Calorie restriction and glycerophospholipid changes in ApoE-deficient mice
In ApoE-deficient mice, calorie restriction consistently changed glycerophospholipid metabolism across liver, heart and serum; the metabolite LPE (16:0/0:0) rose during abdominal aortic aneurysm progression and fell with calorie restriction. Human multi-omics data showed associations, not causes. [1]
Automatic summary · not editorially reviewed
The key findings
In ApoE-/- mice under calorie restriction, the glycerophospholipid metabolism pathway was consistently modulated across liver, heart and serum. [1]
In an angiotensin II-induced abdominal aortic aneurysm model in ApoE-/- mice, LPE (16:0/0:0) was elevated during progression and significantly reduced by calorie restriction. [1]
Glycerophospholipid metabolism and LPE (16:0) were significantly associated with vascular diseases and aging-related indicators in human multi-omics data, including 76 healthy aged individuals. [1]
The source at a glance
- Study type / format
- Abstract of a preclinical multi-tissue metabolomic study with human multi-omics association analyses
- Population / context
- ApoE-deficient mice (liver, heart, serum; angiotensin II aneurysm model) and human multi-omics data including 76 healthy aged individuals
- Summary based on
- Study abstract
- Original publication
- April 21, 2026
Multi-tissue metabolomics in calorie-restricted ApoE-deficient mice
The abstract reports multi-tissue metabolomic profiling of liver, heart and serum in apolipoprotein E-deficient (ApoE-/-) mice subjected to calorie restriction. The stated aim was to clarify the systematic metabolic reprogramming linked to calorie restriction, which the authors describe as unclear. Across these tissues, the glycerophospholipid metabolism pathway was consistently modulated by calorie restriction. This is a description of an animal metabolomic experiment; the abstract does not report sample sizes, feeding details or the full list of changed metabolites.
Supporting source [1]
LPE (16:0/0:0) in an Angiotensin-II aneurysm model
To explore relevance to vascular disease, the authors profiled serum metabolomics in an abdominal aortic aneurysm (AAA) model induced by angiotensin II infusion in ApoE-/- mice. The level of lysophosphatidylethanolamine (LPE) (16:0/0:0), a metabolite in the glycerophospholipid pathway, was elevated during AAA progression and significantly reduced by calorie restriction intervention. The authors suggest it may be a vascular disease risk factor. This is a suggestion from an animal model; the abstract does not show that LPE causes aneurysms or that lowering it prevents them.
Supporting source [1]
Human multi-omics associations with vascular disease and aging
The abstract reports that glycerophospholipid metabolism and LPE (16:0) were significantly associated with vascular diseases and aging-related indicators in human multi-omics data. These data included public transcriptomic and lipidomic data and the authors' serum multi-omics profiling of 76 healthy aged individuals. The authors describe glycerophospholipid metabolism and LPE (16:0) as systemic signatures of calorie restriction with diagnostic potential and as indicators of systemic aging. These are associations in human data, not evidence that calorie restriction or LPE changes cause vascular disease or aging in people.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Sample sizes, feeding protocols, mouse ages and statistical details are not reported here. The mouse experiments are preclinical, and the human data are associations, not causal evidence. Diagnostic potential is proposed, not validated.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Wei ZY, Wang HP, Tang S, Yang B, Lv SJ, Wang HY, Zhang YF, Li M, Zheng W, Wang X, Shi X, Liu DP, Chen HZ. · europepmc.org · April 21, 2026