ArticleArteriosclerosis, thrombosis, and vascular biology2024
Time-Restricted Feeding Reduces Atherosclerosis in LDLR KO Mice but Not in ApoE Knockout Mice.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Effect of 2 Weeks of Time-Restricted Eating on Innate Immunity and Systemic Inflammation in Patients With a History of Myocardial Infarction: A Randomized-Controlled Crossover Study.Journal of the American Heart Association · 2026Trial
- Timing of food intake impacts cardiovascular and neuroendocrine physiology and risk of disease.Cardiovascular research · 2026Review
- Impacts of ketogenic diet intervention on cardiometabolic outcomes in obese, dysglycemic mice.Cardiovascular diabetology · 2026Review
- Immuno-inflammatory-metabolic interactions in cardiovascular diseases: a review from basic mechanisms to clinical translation.Frontiers in immunology · 2026Review
- Established dietary interventions and time-restricted eating for cardiovascular disease prevention.Cell reports. Medicine · 2025Review
- Article
- Time-restricted feeding mediated synchronization of circadian rhythms to sustain cardiovascular health.Journal of molecular and cellular cardiology · 2025Review
- The Effects of a Novel Nutraceutical Composition Containing Coenzyme QFood science & nutrition · 2025Article
- Hyperlipidemia drives tumor growth in a mouse model of obesity-accelerated breast cancer growth.Cancer & metabolism · 2025Article
- Decoding the Liver-Heart Axis in Cardiometabolic Diseases.Circulation research · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
backgroundDyslipidemia increases cardiovascular disease risk, the leading cause of death worldwide. Under time-restricted feeding (TRF), wherein food intake is restricted to a consistent window of <12 hours, weight gain, glucose intolerance, inflammation, dyslipidemia, and hypercholesterolemia are all reduced in mice fed an obesogenic diet. LDLR (low-density lipoprotein receptor) mutations are a major cause of familial hypercholesterolemia and early-onset cardiovascular disease.
methodsWe subjected benchmark preclinical models, mice lacking LDLR-knockout or ApoE knockout to ad libitum feeding of an isocaloric atherogenic diet either ad libitum or 9 hours TRF for up to 13 weeks and assessed disease development, mechanism, and global changes in hepatic gene expression and plasma lipids. In a regression model, a subset of LDLR-knockout mice were ad libitum fed and then subject to TRF.
resultsTRF could significantly attenuate weight gain, hypercholesterolemia, and atherosclerosis in mice lacking the LDLR-knockout mice under experimental conditions of both prevention and regression. In LDLR-knockout mice, increased hepatic expression of genes mediating β-oxidation during fasting is associated with reduced VLDL (very-low-density lipoprotein) secretion and lipid accumulation. Additionally, increased sterol catabolism coupled with fecal loss of cholesterol and bile acids contributes to the atheroprotective effect of TRF. Finally, TRF alone or combined with a cholesterol-free diet can reduce atherosclerosis in LDLR-knockout mice. However, mice lacking ApoE, which is an important protein for hepatic lipoprotein reuptake do not respond to TRF.
conclusionsIn a preclinical animal model, TRF is effective in both the prevention and regression of atherosclerosis in LDLR knockout mice. The results suggest TRF alone or in combination with a low-cholesterol diet can be a lifestyle intervention for reducing cardiovascular disease risk in humans.
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