Naringenin prevents cholesterol-induced systemic inflammation, metabolic dysregulation, and atherosclerosis in Ldlr mice
Why this work is in the frame
A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.
Bibliographic record
Abstract
Metabolic syndrome is a collection of abnormalities, including obesity, dyslipidemia, hypertension, and insulin resistance, all of which contribute to the development of type 2 diabetes and atherosclerosis. Insulin resistance, dyslipidemia, and atherosclerosis are amplifi ed by the development of a chronic low-grade infl ammatory response ( 1 ). In insulin-resistant states, monocyte-derived macrophages infi ltrate visceral adipose tissue, resulting in proinfl ammatory cytokine synthesis, either from adipocytes or resident macrophages, which impairs insulin sensitivity ( 2, 3 ). Administration of diets rich in saturated fats to Ldlr / mice represents a model with many characteristics of the metabolic syndrome ( Recent studies in this Abstract Obesity-associated chronic infl ammation contributes to metabolic dysfunction and propagates atherosclerosis. Recent evidence suggests that increased dietary cholesterol exacerbates infl ammation in adipose tissue and liver, contributing to the proatherogenic milieu. The ability of the citrus fl avonoid naringenin to prevent these cholesterol-induced perturbations is unknown. To assess the ability of naringenin to prevent the amplifi ed infl ammatory response and atherosclerosis induced by dietary cholesterol, male Ldlr / mice were fed either a cholesterol-enriched high-fat or low-fat diet supplemented with 3% naringenin for 12 weeks. Naringenin, through induction of hepatic fatty acid (FA) oxidation and attenuation of FA synthesis, prevented hepatic steatosis, hepatic VLDL overproduction, and hyperlipidemia induced by both cholesterol-rich diets. Naringenin attenuated hepatic macrophage infi ltration and infl ammation stimulated by dietary cholesterol. Insulin resistance, adipose tissue expansion, and infl ammation were alleviated by naringenin. Naringenin attenuated the cholesterol-induced formation of both foam cells and expression of infl ammatory markers in peritoneal macrophages. Naringenin signifi cantly decreased atherosclerosis and inhibited the formation of complex lesions, which was associated with normalized aortic lipids and a reversal of aortic infl ammation. We demonstrate that in mice fed cholesterolenriched diets, naringenin attenuates peripheral and systemic infl ammation, leading to protection from atherosclerosis. These studies offer a therapeutically relevant alternative for the prevention of cholesterol-induced metabolic dysregulation.
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Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.006 | 0.001 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.001 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
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 it