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

Li, Longlong; Lu, Ze; Wang, Yulei; Yang, Ying; Wang, Huihui; Ma, Haitian

doi:10.1016/j.psj.2023.103251

Cited by 3 publications

(2 citation statements)

References 37 publications

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“…These findings are consistent with those of Bayraktar et al (2023), who reported decreased T4 concentrations when Moringa oleifera essential oil was incorporated into quail diets. Similarly, the use of feed additives such as genistein or sodium butyrate also reduced T4 concentrations (El-Maaty et al, 2023;Li et al, 2024). On the other hand, Skomorucha and Sosnówka-Czajka (2017) highlighted the considerable variability in thyroid hormone levels reported by different authors, independent of the experimental factor, such as heat stress exposure.…”

Section: Discussionmentioning

confidence: 89%

Implementation of a metabolizable energy regression model for black soldier fly larvae fat in broiler chicken diets: effect on growth performance, nutrient digestibility, and selected physiological indices

Kierończyk,

Kaczmarek,

Hejdysz

et al. 2024

J. Anim. Feed Sci.

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Section: Discussionmentioning

confidence: 89%

Implementation of a metabolizable energy regression model for black soldier fly larvae fat in broiler chicken diets: effect on growth performance, nutrient digestibility, and selected physiological indices

Kierończyk,

Kaczmarek,

Hejdysz

et al. 2024

J. Anim. Feed Sci.

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“…The proper function of the mitochondrial TCA cycle depends on the maintenance of mitochondrial homeostasis [ 40 ]. HS impairs mitochondrial homeostasis is generally accompanied by the decreased antioxidant capacity and increased ROS content [ 10 , 41 ]. The impaired antioxidant capacity of muscle is generally accompanied by poor meat quality [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

Nano-Se exhibits limited protective effect against heat stress induced poor breast muscle meat quality of broilers compared with other selenium sources

Jing,

Wang,

et al. 2024

J Animal Sci Biotechnol

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Background At present, heat stress (HS) has become a key factor that impairs broiler breeding industry, which causes growth restriction and poor meat quality of broilers. Selenium (Se) is an excellent antioxidant and plays a unique role in meat quality improvement. Recent years, nano-selenium (NanoSe) has received tremendous attention in livestock production, due to its characteristic and good antibacterial performance in vitro. Here, we developed the heat stressed-broiler model to investigate the protective effects of NanoSe on growth performance and meat quality of broilers and compare whether there are differences with that of other Se sources (Sodium selenite, SS; Selenoyeast, SeY; Selenomethionine, SeMet). Results HS jeopardized the growth performance and caused poor meat quality of breast muscle in broilers, which were accompanied by lowered antioxidant capacity, increased glycolysis, increased anaerobic metabolism of pyruvate, mitochondrial stress and abnormal mitochondrial tricarboxylic acid (TCA) cycle. All Se sources supplementation exhibited protective effects, which increased the Se concentration and promoted the expression of selenoproteins, improved the mitochondrial homeostasis and the antioxidant capacity, and promoted the TCA cycle and the aerobic metabolism of pyruvate, thus improved the breast muscle meat quality of broilers exposed to HS. However, unlike the other three Se sources, the protective effect of NanoSe on meat quality of heat stressed-broilers was not ideal, which exhibited limited impact on the pH value, drip loss and cooking loss of the breast muscle. Compared with the other Se sources, broilers received NanoSe showed the lowest levels of slow MyHC, the highest levels of fast MyHC and glycogen, the highest mRNA levels of glycolysis-related genes (PFKM and PKM), the highest protein expression of HSP60 and CLPP, and the lowest enzyme activities of GSH-Px, citroyl synthetase (CS) and isocitrate dehydrogenase (ICD) in breast muscle. Consistent with the SS, the Se deposition in breast muscle of broilers received NanoSe was lower than that of broilers received SeY or SeMet. Besides, the regulatory efficiency of NanoSe on the expression of key selenoproteins (such as SELENOS) in breast muscle of heat stressed-broilers was also worse than that of other Se sources. Conclusion Through comparing the meat quality, Se deposition, muscle fiber type conversion, glycolysis, mitochondrial homeostasis, and mitochondrial TCA cycle-related indicators of breast muscle in heat stressed broilers, we found that the protective effects of organic Se (SeY and SeMet) are better than that of inorganic Se (SS) and NanoSe. As a new Se source, though NanoSe showed some protective effect on breast muscle meat quality of heat stressed broilers, the protective effect of NanoSe is not ideal, compared with other Se sources.

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Selenium restored mitophagic flux to alleviate cadmium-induced hepatotoxicity by inhibiting excessive GPER1-mediated mitophagy activation

Zhang,

Yan,

Xie

et al. 2024

Journal of Hazardous Materials

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

Cited by 3 publications

References 37 publications

Implementation of a metabolizable energy regression model for black soldier fly larvae fat in broiler chicken diets: effect on growth performance, nutrient digestibility, and selected physiological indices

Implementation of a metabolizable energy regression model for black soldier fly larvae fat in broiler chicken diets: effect on growth performance, nutrient digestibility, and selected physiological indices

Nano-Se exhibits limited protective effect against heat stress induced poor breast muscle meat quality of broilers compared with other selenium sources

Selenium restored mitophagic flux to alleviate cadmium-induced hepatotoxicity by inhibiting excessive GPER1-mediated mitophagy activation

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