Evidence map›Paper›PMID 27438680›Full record

ReviewCurrent opinion in lipidology2016

Intestinal phospholipid and lysophospholipid metabolism in cardiometabolic disease.

David Y Hui

Abstract readReview
In one paragraph

Review in Current opinion in lipidology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

36 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. Review
  7. Development of anFrontiers in pharmacology · 2025
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  16. Male-Biased Gut Microbiome and Metabolites Aggravate Colorectal Cancer Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
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  18. Article
  19. Review
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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

1 author.

David Y HuiDepartment of Pathology, Metabolic Disease Research Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA.

Funding

Role of Lipoprotein Receptors in Diet-induced Obesity and DiabetesR01DK074932 · NIDDK · UNIVERSITY OF CINCINNATI · PI HUI, DAVID YIU-KWAN · 2007 to 2019
$4.4M
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
Role of Endothelial and Macrophage ApoER2 in Atherosclerosis ModulationR01HL118001 · NHLBI · UNIVERSITY OF CINCINNATI · PI HUI, DAVID YIU-KWAN, SHAUL, PHILIP W · 2014 to 2017
$2.8M
Cell Type Specific Roles of ApoE2 in Tissue Inflammation and AtherosclerosisR01HL131028 · NHLBI · UNIVERSITY OF CINCINNATI · PI HUI, DAVID YIU-KWAN, REARDON-ALULIS, CATHERINE A · 2016 to 2019
$2.6M
Intestinal LPC/LPA modulation of gut microbiota and metabolic diseaseR01DK112657 · NIDDK · UNIVERSITY OF CINCINNATI · PI HUI, DAVID YIU-KWAN · 2016 to 2020
$1.8M
NHLBI NIH HHS R01 HL118001NHLBI NIH HHS R01 HL131028NIDDK NIH HHS R01 DK069967NIDDK NIH HHS R01 DK074932NIDDK NIH HHS R01 DK112657
6 · The paper itself

Abstract

purpose of reviewPhospholipids are major constituents in the intestinal lumen after meal consumption. This article highlights current literature suggesting the contributory role of intestinal phospholipid metabolism toward cardiometabolic disease manifestation. RECENT

findingsGroup 1b phospholipase A2 (PLA2g1b) catalyzes phospholipid hydrolysis in the intestinal lumen. The digestive product lysophospholipid, particularly lysophosphatidylcholine (LPC), has a direct role in mediating chylomicron assembly and secretion. The LPC in the digestive tract is further catabolized into lysophosphatidic acid and choline via autotaxin-mediated and autotaxin-independent mechanisms. The LPC and lysophosphatidic acid absorbed through the digestive tract and transported to the plasma directly promote systemic inflammation and cell dysfunction, leading to increased risk of cardiovascular disease and obesity/diabetes. The choline moiety generated in the digestive tract can also be used by gut bacteria to generate trimethylamine, which is subsequently transported to the liver and oxidized into trimethylamine-N-oxide that also enhances atherosclerosis and cardiovascular abnormalities. SUMMARY: Products of phospholipid metabolism in the intestine through PLA2g1b and autotaxin-mediated pathways directly contribute to cardiometabolic diseases through multiple mechanisms. The implication of these studies is that therapeutic inhibition of PLA2g1b and autotaxin in the digestive tract may be a viable approach for cardiovascular and metabolic disease intervention.

Indexed as

AnimalsCholineHumansIntestinal MucosaLysophospholipidsMetabolic DiseasesMyocardiumCholineLysophospholipids

Identifiers

PMID27438680
PMCPMC5125253

What OpenQuestion holds

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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.