ArticleMedComm2026
Increased Brown Adipose Tissue Thermogenesis in Phenylketonuria.
Article in MedComm, 2026. 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.
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Who cites it
1 citing paper in PubMed.
- POMC AMPKα1 deletion drives male-specific BAT thermogenesis and obesity resistance.EMBO reports · 2026Article
Corrections and comments
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Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phenylketonuria (PKU), the most common autosomal‑recessive disorder of amino acid metabolism, is characterized by neurological impairment and systemic metabolic alterations caused by chronically elevated phenylalanine (Phe) levels. PKU patients have long been reported to display reduced metabolic rate and impaired thermoregulation, yet the role of brown adipose tissue (BAT) in this condition remains unknown. Here, noninvasive infrared thermography was used to assess BAT activity in a cohort primarily comprising children and adolescents including controls, mild hyperphenylalaninemia (MHPA), and PKU patients, while circulating metabolic and hormonal parameters were analyzed for associations with BAT temperature. Despite overall normothermia, individuals with PKU exhibited higher BAT temperature than both control and MHPA patients, which correlated with circulating fibroblast growth factor 21 (FGF21) and thyroid hormones. To gain mechanistic insight, rats and mice were centrally treated with FGF21, reproducing the BAT thermogenic phenotype along with decreased hypothalamic AMP‑activated protein kinase (AMPK) activity and increased sympathetic drive to BAT. Consistently, analysis of public single‑cell RNA‑sequencing data revealed convergent expression of AMPK, thyroid hormone receptor, and FGF21 receptor signaling in specific hypothalamic neuronal populations. These findings reveal enhanced BAT thermogenesis in PKU and demonstrate that Phe-induced FGF21 disrupts energy homeostasis via hypothalamic AMPK inhibition.
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Registered trials
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