ReviewNutrients2025
Thyroid-Microbiome Allostasis and Mitochondrial Performance: An Integrative Perspective in Exercise Physiology.
Review in Nutrients, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Thyroid hormones and metabolic flexibility: tissue-specific control of energy homeostasis.Frontiers in physiology · 2026Review
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
Exercise acts as a physiological stimulus, requiring precise coordination among endocrine, microbial, and mitochondrial systems to maintain metabolic stability through allostatic regulation. The goal of the article is to integrate multidisciplinary evidence to characterize the thyroid-microbiome-mitochondrial axis as a key regulator of the allostatic state in athletic physiological response. During acute, chronic, and overload training phases, the thyroid-microbiome-mitochondrial axis operates bidirectionally, coupling microbial signaling with endocrine and mitochondrial networks to mediate metabolic response to exercise. This response shows interindividual variability driven by sex, age, genetics, and nutritional status, shaping the boundaries between adaptive efficiency and allostatic overload. Microbial metabolites, such as short-chain fatty acids (SCFA) and secondary bile acids, modulate deiodinase activity, bile acid recycling, and mitochondrial biogenesis through AMPK-SIRT1-PGC1α signaling, optimizing substrate use and thermogenic capacity. Thyroid hormones reciprocally regulate gut motility, luminal pH, and bile secretion, maintaining microbial diversity and mineral absorption. Under excessive training load, caloric restriction, or inadequate recovery, this network becomes transiently unbalanced: SCFA synthesis decreases, D3 activity increases, and a reversible low-T
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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 Socratic graph.