Abstract

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 hypothalamic–pituitary–adrenocortical axes in stress-induced food intake behavior in fish.

Highlights

  • Feeding behavior is a complex activity that is associated with food intake

  • The feeding behavior control resides in the arcuate nucleus of the hypothalamus (ARH), where the pro-opiomelanocortin (Pomc) neurons and the neuropeptide Y (Npy)/agouti-related peptide (Agrp) neurons suppress or increase the appetite, respectively [4]

  • To address whether food intake behavior is modified by a stress condition, we exposed salmon parr to an infectious pancreatic necrosis virus (IPNV) challenge

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Summary

Introduction

Feeding behavior is a complex activity that is associated with food intake. Fish are excellent experimental models for studying the regulation of feeding behavior because they have versatile feeding habits and patterns. The feeding behavior control resides in the arcuate nucleus of the hypothalamus (ARH), where the pro-opiomelanocortin (Pomc) neurons (anorexigenic) and the neuropeptide Y (Npy)/agouti-related peptide (Agrp) neurons (orexigenic) suppress or increase the appetite, respectively [4]. The Pomc neurons initiate a cascade of signaling events under the action of leptin including activation of the signal transducer and activator of transcription 3 (Stat). The Pomc neurons initiate a cascade of signaling events under the action of leptin including activation of the signal transducer and activator of transcription 3 (Stat3) This activation drives the expression of the pomc gene, triggering the secretion of the anorexigenic Pomc-derived peptide α-melanocyte-stimulating hormone (α-Msh) [8]. Pomc neurons through α-Msh inhibit the release of orexigenic signals from Npy/Agrp neurons [9]

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