Some mechanisms regulating nutrient utilisation in livestock during immune activation: an overview

Abstract

The pro-inflammatory cytokines, IL-1, IL-6, TNFα and IFN α/β, produced during immune activation and tissue injury, override control of nutrient utilisation by the hypothalamic-somatotropic axis. The many effects of these cytokines include induction of fever and sickness behaviour, reduced fatty acid uptake by adipose tissue, reduced protein synthesis and enhanced protein breakdown in skeletal muscle, and gluconeogenesis, increased fatty acid synthesis and synthesis of acute phase proteins in the liver. Resistance to the effects of insulin, GH and IGF-1 is induced in adipose tissues, liver and muscle, at least in part through induction by pro-inflammatory cytokines of SOCS proteins which inhibit signal transduction and activation of gene transcription via the JAK/STAT pathway. These homeorhetic changes mobilise nutrients to fuel host defence responses. While an understanding of the mechanisms contributing to the catabolic state have arisen largely from studies of sepsis, trauma and acute challenge with biological mediators of the acute phase response, recent evidence in livestock suggests that graded production of pro-inflammatory cytokines during challenge with pathogens or subclinical infection can induce an incremental reduction in nutrient accretion in products of commercial value from livestock. This relationship highlights the value of good hygiene and reduced stress to improved feed utilisation for growth.