4.7 Article

Viral Infection Drives the Regulation of Feeding Behavior Related Genes in Salmo salar

Journal

Publisher

MDPI
DOI: 10.3390/ijms222111391

Keywords

feeding behavior; lipid metabolism; inflammation; infection

Funding

  1. ANID (Chile) funds (FONDECYT) [1190627]
  2. CONICYT-PCHA/National PhD 2018 grant from Nataly Sanhueza [21181886]
  3. CONICYT-PCHA/National PhD grant from Beatriz Carnicero [21181886]
  4. FONDEQUIP Chile funds [EQM180201]

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Feeding behavior in fish is influenced by multiple signals in the brain, with stress cues such as viral infection triggering responses from hypothalamic neurons to regulate energy storage and expenditure. This study provides evidence of a molecular linkage between inflammation and food intake in Salmon salar, highlighting the importance of understanding the interplay between energy homeostasis and pathogenesis in fish.
The feeding behavior in fish is a complex activity that relies on the ability of the brain to integrate multiple signals to produce appropriate responses in terms of food intake, energy expenditure, and metabolic activity. Upon stress cues including viral infection or mediators such as the proinflammatory cytokines, prostaglandins, and cortisol, both Pomc and Npy/Agrp neurons from the hypothalamus are stimulated, thus triggering a response that controls both energy storage and expenditure. However, how appetite modulators or neuro-immune cues link pathogenesis and energy homeostasis in fish remains poorly understood. Here, we provide the first evidence of a molecular linkage between inflammation and food intake in Salmon salar. We show that in vivo viral challenge with infectious pancreatic necrosis virus (IPNV) impacts food consumption by activating anorexic genes such as mc4r, crf, and pomcb and 5-HT in the brain of S. salar. At the molecular level, viral infection induces an overall reduction in lipid content in the liver, favoring the production of AA and EPA associated with the increment of elovl2 gene. In addition, infection upregulates leptin signaling and inhibits insulin signaling. These changes are accompanied by a robust inflammatory response represented by the increment of Il-1b, Il-6, Tnfa, and Pge2 as well as an increased cortisol level in vivo. Thus, we propose a model in which hypothalamic neurons respond to inflammatory cytokines and stress-related molecules and interact with appetite induction/inhibition. These findings provide evidence of crosstalk between pathogenesis-driven inflammation and hypothalamicpituitary-adrenocortical axes in stress-induced food intake behavior in fish.

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