4.7 Article

Genistein alleviates chronic heat stress-induced lipid metabolism disorder and mitochondrial energetic dysfunction by activating the GPR30-AMPK-PGC-1a signaling pathways in the livers of broiler chickens

Journal

POULTRY SCIENCE
Volume 103, Issue 1, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.psj.2023.103251

Keywords

genistein; heat stress; lipid metabolism disorder; G protein-coupled estrogen receptor; broiler chicken

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The study investigated the preventive effects and mechanisms of genistein (GEN) on production performance and metabolic disorders in broilers under chronic heat stress (HS). The results showed that GEN improved growth performance and hormone secretion in broilers under HS, reduced liver index and abdominal fat rate, and alleviated excessive lipid accumulation in the liver and serum. GEN also effectively regulated gene expression related to lipid metabolism and improved hepatic mitochondrial energetic dysfunction. Therefore, GEN can be used as a feed additive to alleviate heat stress in broilers.
The objective of this study was to investigate the preventive effects and mechanisms of genistein (GEN) on production performance and metabolic disorders in broilers under chronic heat stress (HS). A total of 120 male 3-wk-old Ross broilers were randomly assigned to 5 groups: a thermoneutral zone (TN) group maintained at normal temperature (21 degrees C +/- 1 degrees C daily), an HS group subjected to cyclic high temperature (32 degrees C +/- 1 degrees C for 8 h daily), and 3 groups exposed to HS with varying doses of GEN (50, 100, or 150 mg/kg diet). The experimental period lasted for 3 wk. Here, HS led to a decline in growth performance parameters and hormone secretion disorders (P < 0.05), which were improved by 100 and 150 mg/kg GEN treatment (P < 0.05). Moreover, the HS-induced increases in the liver index (P < 0.01) and abdominal fat rate (P < 0.05) were attenuated by 150 mg/kg GEN (P < 0.05). The HS-induced excessive lipid accumulation in the liver and serum (P < 0.01) was ameliorated after 100 and 150 mg/kg GEN treatment (P < 0.05). Furthermore, the HS-induced decreases in lipolysis-related mRNA levels and increases in lipid synthesis-related mRNA levels in the liver (P < 0.01) were effectively blunted after 100 and 150 mg/kg GEN treatment (P < 0.05). Importantly, the HS-stimulated hepatic mitochondrial energetic dysfunction and decreases in the mRNA or protein levels of peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1 alpha), nuclear respiratory factor 1, and mitochondrial transcription factor A in the liver were ameliorated by 150 mg/kg GEN (P < 0.05). Moreover, 50 to 150 mg/kg GEN treatment resulted in a significant increase in the mRNA or protein levels of G protein-coupled estrogen receptor (GPR30), AMP-activated protein kinase (AMPK) alpha 1, phosphorylated AMPK alpha, and phosphorylated acetyl-CoA carboxylase alpha. Collectively, GEN alleviated metabolic disorders and hepatic mitochondrial energetic dysfunction under HS, possibly through the activation of GPR30-AMPM-PGC-1 alpha pathways. These data provide a sufficient basis for GEN as an additive to alleviate HS in broilers.

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