Heat stress and β-adrenergic agonists alter the adipose transcriptome and fatty acid mobilization in ruminant livestock

Authors

Rachel R. Reith, University of Nebraska-LincolnFollow
Renae L. Sieck, University of Nebraska - LincolnFollow
Pablo C. Grijalva, University of Arizona–TucsonFollow
Erin M. Duffy, University of Nebraska-LincolnFollow
Rebecca M. Swanson, University of Nebraska - LincolnFollow
Anna M. Fuller, University of Nebraska-LincolnFollow
Kristin A. Beede, University of Nebraska - LincolnFollow
Joslyn K. Beard, University of Nebraska-LincolnFollow
Duarte E. Diaz, University of Arizona–TucsonFollow
Ty B. Schmidt, University of Nebraska-LincolnFollow
Dustin T. Yates, University of Nebraska LincolnFollow
Jessica L. Petersen, University of Nebraska - LincolnFollow

Date of this Version

2020

Citation

Transl. Anim. Sci. 2020.4:S141–S144

doi: 10.1093/tas/txaa122

Comments

© The Author(s) 2020. Published by Oxford University Press on behalf of the American Society of Animal Science. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License

Abstract

Growth and feed efficiency of cattle are improved by supplementation with the beta-adrenergic agonists (βAA), ractopamine hydrochloride (RH; β₁AA) or zilpaterol hydrochloride (ZH; β₂AA) (Elam et al., 2009). βAA supplementation alters adipose deposition by inhibiting fatty acid biosynthesis and promoting lipolysis of stored triacylglycerols into free fatty acids (FFAs) (Johnson et al., 2014). However, β₂ adrenoceptors (βAR) desensitize with chronic activation (Re et al., 1997); supplementation is thus limited to the last 20 to 40 d of feeding.

The annual economic impact of heat stress (HS) has been estimated to exceed $2.4 billion (St-Pierre et al., 2003). Heat-stressed livestock have reduced growth rates, dry matter intake, and average daily gain (Mitlöhner et al., 2001; St-Pierre et al., 2003). In response to acute stress, signaling pathways for lipolysis of circulating and stored triglycerides are activated, while chronic stress increases lipogenesis and adipogenesis (Campbell et al., 2009; Peckett et al., 2011). In cattle, HS also increases the responsiveness of adipocytes to lipolytic signals, increasing lipolysis (Faylon et al., 2015).

The objective of this study was to understand how HS and βAA independently and interactively affect adipose tissue. Prior work identified minimal impact of RH on metabolic properties (Barnes et al., 2019) and on the transcriptome of skeletal muscle (Kubik et al., 2018). We therefore hypothesized that RH may be primarily affecting adipose; specifically, that lipolytic activity is increased due to heat and βAA in an additive fashion. We tested this hypothesis in RH-supplemented lambs and ZH-supplemented cattle exposed to HS for 30 and 21 d, respectively.