| Human healthy eating is closely linked with animal health.And the quality of animal products directly affects their productions,even health of human being.Obesity,one of the greatest threats to human health,is proverbially caused mainly by the excessive intake of sugar and fat.As one of the broad and relatively inexpensive sources of dietary animal protein for humans,the quality of broilers had arised a widespread attention by human being.However,some feeders are only pursuing growth rates of broilers to maximizing economic benefits under the current developing tendency of intensive and large-scale farming.This gives rise to the current excessive fat deposition in chicken body has been ignored.Excessive fat deposition in broiler chicken not only worsens carcass quality,utilization of feed but increases the incidence of metabolic diseases.More seriously,intake of ungraded chicken productions also similarly induces human’s diseases such as obesity,diabetes and atherosclerosis.Therefore,it becomes one of the key issues in poultry production to reduce abdominal fat deposition and improve meat quality.On the other hands,in term of animal performance,some key metabolic intermediates or structural analogs whcih act as chemical signals have extents of regulating-function through controling the metabolic pathways.Citric acid is proverbially acts as an important metabolic intermediate in the pathway of glucose and lipid metabolism.As a structural analogue of citric acid,(-)-hydroxycitric acid[(-)-HCA]can reduce fat deposition and body weight gain.Many study had showed that(-)-HCA can control fat deposition in animals and humans.But the biological mechanisms are still not fully clear,especially on this point whether it indirectly regulates fat metabolism by affecting glucose metabolism.Therefore,present study aimed to investigate the impact of(-)-HCA on glucose and energy metabolism in chicken embryonic development,and further evaluation whether it’s action are associated with modulation of the cAMP/CREB-PGC1α signaling pathway.These results revealed details of the biochemical mechanism of(-)-HCA-mediated glycolipid metabolism,and support it as a nutritional supplemental to control fat deposition and prevent metabolic disorder-related diseases in animals and humans.1 Effect of(-)-hydroxycitric acid on glucose metabolism in chicken embryosTo investigate the effect of(-)-hydroxycitric acid[(-)-HCA]on glucose metabolism in chicken embryos,a total of 270 Ross 308 broiler fertilized eggs(65±0.2 g)were randomly divided into three groups and injected with 0,1.0 and 10 mg/kg embryos weight of(-)-HCA which dissolved in 50μL of DMSO.Fertilized eggs were incubated in an electric forced-draft incubator at 37±0.5℃ and 65%relative humidity.At 14 days of age(E14),19 days of age(E19),and 1 day of ageing(H1)of chicken embryos,serum and liver samples were collected for further analysis.Results showed that(-)-HCA treatment significantly increased serum glucose and citric acid content while reduced lactic acid content at E19 and H1 of chicken embryos when compared with the control group(P<0.05);(-)-HCA treatment increased the glycogen content at E19 and H1 of chicken embryos through increasing glycogen synthase mRNA level(P<0.05).In addition,(-)-HCA treatment significantly reduced fructose-2,6-diphosphate(F-2,6-BP)content,fructose phosphate kinase-1(PFK-1)activity and pyruvate kinase(PK)activity and protein expression level at E19 and H1 of chicken embryos(P<0.05).The mRNA level of fructose-6-phosphatase(G6P),pyruvate carboxylase(PC),fructose-1,6-bisphosphatase(FBP1)and the activity of phosphoenolpyruvate carboxykinase(PEPCK)at E19 and H1 of chicken embryos were increased after(-)-HCA treated(P<0.05).These results indicated that(-)-HCA inhibits glycolysis and accelerates gluconeogenesis by regulating the key factors expression in chicken embryos.2 Effect of(-)-hydroxycitric acid on fat and energy metabolism in chicken embryosThis study investigate the effect of(-)-hydroxycitric acid[(-)-HCA]on fat and energy metabolism in chicken embryos.a total of 270 Ross 308 broiler fertilized eggs(65±0.2 g)were randomly divided into three groups and injected with 0,1.0 and 10 mg/kg embryos weight of(-)-HCA which dissolved in 50 μL of DMSO.Fertilized eggs were incubated in an electric forced-draft incubator at 37±0.5℃ and 65%relative humidity.At 14 days of age(E14),19 days of age(E19),and 1 day of ageing(H1)of chicken embryos,liver were collected for further analysis.Results showed that(-)-HCA treatment obviously reduced hepatic triglyceride content,while increased hepatic non-esterified fatty acid at different stage of chicken embryonic development when compared to control group(P<0.05).Peroxisome proliferator-activated receptor-γ coactivator-1α(PGC-1α),peroxisome proliferator-activated receptor α(PPARα)mRNA level and enoyl-CoA hydratase short chain 1(ECHS1)protein level were increased in chicken embryos treated with(-)-HCA(P<0.05).Compared with the control group,(-)-HCA treatment increased the citrate content of mitochondria,succinate dehydrogenase(SDH)activity and protein expression level at E19 and H1 of chicken embryos(P<0.05).The above results indicated that(-)-HCA promoted the fat oxidative decomposition and then improved the key factors expression level in citric acid cycle and oxidative respiratory chain,which finally accelerated the energy metabolism in chicken embrys.3 Effect of(-)-hydroxycitrate on cAMP/CREB-PGC-1α signaling pathway in chicken embryosTo investigate the effect of(-)-hydroxycitric acid[(-)-HCA]on cAMP/CREB-PGC-1αsignaling pathway in chicken embryos,a total of 270 Ross 308 broiler fertilized eggs(65±0.2 g)were randomly divided into three groups and injected with 0,1.0 and 10 mg/kg embryos weight of(-)-HCA which dissolved in 50 μL of DMSO.Fertilized eggs were incubated in an electric forced-draft incubator at 37±0.5℃ and 65%relative humidity.At 14 days of age(E14),19 days of age(E19),and 1 day of ageing(H1)of chicken embryos,liver were collected for further analysis.The results showed that(-)-HCA treatment significantly increased cAMP content at E19 and H1 of chicken embryos when compared to control group(P<0.05).No significant difference on total protein level of cAMP responsive element binding protein(CREB),while(-)-HCA significantly increased p-CREB protein level at E19 and H1 of chicken embryos(P<0.05).Compared with control group,(-)-HCA treatment significantly enhanced the protein level of peroxisome proliferator-activated receptor-y coactivator-1α(PGC-α),hepatic nuclear factor-4 A(HNF4A)and nuclear respiratory factor-1(NRF-1)at E19 and H1 of chicken embryos(P<0.05).In addition,the protein expression level of phosphoenolpyruvate carboxykinase(PEPCK),pyruvate carboxylase(PC),fructose-1,6-bisphosphatase(FBP1)and MT-ND1(NADH dehydrogenase)were also significantly increased at E19 and H1 of chicken embryos after(-)-HCA treated(P<0.05).These results suggest that(-)-HCA improved gluconeogenesis by activating the cAMP/CREB-PGC1α-HNF4A signaling pathway and accelerated energy metabolism by activating the cAMP/CREB-PGC1α-NRF-1 signaling pathway. |
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