An 8-week feeding experiment was carried out to explore the effects of dietary n-3/n-6 polyunsaturated fatty acid(PUFA)ratio on growth performance,lipid metabolism,hepatic antioxidant status,and gut flora of spotted s...An 8-week feeding experiment was carried out to explore the effects of dietary n-3/n-6 polyunsaturated fatty acid(PUFA)ratio on growth performance,lipid metabolism,hepatic antioxidant status,and gut flora of spotted seabass(Lateolabrax maculatus).Six experimental diets were formulated to contain different levels of two purified oil sources including docosahexaenoic and eicosapentaenoic acids enriched oil(n-3)and linoleic acid-enriched oil(n-6)leading to n-3/n-6 PUFA ratios of 0.04,0.35,0.66,1.35,2.45 and16.17.Each diet was fed to triplicate groups of juvenile L.maculatus(11.06±0.20 g,30 fish/tank).Final body weight(FBW),weight gain(WG),specific growth rates(SGR),protein efficiency ratio(PER)and feed utilization efficiency increased as n-3/n-6 PUFA ratio increased up to a certain level,and then decreased thereafter.Fish fed the diet with n-3/n-6 PUFA ratio of 0.66 exhibited the highest FBW,WG,SGR and PER and the lowest feed conversion ratio.Lower n-3/n-6 PUFA ratios induced up-regulated expression of lipid synthesis-related genes(fas,acc2 and srebp-1c)and down-regulated expression of lipolysis related genes(atgl,ppara,cpt-1 and aox).Higher expression of lipolysis-related genes(atgl,ppara and cpt-1)was recorded at moderate n-3/n-6 PUFA ratios(0.66 to 1.35).Moreover,inappropriate n-3/n-6 PUFA ratios triggered up-regulation of pro-inflammatory genes(il-6 and tnf-a)and down-regulation of antiinflammatory genes(il-4 and il-10)in the intestine.The diet with n-3/n-6 PUFA ratio of 0.66 inhibited intestine inflammation,improved intestinal flora richness,increased the abundance of beneficial bacteria such as Lactobacillus,Alloprevotella and Ruminococcus,and reduced the abundance of harmful bacteria including Escherichia-Shigella and Enterococcus.In summary,it could be suggested that a dietary n-3/n-6PUFA ratio of 0.66 can improve growth performance and feed utilization in L.maculatus,as is deemed to be mediated through regulation of lipid metabolism and intestinal flora.展开更多
OBJECTIVE: To assess whether dietary fat intake influences Parkinson’s disease risk. DATA SOURCES: We systematically surveyed the Embase and PubMed databases, reviewing manuscripts published prior to October 2018. Th...OBJECTIVE: To assess whether dietary fat intake influences Parkinson’s disease risk. DATA SOURCES: We systematically surveyed the Embase and PubMed databases, reviewing manuscripts published prior to October 2018. The following terms were used:(“Paralysis agitans” OR “Parkinson disease” OR “Parkinson” OR “Parkinson’s” OR “Parkinson’s disease”) AND (“fat” OR “dietary fat” OR “dietary fat intake”). DATA SELECTION: Included studies were those with both dietary fat intake and Parkinson’s disease risk as exposure factors. The Newcastle-Ottawa Scale was adapted to investigate the quality of included studies. Stata V12.0 software was used for statistical analysis. OUTCOME MEASURES: The primary outcomes included the relationship between high total energy intake, high total fat intake, and Parkinson’s disease risk. The secondary outcomes included the relationship between different kinds of fatty acids and Parkinson’s disease risk. RESULTS: Nine articles met the inclusion criteria and were incorporated into this meta-analysis. Four studies scored 7 and the other five studies scored 9 on the Newcastle-Ottawa Scale, meaning that all studies were of high quality. Meta-analysis results showed that high total energy intake was associated with an increased risk of Parkinson’s disease (P = 0.000, odds ratio (OR)= 1.49, 95% confidence interval (CI): 1.26–1.75);in contrast, high total fat intake was not associated with Parkinson’s disease risk (P = 0.123, OR = 1.07, 95% CI: 0.91–1.25). Subgroup analysis revealed that polyunsaturated fatty acid intake (P = 0.010, OR = 1.03, 95% CI: 0.88–1.20) reduced the risk of Parkinson’s disease, while arachidonic acid (P = 0.026, OR = 1.15, 95% CI: 0.97–1.37) and cholesterol (P = 0.002, OR = 1.09, 95% CI: 0.92–1.29) both increased the risk of Parkinson’s disease. Subgroup analysis also demonstrated that, although the results were not significant, consumption of n-3 polyunsaturated fatty acids (P = 0.071, OR = 0.88, 95% CI: 0.73–1.05展开更多
目的研究不同n-3/n-6配比脂肪酸对大鼠磷酸腺苷酸活化蛋白激酶(AMP-activated protein kinase,AMPK)蛋白及活性表达的影响。方法58只SD大鼠适应性喂养7d后,尾静脉取血。根据血清总胆固醇水平随机分为:空白(基础饲料);高脂(高脂饲料);高...目的研究不同n-3/n-6配比脂肪酸对大鼠磷酸腺苷酸活化蛋白激酶(AMP-activated protein kinase,AMPK)蛋白及活性表达的影响。方法58只SD大鼠适应性喂养7d后,尾静脉取血。根据血清总胆固醇水平随机分为:空白(基础饲料);高脂(高脂饲料);高脂1:1(高脂饲料+n-3/n-6=1:1配方油);高脂1:5(高脂饲料+n3/n6=1:5配方油);低脂1:1(脱脂基础饲料+n-3/n-6=1:1配方油);低脂1:5(脱脂基础饲料+n3/n6=1:5配方油)6组,喂养45d,观察大鼠摄食与体重增长。于实验前1d,15d,30d,45d分别各取血测血清总胆固醇水平,于D45处死动物。Western blotting分别分析肝和下丘脑组织中AMPK-α总蛋白及其活性表达。结果添加PUFA的4个比例组血清TC、体重与高脂组相比,显著降低,且低脂2个比例组和高脂1:1组均与高脂1:5组相比有显著差异。添加PUFA的4个比例组均与高脂组相比,大鼠下丘脑AMPK-α总蛋白表达水平明显降低,肝AMPK-α蛋白表达水平均比高脂组明显升高。结论PUFA改善血脂可能是通过增加肝AMPK表达,抑制下丘脑AMPK表达,增加肝脂肪酸氧化和抑制食欲,影响血脂代谢。展开更多
The title complex Cu[C5H3N(CCH3=N-C6H5)2]2(PF6)2 has been synthesized by r eaction of Schiff base C5H3N(CCH3=N-C6H5)2 and cupric sulfate in toluene solut ion. The crystal structure was determined by X-ray diffraction ...The title complex Cu[C5H3N(CCH3=N-C6H5)2]2(PF6)2 has been synthesized by r eaction of Schiff base C5H3N(CCH3=N-C6H5)2 and cupric sulfate in toluene solut ion. The crystal structure was determined by X-ray diffraction method and the chemical formula weight of the complex is 1041.85. The crystal structure belongs to triclinic system with spacegroup and cell parameters: a=12.6470(10) , b=14. 123(2) , c=15.613(2);á=66.150(10)a=79.470(10)?=78.290(10)穖-3 and F(000)=1064. The final R:R1=0.0668, wR 2=0.1927; R(all data): R1=0.1133, wR2=0.2357. The Cu was coordinated by six nitrogen, at the same time the Cu formed a distorted octahedron, besides the angles and pl anes of this compound were discussed . The result of kinetics of the thermal dec omposition indicated that the first step of it is 2 series chemical reactions, t he function of machanism is f(a)=(1-a)2, and the activation energy is 144.64E/ kJ. CCDC: 180872.展开更多
基金funded by the National Natural Science Foundation of China(32072984)the Natural Science Foundation of Fujian Province(2020J01664)China Agricultural Research System(CARS-47)。
文摘An 8-week feeding experiment was carried out to explore the effects of dietary n-3/n-6 polyunsaturated fatty acid(PUFA)ratio on growth performance,lipid metabolism,hepatic antioxidant status,and gut flora of spotted seabass(Lateolabrax maculatus).Six experimental diets were formulated to contain different levels of two purified oil sources including docosahexaenoic and eicosapentaenoic acids enriched oil(n-3)and linoleic acid-enriched oil(n-6)leading to n-3/n-6 PUFA ratios of 0.04,0.35,0.66,1.35,2.45 and16.17.Each diet was fed to triplicate groups of juvenile L.maculatus(11.06±0.20 g,30 fish/tank).Final body weight(FBW),weight gain(WG),specific growth rates(SGR),protein efficiency ratio(PER)and feed utilization efficiency increased as n-3/n-6 PUFA ratio increased up to a certain level,and then decreased thereafter.Fish fed the diet with n-3/n-6 PUFA ratio of 0.66 exhibited the highest FBW,WG,SGR and PER and the lowest feed conversion ratio.Lower n-3/n-6 PUFA ratios induced up-regulated expression of lipid synthesis-related genes(fas,acc2 and srebp-1c)and down-regulated expression of lipolysis related genes(atgl,ppara,cpt-1 and aox).Higher expression of lipolysis-related genes(atgl,ppara and cpt-1)was recorded at moderate n-3/n-6 PUFA ratios(0.66 to 1.35).Moreover,inappropriate n-3/n-6 PUFA ratios triggered up-regulation of pro-inflammatory genes(il-6 and tnf-a)and down-regulation of antiinflammatory genes(il-4 and il-10)in the intestine.The diet with n-3/n-6 PUFA ratio of 0.66 inhibited intestine inflammation,improved intestinal flora richness,increased the abundance of beneficial bacteria such as Lactobacillus,Alloprevotella and Ruminococcus,and reduced the abundance of harmful bacteria including Escherichia-Shigella and Enterococcus.In summary,it could be suggested that a dietary n-3/n-6PUFA ratio of 0.66 can improve growth performance and feed utilization in L.maculatus,as is deemed to be mediated through regulation of lipid metabolism and intestinal flora.
基金supported by the National Natural Science Foundation of China,No.31200868(to XC)
文摘OBJECTIVE: To assess whether dietary fat intake influences Parkinson’s disease risk. DATA SOURCES: We systematically surveyed the Embase and PubMed databases, reviewing manuscripts published prior to October 2018. The following terms were used:(“Paralysis agitans” OR “Parkinson disease” OR “Parkinson” OR “Parkinson’s” OR “Parkinson’s disease”) AND (“fat” OR “dietary fat” OR “dietary fat intake”). DATA SELECTION: Included studies were those with both dietary fat intake and Parkinson’s disease risk as exposure factors. The Newcastle-Ottawa Scale was adapted to investigate the quality of included studies. Stata V12.0 software was used for statistical analysis. OUTCOME MEASURES: The primary outcomes included the relationship between high total energy intake, high total fat intake, and Parkinson’s disease risk. The secondary outcomes included the relationship between different kinds of fatty acids and Parkinson’s disease risk. RESULTS: Nine articles met the inclusion criteria and were incorporated into this meta-analysis. Four studies scored 7 and the other five studies scored 9 on the Newcastle-Ottawa Scale, meaning that all studies were of high quality. Meta-analysis results showed that high total energy intake was associated with an increased risk of Parkinson’s disease (P = 0.000, odds ratio (OR)= 1.49, 95% confidence interval (CI): 1.26–1.75);in contrast, high total fat intake was not associated with Parkinson’s disease risk (P = 0.123, OR = 1.07, 95% CI: 0.91–1.25). Subgroup analysis revealed that polyunsaturated fatty acid intake (P = 0.010, OR = 1.03, 95% CI: 0.88–1.20) reduced the risk of Parkinson’s disease, while arachidonic acid (P = 0.026, OR = 1.15, 95% CI: 0.97–1.37) and cholesterol (P = 0.002, OR = 1.09, 95% CI: 0.92–1.29) both increased the risk of Parkinson’s disease. Subgroup analysis also demonstrated that, although the results were not significant, consumption of n-3 polyunsaturated fatty acids (P = 0.071, OR = 0.88, 95% CI: 0.73–1.05
文摘目的研究不同n-3/n-6配比脂肪酸对大鼠磷酸腺苷酸活化蛋白激酶(AMP-activated protein kinase,AMPK)蛋白及活性表达的影响。方法58只SD大鼠适应性喂养7d后,尾静脉取血。根据血清总胆固醇水平随机分为:空白(基础饲料);高脂(高脂饲料);高脂1:1(高脂饲料+n-3/n-6=1:1配方油);高脂1:5(高脂饲料+n3/n6=1:5配方油);低脂1:1(脱脂基础饲料+n-3/n-6=1:1配方油);低脂1:5(脱脂基础饲料+n3/n6=1:5配方油)6组,喂养45d,观察大鼠摄食与体重增长。于实验前1d,15d,30d,45d分别各取血测血清总胆固醇水平,于D45处死动物。Western blotting分别分析肝和下丘脑组织中AMPK-α总蛋白及其活性表达。结果添加PUFA的4个比例组血清TC、体重与高脂组相比,显著降低,且低脂2个比例组和高脂1:1组均与高脂1:5组相比有显著差异。添加PUFA的4个比例组均与高脂组相比,大鼠下丘脑AMPK-α总蛋白表达水平明显降低,肝AMPK-α蛋白表达水平均比高脂组明显升高。结论PUFA改善血脂可能是通过增加肝AMPK表达,抑制下丘脑AMPK表达,增加肝脂肪酸氧化和抑制食欲,影响血脂代谢。
文摘The title complex Cu[C5H3N(CCH3=N-C6H5)2]2(PF6)2 has been synthesized by r eaction of Schiff base C5H3N(CCH3=N-C6H5)2 and cupric sulfate in toluene solut ion. The crystal structure was determined by X-ray diffraction method and the chemical formula weight of the complex is 1041.85. The crystal structure belongs to triclinic system with spacegroup and cell parameters: a=12.6470(10) , b=14. 123(2) , c=15.613(2);á=66.150(10)a=79.470(10)?=78.290(10)穖-3 and F(000)=1064. The final R:R1=0.0668, wR 2=0.1927; R(all data): R1=0.1133, wR2=0.2357. The Cu was coordinated by six nitrogen, at the same time the Cu formed a distorted octahedron, besides the angles and pl anes of this compound were discussed . The result of kinetics of the thermal dec omposition indicated that the first step of it is 2 series chemical reactions, t he function of machanism is f(a)=(1-a)2, and the activation energy is 144.64E/ kJ. CCDC: 180872.
