Choline status modulates the development of atherosclerosis in LDL receptor knockout mice (272.7)
Bibliographic record
Abstract
Background: Phosphatidylethanolamine N‐methyltransferase (Pemt) is the only de novo pathway for phosphatidylcholine (PC) synthesis in mammals; as such, Pemt ‐/‐ mice are chronically choline‐deficient. PEMT deficiency dramatically reduces atherosclerosis development in LDL receptor (LDLR) knockout mice. This atheroprotective effect is believed to be mediated by reduction in circulating lipid levels. Purpose: to investigate the effect of altering choline status on plasma lipid profiles and atherosclerosis development in LDLR‐/‐ mice, and to test the hypothesis that choline supplementations reverse the atheroprotective effect of PEMT deletion via normalization plasma lipid profiles. Methods: LDLR‐/‐ and PEMT‐/‐/ LDLR‐/‐ male mice were given free access to high fat high cholesterol diet. Choline in diet (g/Kg) ranged from 0‐10. Atherosclerosis development was assessed by measuring plaque area in cross sectional aortic root. Results: In LDLR‐/‐ mice, choline‐deficient group gained less weight, presented higher liver TG, CE and PL compared to other groups. Excessive choline group presented significantly higher liver PC and plasma TG. Choline supplementation caused step‐wise increase in atherosclerosis development in LDLR‐/‐ mice. Significant correlations were observed between choline in diet and plasma PL (r=0.8075, P<0.0001), plasma total cholesterol (r=0.8369, P<0.0001), plasma TG (r=0.7551, P<0.0001), and aortic root atherosclerotic plaque area (r=0.6985, P<0.0001). As previously reported, PEMT‐/‐/ LDLR‐/‐ mice were protected from atherosclerosis. Increasing dietary choline from 3‐10 (g/Kg) decreased liver weight, TG, and PL. Surprisingly; it didn’t promote atherogenic plasma lipid profiles nor increased plaque formation. Conclusion: There is a positive correlation between dietary choline and the development of atherosclerosis in the LDLR‐/‐ mice. Choline deficiency cannot solely explain the atheroprotective effect of PEMT deletion in the LDLR‐/‐ mice. Grant Funding Source : Supported by Canadian Institutes of Health Research (CIHR) & Alberta Innovates Bio Solutions (AI B)
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.001 | 0.001 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.001 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.003 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".