Dietary taurine supplementation ameliorates muscle loss in chronic heat stressed broilers via suppressing the perk signaling and reversing endoplasmic reticulum‐stress‐induced apoptosis. (10th October 2020)

• Record Type: Journal Article
• Authors: Ma, Bingbing; Zhang, Lin; Li, Jiaolong; Xing, Tong; Jiang, Yun; Gao, Feng
• Is Part Of: Journal of the science of food and agriculture. Volume 101:Number 5(2021)
• Page Start: 2125
• Page End: 2134
• Publication Date: 2020-10-10
• Subjects: heat stress -- taurine -- chicken -- unfolded protein response -- protein metabolism; Food -- Periodicals; Agriculture -- Periodicals; 664
• DOI: 10.1002/jsfa.10835
• Languages: English
• ISSNs: 0022-5142

Abstract

Abstract: BACKGROUND: Heat stress seriously affects animal health and induces enormous financial losses in poultry production. Exploring the appropriate means for ameliorating unfavorable effects caused by heat stress is essential. We investigated whether taurine supplementation could attenuate breast muscle loss in chronic heat‐stressed broilers, as well as its mechanism. We designed three groups: a normal control group (22 °C), a heat stress group (32 °C) and a taurine treatment group (32 °C, basal diet + 5 g·kg −1 taurine). RESULTS: We found that taurine significantly moderated the decreases of breast muscle mass and yield, as well as the increases of serum aspartate aminotransferase activity and serum urine acid level in chronic heat‐stressed broilers. Additionally, supplementary taurine significantly alleviated elevations of the cytoplasm Ca 2+ concentration, protein expressions of GRP78 and p‐PERK, mRNA expressions of Ca 2+ channels ( RyR1, IP3R3 ) and endoplasmic reticulum (ER) stress factors ( GRP78, GRP94, PERK, EIF2α, ATF4, IRE1, XBP1, ATF6 and CHOP ), apoptosis ( Caspase‐3 and TUNEL), protein catabolism, and the reduction of taurine transporter ( TauT ) mRNA expression in the breast muscle induced by chronic heat stress. CONCLUSION: Supplementary taurine could attenuate chronic heat stress‐induced breast muscle loss via reversing ER stress‐induced apoptosis and suppressing protein catabolism. © 2020 Society of Chemical Industry