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Increased Brown Adipose Tissue Thermogenesis in Phenylketonuria
Journal article   Open access   Peer reviewed

Increased Brown Adipose Tissue Thermogenesis in Phenylketonuria

Noemí López-Rey, Alba Cabaleiro, María P Pata, Marion Peyrou, Ánxela Estévez-Salguero, Paola Fernández-Sanmartín, Donald A Morgan, Vitor Ferreira, Paula Sánchez-Pintos, Cintia Folgueira, …
MedComm (2020), Vol.7(6), e70820
06/01/2026
DOI: 10.1002/mco2.70820
PMCID: PMC13263790
PMID: 42292855
url
https://doi.org/10.1002/mco2.70820View
Published (Version of record) Open Access

Abstract

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.
Amino Acids Catecholamines Dopamine Enzymes Metabolism Body fat Phenylketonuria Thermogenesis

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