Western Blot 快速封闭液

Introduction Human beings and animals have been exposed to long-term artificial lighting environments to induce glucose metabolism disorder. Melatonin (MT) is involved in the regulation of glucolipid metabolism, and can prevent skeletal muscle wasting as well as sarcopenia-associated diseases. However, the effect of exogenous MT on skeletal muscle glucose metabolism and the involvement of the parasympathetic pathway have not been clarified. Objectives: To investigate the role of parasympathetic regulatory pathway in the mediating the effects of exogenous MT on skeletal muscle glucose metabolism following long-term light exposure. Methods: This study established rapid growth period broiler models, while characterized muscle histological analysis, glucose metabolism indexes and related genes expression through parasympathetic activation, exogenous MT administration and exogenous MT with parasympathetic inhibition experiments. Results: Long-term light exposure inhibited muscle glycogen synthesis, promoted muscle glycogen decomposition, increased anaerobic glycolysis, decreased aerobic respiration and induced the injury in breast muscle. Parasympathetic activation and exogenous MT caused a marked improvement in muscle glycogen accumulation, aerobic glycolysis and the injury in breast muscle. The exogenous MT beneficial functions were alleviated by parasympathetic inhibition. Furthermore, parasympathetic activation and exogenous MT administration protected cecal microbiota homeostasis, by improving stability of the gut microbiota community and increasing the relative abundance of Lactobacillus . Lactobacillus abundance was positively associated with muscle glycogen accumulation. Conclusion: Taken together, this study highlighted the role of the novel parasympathetic regulatory pathway in the effects of exogenous MT in maintaining glucose metabolism homeostasis and restoring the damage in skeletal muscle with long-term light exposure. The results indicate that gut microbiota are involved in the MT-parasympathetic regulatory network. This study filles the gap in autonomic nervous-endocrine regulation under long light exposure, and provides a new insight to alleviate long light exposure-induced glucose metabolism disorders to improve the growth and health of humans and animals.

To date, extensive research has shown that heat stress disturbs glucose and lipid metabolism in broiler chickens. Recent evidence suggests that chromium supplementation influences metabolic regulation, particularly in glucose and lipid homeostasis in mammals. This study aimed to evaluate the effects of chromium picolinate supplementation on glucose and lipid metabolism in the breast muscle of broiler chickens under chronic heat stress. A total of 180 male Arbor Acres ( AA ) broilers (22 days old) were randomly assigned to three groups: a thermoneutral control group (21°C), a heat stress group (31°C), and a heat stress group receiving chromium picolinate (31°C + 400 μg/Kg elemental chromium). After 14 days, heat stress significantly impaired growth performance, induced insulin resistance, increased fat deposition, and suppressed the expression of key glucose and lipid metabolic genes. In contrast, chromium picolinate improved the average daily feed intake ( ADFI ), average daily gain ( ADG ), and reduced feed conversion ratio ( FCR ). It also upregulated glucose metabolism genes ( GLUT1, PI3K, GS ) and lipid metabolism genes ( PPARα, CPT-1, LPL ) in breast muscle. Overall, chromium picolinate alleviated heat stress-induced skeletal muscle glucose and lipid metabolism disturbances in broiler chickens.

Prolonged light periods resulted in up-regulation of cecal 5-hydroxytryptamine ( 5-HT ) synthesis and secretion, disorders of breast muscle glucose metabolism and alteration in gut microbiota composition. The present study was conducted to investigate the effects of cecal microbiota on peripheral 5-HT metabolism and breast muscle glucose metabolism in broiler chickens underlying prolonged light periods. A total of 144 5-day-old male Arbor Acres ( AA ) broiler chickens were randomly divided into four treatment groups i.e., 12 hours light: 12 hours dark ( 12L:12D ) photoperiod group, 18 hours light: 6 hours dark ( 18L:6D ) photoperiod group, 18L:6D photoperiod with phosphate buffered saline ( PBS ) solution administration group ( 18L:6D+PBS ) and 18L:6D photoperiod with cecal microbiota transplantation ( CMT ) group ( 18L:6D+CMT ) for 14 days. The results demonstrated that the 18L:6D photoperiod increased breast muscle rate ( P < 0.05) but induced the morphological damage of breast muscle, dysregulation of breast muscle glucose metabolism and higher peripheral 5-HT synthesis ( P < 0.05). In contrast, CMT significantly improved breast muscle weight and breast muscle ratio while reducing the breast muscle injury. Furthermore, CMT alleviated glucose metabolism dysregulation, as evidenced by significant reductions in serum glucose ( P < 0.05), insulin ( INS ) ( P < 0.05), homeostasis model assessment of insulin resistance ( HOMA-IR ) ( P < 0.05), and the lactic acid-to-pyruvate ratio ( L/P ) ( P < 0.05), as well as an increase in muscle glycogen concentrations ( P < 0.05). Additionally, the expression of glycogen synthase ( GS ), pyruvate dehydrogenase ( PDH ) and glucose transporter-4 ( GLUT4 ) up-regulated, while the expression of glycogen phosphorylase L ( PYGL ), hexokinase ( HK ), 6-phosphofructokinase ( PFK ), pyruvate kinase ( PK ) and lactate dehydrogenase ( LDH ) down-regulated ( P < 0.05) in breast muscle of CMT-treated broiler chickens. Notably, both peripheral 5-HT concentrations and cecal 5-HT synthesis was significantly reduced ( P < 0.05) in the 18L:6D+CMT group. In summary, these findings indicate that CMT promotes breast muscle rate, reduces breast muscle injury, alleviates breast muscle glucose metabolism disorder in broiler chickens exposed to prolonged light periods. Moreover, peripheral 5-HT metabolism may serve as a key pathway through which cecal microbiota regulates skeletal muscle glucose metabolism.

Heat stress poses a considerable challenge to the modern poultry industry by negatively impacting immune system maturation and eliciting inflammatory responses. Peroxisome proliferators-activated receptors α (PPARα), predominantly expressed in metabolically active tissues such as skeletal muscle, are essential for regulating the inflammatory process. Moreover, our recent research has found that heat stress down-regulates the transcription of PPARα in broiler chickens. To study if PPARα regulation is involved in heat-stress-induced skeletal muscle inflammatory response in broiler chickens, 180 male Arbor Acres (AA) broilers aged 22 days were randomly assigned to three experimental groups: a thermoneutral condition group at 21 °C, a heat stress group at 31 °C and a heat stress group at 31 °C supplemented with the PPARα activator fenofibrate. After 7 days of adaptive feeding, the broilers were subjected to a 14-day formal experimental phase. Results demonstrated that heat stress decreased the spleen and thymus index and increased serum and breast muscle inflammatory factor concentrations (p< 0.05). Moreover, heat-stress-induced abnormal breast muscle fiber morphology in broiler chickens. Furthermore, heat stress significantly up-regulated nuclear factor kappa-B (NF-κB) expression in boiler chickens (p< 0.05). However, activating PPARα through fenofibrate improved the growth performance (p< 0.05), enhanced immune organ indexes (p< 0.05), reduced inflammatory factor concentrations (p< 0.05), alleviated breast muscle fiber morphology damage and suppressed NF-κB expression (p< 0.05) in the breast muscle of broiler chickens. Based on our previous research, these results collectively underscore that heat stress induced inflammation and up-regulated NF-κB in the breast muscle of broiler chickens by inhibiting PPARα.