB Phospholipases A2HyperlipidemiasLipoproteins, VLDLLiverLysophosphatidylcholinesMaleMicePostprandial PeriodTriglyceridesDietary CarbohydratesGroup IB Phospholipases A2Lipoproteins, VLDLLysophosphatidylcholinesTriglycerides

Identifiers

PMID21908646
PMCPMC3196232
OpenAlexW2071034679

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.