ArticleAnimal cells and systems2025
Regulation of BAT thermogenesis via TRPA1-expressing hypothalamic POMC neurons.
Article in Animal cells and systems, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- TRPA1 deficiency alters brown adipose tissue proteome and thermogenic gene expression during cold exposure in mice.Biochemistry and biophysics reports · 2026Article
- Review
- Cross-Talk Between Signaling and Transcriptional Networks Regulating Thermogenesis-Insights into Canonical and Non-Canonical Regulatory Pathways.International journal of molecular sciences · 2026Review
- Therapeutic potential of modulating endogenous PYY expression for controlling overweight and obesity: a narrative review.Frontiers in nutrition · 2026Review
- Enhancer RNA-mediated transcriptional regulation of TDP-43 during early neural lineage specification.Animal cells and systems · 2026Article
- The roles, mechanisms, and therapeutic implications of glucocorticoids in glucose and lipid metabolism.Military Medical Research · 2026Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pro-opiomelanocortin (POMC) neurons in the hypothalamic arcuate nucleus (ARC) play a pivotal role in regulating brown adipose tissue (BAT) thermogenesis via the sympathetic nervous system. The activation of transient receptor potential ankyrin 1 (TRPA1) has been demonstrated to enhance heat production, particularly in BAT. However, no direct evidence has been reported regarding BAT thermogenesis mediated by TRPA1-regulated ARC POMC neurons. This study aimed to investigate the role of TRPA1-expressing hypothalamic POMC neurons in BAT thermogenesis. To confirm TRPA1 expression in ARC POMC neurons, we employed single-cell reverse transcriptase polymerase chain reaction and immunolabeling techniques. Selective TRPA1 agonists, including capsiate and ASP7663, induced depolarization of ARC POMC neurons, an effect that was inhibited by A967079, a TRPA1-selective antagonist. Furthermore, intracerebroventricular (i.c.v.) administration of ASP7663 increased BAT and core body temperature. The thermogenic effect of ASP7663 in BAT was abolished by co-administration of A967079. Among the BAT thermogenic markers, peroxisome proliferator-activated receptor gamma coactivator 1-alpha and PR domain containing 16 (PRDM16) expressions were considerably upregulated following i.c.v. administration of ASP7663. However, this increase was reversed by A967079, except for PRDM16. These findings indicate that TRPA1-mediated activation of hypothalamic POMC neurons is critical in regulating BAT thermogenesis and promoting energy expenditure.
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