ArticleMetabolic brain disease2026
Intensity-dependent effects of interval training on brain mitophagy, metabolic signaling pathways, and neuroinflammation in a rat model of type 2 diabetes.
Article in Metabolic brain disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes mellitus impairs brain metabolic and mitochondrial homeostasis, yet the intensity-dependent neuroprotective effects of exercise remain poorly defined. This study examined the intensity‑dependent effects of interval training on brain mitophagy, metabolic signaling, oxidative stress, and neuroinflammation in a type 2 diabetes model. Fifty male rats were assigned to five groups (n = 10 each): healthy control (HC), diabetic control (DC), diabetic + low-intensity interval training (LIIT), diabetic + moderate-intensity interval training (MIIT), and diabetic + high-intensity interval training (HIIT). Following the intervention, hippocampal and cortical tissues were analyzed for metabolic signaling markers (AMPK, ULK1, mTOR), mitophagy-related proteins (PINK1, Parkin, LC3-II/I, p62), oxidative and antioxidant indices (MDA, SOD, CAT, TAC), pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), and lipid peroxidation (4-HNE). Statistical significance was set at p < 0.05. MIIT and HIIT activated AMPK-ULK1 signaling and suppressed mTOR in the hippocampus and cortex, leading to enhanced mitophagy, particularly in the hippocampus. These adaptations were accompanied by improved redox balance, reduced lipid peroxidation, and attenuated neuroinflammation, with effects increasing in an intensity-dependent manner (LIIT < MIIT < HIIT). Interval training may support neuroprotective adaptations in type 2 diabetes, with moderate- and high-intensity protocols potentially offering greater benefits than low intensity. Still, these effects require confirmation in broader experimental contexts.
Indexed as
Identifiers
42667305What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.