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Journal Article

White Adipose Tissue as a Functional Target of Secondary Bile Acids in Rainbow Trout (Oncorhynchus mykiss)

Gabriel Pérez-Tierra; Jessica Calo; Ayelén M. Blanco; José L. Soengas
Marine Biotechnology · Vol. 28, Issue 3 · 2026

Abstract

Secondary bile acids (SBAs) are increasingly recognized as hormone-like signals in vertebrates, yet their regulatory potential in fish adipose tissue remains largely unexplored. This study evaluated the acute effects of SBAs (500 µM lithocholic acid -LCA-, 1500 µM deoxycholic acid -DCA-, and their taurine conjugates: 1000 µM T-LCA and 600 µM T-DCA) on the transcriptomic profile, glucose and lipid homeostasis, and bile acid (BA)–related pathways in rainbow trout white adipose tissue (WAT) six hours after intragastric administration. The main results showed that LCA emerged as the main metabolic modulator, enhancing glycolytic entry points via increased hexokinase and pyruvate kinase activities, modulating energy-sensing genes prkaa1/2 (Ampk) and mtor (mTOR), and promoting coordinated adjustments in lipid metabolism, including upregulation of acly and hadh (Hoad), increased Acly activity, and reduced NEFA levels suggesting a potential enhancement of metabolic flexibility and intracellular lipid turnover. In contrast, DCA induced a more restricted response, upregulating mRNA abundance of genes encoding the BA transporters Ostα1 and Ostβ, the receptor FXRα-1, and Cyp8b1 isoforms, suggesting a targeted role in local BA sensing and signaling. Taurine-conjugated SBAs generally produced attenuated effects, with T-DCA tending to promote lipid retention and T-LCA evoking minimal changes. Overall, this study provides the first evidence of BA–related elements in rainbow trout WAT and suggests that SBAs can potentially modulate adipose tissue function in a manner dependent on BA identity, laying the foundation for future studies on their physiological and nutritional roles.

Bibliographic Information

JournalMarine Biotechnology
PublisherSpringer
Publication Date2026-06-01
Publication Year2026
Volume28
Issue3
Document TypeJournal Article
Print ISSN1436-2228
eISSN1436-2236
DOI10.1007/s10126-026-10622-5

Access Information

NARA Access Coverage1999-01-01~Current
Journal Homepagehttps://www.springer.com/journal/10126
Publisher PageOpen Publisher Page
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