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Vitamin A status and its metabolism contribute to the regulation of hepatic genes during the cycle of fasting and refeeding in rats
Institution:1. Department of Pharmacology & Therapeutics, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263, USA;2. Key Lab of Agricultural Animal Genetics and Breeding, Ministry of Education, College of Animal Science and Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
Abstract:Vitamin A (VA) status and its metabolism affect hepatic metabolic homeostasis. We investigated if VA status and metabolism contribute to energy metabolism and expression of hepatic genes in the cycle of fasting and refeeding. Zucker lean rats with VA sufficient (VAS) or VA deficient (VAD) status were respectively grouped as: ad libitum (VAS-AD or VAD-AD), 48-h fasted (VAS-Fasted or VAD-Fasted), 48-h fasted and refed a VAS diet (VAS-Refed-VAS or VAD-Refed-VAS), or refed a VAD diet (VAS-Refed-VAD or VAD-Refed-VAD) for 6 h. Respiratory exchange ratio (RER) of rats fed the VAS or VAD diet was monitored for 6 weeks. From week four, rats fed the VAS diet had higher RER than those fed the VAD diet. VAS-Refed rats had higher plasma levels of glucose, triglyceride, insulin and leptin than VAD-Refed rats. The mRNA and protein levels of hepatic genes for fuel metabolism in the fasting and refeeding cycle were determined using real-time polymerase chain reaction and immunoblot, respectively. The mRNA levels of glucokinase (Gck), sterol regulatory element-binding protein 1c (Srebp-1c), and fatty acid synthase (Fas) were lowered in VAS-Fasted and VAD-Fasted rats, and increased in VAS-Refed-VAS, VAS-Refed-VAD and VAD-Refed-VAS, but not VAD-Refed-VAD, rats. The ACL and FAS protein levels only dropped in VAS-Fasted rats and increased in VAS-Refed-VAS rats. The GK protein level decreased only in VAS-Fasted rats, and increased in VAS-Refed-VAS, VAS-Refed-VAD and VAD-Refed-VAS (but not VAD-Refed-VAD) rats. We conclude that VA status and its metabolism in the fasting and refeeding cycle contribute to the regulation of hepatic gene expression in rats.
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