Time-restricted feeding plus exercise in aged mice: liver ER stress and collagen
In aged male mice on a standard diet, time-restricted feeding alone partly reduced PERK-related ER stress and tissue changes in the liver; only the combination with exercise significantly lowered upstream PERK phosphorylation, while CHOP stayed elevated. [1]
Automatic summary · not editorially reviewed
The key findings
Aged male mice on a standard diet showed sustained PERK-associated ER stress signaling, mild inflammatory cell infiltration, increased collagen deposition and a higher MASLD score, without increased adiposity or impaired glucose tolerance. [1]
Time-restricted feeding alone partly attenuated PERK-associated ER stress signaling and histological alterations, but only the combined intervention significantly reduced upstream PERK phosphorylation. [1]
CHOP remained elevated across the aged groups, suggesting downstream PERK-associated stress signaling was not fully reversible. [1]
The source at a glance
- Study type / format
- Animal intervention study (abstract)
- Population / context
- Adult (6-month-old) and aged (24-month-old) male C57BL/6 J mice on a standard diet.
- Summary based on
- Study abstract
- Original publication
- July 1, 2026
Aged versus adult mice on a standard diet
The study compared adult (6-month-old) and aged (24-month-old) male C57BL/6 J mice kept on a standard diet. Aged mice showed sustained activation of PERK-associated ER stress signaling, especially along the PERK-CHOP axis, plus mild inflammatory cell infiltration, increased collagen deposition and a higher MASLD score. This occurred even though the aged mice did not have increased adiposity or impaired glucose tolerance.
Supporting source [1]
Feeding schedule alone versus combined with exercise
Time-restricted feeding was a 12-hour fasting/feeding cycle on 5 days per week for 8 weeks. Exercise consisted of alternating aerobic and resistance sessions, 1 hour per day. Time-restricted feeding alone partly attenuated PERK-associated ER stress signaling and the histological changes. However, only the combined intervention significantly reduced upstream PERK phosphorylation. CHOP remained elevated across the aged groups, suggesting the downstream PERK-associated stress signaling was not fully reversible.
Supporting source [1]
Mouse findings on liver aging without obesity
The authors conclude that liver aging under non-obesogenic conditions in these mice is characterized by sustained PERK-associated ER stress signaling together with mild inflammatory cell infiltration and increased collagen deposition. They state that coordinated nutritional and exercise strategies can modulate stress-responsive pathways linked to liver resilience during aging. These are findings in male mice; the abstract does not report effects on lifespan or human outcomes.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. This is a study in male C57BL/6 J mice, so the findings do not establish effects in humans. The abstract reports no lifespan data and no long-term follow-up beyond the 8-week intervention.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Antonio GCF, Pitoli BS, Macêdo APA, de Lima RD, Muñoz VR, Vieira RFL, Dias LM, Cintra DE, Silva ASRD, Ropelle ER, Pauli JR. · europepmc.org · July 1, 2026