# One-month early time-restricted eating mitigates brain aging and enhances memory in males with metabolic syndrome: an MRI structural study

**Authors:** Yue Qin, Xiaoshi Li, Lei Wang, FengLin Shuang, Xin Jin, Tingting Qu, Yuying Wang, Yunbing Wu, Juan Tian, Yifan Qian, Qianqian Lv, Zirui Wang, Yarong Wang, Ying Xing

PMC · DOI: 10.3389/fragi.2026.1752738 · Frontiers in Aging · 2026-02-18

## TL;DR

A one-month time-restricted eating plan improved brain health and memory in men with metabolic syndrome.

## Contribution

This study shows that short-term time-restricted eating can reduce brain aging and improve memory in men with metabolic syndrome.

## Key findings

- A one-month eTRE intervention reduced brain age gap and improved metabolic markers in males with MetS.
- Memory recall scores increased significantly after the eTRE intervention.
- Gray matter volume increased in brain regions like the hippocampus and thalamus, linked to memory improvements.

## Abstract

Metabolic syndrome (MetS) has emerged as a global health concern challenges to human brain aging and memory function. While early time-restricted eating (eTRE) has been widely recognized as an effective dietary approach for improving metabolic regulation, its potential influence on brain aging and memory performance in individuals with MetS has not yet been fully elucidated.

Twenty three males with MetS were enrolled and underwent a 1-month eTRE intervention. Assessments included metabolic profiling, memory evaluation, and MRI scanning at both baseline and post-intervention. Brain age gap (BAG) was estimated using the brainageR package, after which voxel-based morphometry (VBM) was applied to identify gray matter regions whose structural changes contributed most to brain age alterations. Subsequently, correlation analyses were performed to examine the associations between these regional changes and memory function.

After 1-month of eTRE, males with MetS showed a significant reduction in BAG difference (p < 0.05), along with improvements in BMI, fasting glucose, and lipid profiles (All p < 0.05). Moreover, delayed recall and immediate recall scores demonstrated a significant increase (All p < 0.05). VBM identified gray matter volume increases in left hippocampus, left thalamus, left red nucleus, and left substantia nigra, with left thalamic gray matter volume changes significantly negative correlation with changes of immediate recall scores (r = −0.512, p = 0.01).

The 1-month eTRE intervention improved metabolic health, reduced brain aging, and enhanced memory in males with MetS. These benefits were associated with structural changes in the brain, indicating that even a short-term eTRE intervention serve as an effective strategy to promote brain health in individuals with MetS.

## Linked entities

- **Diseases:** metabolic syndrome (MONDO:0000816)

## Full-text entities

- **Genes:** PKM (pyruvate kinase M1/2) [NCBI Gene 5315] {aka CTHBP, HEL-S-30, OIP3, PK3, PKM2, TCB}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, CCK (cholecystokinin) [NCBI Gene 885], TRE-TTC3-1 (tRNA-Glu (anticodon TTC) 3-1) [NCBI Gene 7193] {aka TRE, TRNAE1, TRNE}
- **Diseases:** Parkinson's disease (MESH:D010300), head injury (MESH:D006259), MetS (MESH:D024821), inflammation (MESH:D007249), neurodegenerative disorders (MESH:D019636), Anxiety (MESH:D001007), intracranial lesions (MESH:D020765), neuroinflammation (MESH:D000090862), chronic kidney disease (MESH:D051436), liver cirrhosis (MESH:D008103), malignant tumours (MESH:D009369), diabetes (MESH:D003920), mental disorders (MESH:D001523), Alzheimer's disease (MESH:D000544), decline in memory ability (MESH:D060825), hypothalamic obesity (MESH:D009765), acquired immunodeficiency syndrome (MESH:D000163), hypoglycemic (MESH:C000721848), adrenal diseases (MESH:D000307), Cushing's syndrome (MESH:D003480), metabolic dysregulation (MESH:D021081), neurological disorders (MESH:D009461), hypogonadism (MESH:D007006), acromegaly (MESH:D000172), vascular dementia (MESH:D015140), hypertension (MESH:D006973), brain dysfunction (MESH:D001927), microvascular injury (MESH:D017566), insulin resistance (MESH:D007333), rheumatic autoimmune diseases (MESH:D012216), weight loss (MESH:D015431), cerebrovascular disease (MESH:D002561), endocrine disorders (MESH:D004700), gastrointestinal diseases (MESH:D005767), cardiovascular disease (MESH:D002318), eating (MESH:D001068), systemic (MESH:D015619), dementia (MESH:D003704), type 1 diabetes (MESH:D003922), insulinoma (MESH:D007340), Depression (MESH:D003866), type 2 diabetes (MESH:D003924), neuronal damage (MESH:D009410), memory deterioration (MESH:D008569), cognitive decline (MESH:D003072), caloric restriction (MESH:D002313)
- **Chemicals:** TC (MESH:D013667), sugar (MESH:D000073893), fat (MESH:D005223), triglycerides (MESH:D014280), water (MESH:D014867), blood glucose (MESH:D001786), Cholesterol (MESH:D002784), TG (MESH:D013866), BAG (-), lipid (MESH:D008055), ROS (MESH:D017382), Glucose (MESH:D005947), alcohol (MESH:D000438)
- **Species:** Nicotiana tabacum (American tobacco, species) [taxon 4097], Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12957201/full.md

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12957201/full.md

## References

38 references — full list in the complete paper: https://tomesphere.com/paper/PMC12957201/full.md

---
Source: https://tomesphere.com/paper/PMC12957201