Accelerated BDNF expression in visceral white adipose tissues following high‐fat diet feeding in mice

Brain‐derived neurotrophic factor (BDNF) is expressed in the white adipose tissues (WATs), and the expression increases during high‐fat diet (HFD) feeding, implicating its role in obesity. Here, we focused on BDNF expression in epididymal WAT (eWAT), a visceral adipose tissue, in mice. During 2 week...

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Veröffentlicht in:Genes to cells : devoted to molecular & cellular mechanisms 2024-11, Vol.29 (11), p.1077-1084
Hauptverfasser: Sakata, Kurumi, Fukuchi, Mamoru
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Sprache:eng
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Zusammenfassung:Brain‐derived neurotrophic factor (BDNF) is expressed in the white adipose tissues (WATs), and the expression increases during high‐fat diet (HFD) feeding, implicating its role in obesity. Here, we focused on BDNF expression in epididymal WAT (eWAT), a visceral adipose tissue, in mice. During 2 weeks of HFD feeding, Bdnf mRNA expression in eWAT slightly increased, but a robust increase was observed after 8 weeks of HFD feeding. This upregulation of Bdnf mRNA was correlated with significant induction of hypoxia‐inducible factor 1α (Hif1α) and platelet‐derived growth factor subunit B (Pdgfb) mRNA in eWAT following 8 weeks of HFD feeding. Furthermore, the increased expression of the M1 macrophage markers was strongly correlated with the elevation of Bdnf mRNA in the eWAT. Notably, 8 weeks of HFD feeding significantly elevated Tnfα mRNA expression in eWAT, while no such induction was observed in inguinal WAT (iWAT). In contrast, the expression of Adipoq (adiponectin), implicated in improved insulin sensitivity and anti‐inflammatory effects, was significantly upregulated in iWAT, but not in eWAT. Thus, our study may show the role of BDNF in eWAT in obesity models, potentially contributing to the pathological state of visceral adipose tissues. A robust induction of brain‐derived neurotrophic factor mRNA expression was observed particularly in epididymal white adipose tissue of mice fed with high‐fat diet for 8 weeks.
ISSN:1356-9597
1365-2443
1365-2443
DOI:10.1111/gtc.13162