铬、鱼油对肥胖模型大鼠瘦素和胰岛素的影响

目的铬、鱼油参与并调节糖、脂肪代谢,选择铬、鱼油作为影响因素,观察其对饮食诱导肥胖大鼠的影响。方法将肥胖模型大鼠按体重随机分为4组,每组8只。分别为肥胖组、鱼油组、鱼油+铬组和铬组,另设基础对照组。在实验的第0周和第6周空腹采尾血,测定血清瘦素和胰岛素水平。结果3个实验组的胰岛素和瘦素水平在第0周时,与肥胖组差异无显著性(P>0.05),第6周时,显著低于肥胖组(P<0.05)。结论结果提示铬、鱼油有缓解肥胖大鼠高胰岛素和高瘦素水平的作用。     

营养与食品卫生学校外实践教学基地建设的必要性

营养与食品卫生学是具有较强应用性质的学科。现有的营养与食品卫生学实践教学不能满足学生对实践经验的需求,而从事教学工作的教师由于缺乏实践经验也严重影响了教学效果和教学能力的提高。因此,为提高营养与食品卫生学专业课教学水平,提升青年教师自身素质,增强医学院校预防专业毕业生的从业能力,有必要加强营养与食品卫生学实践教学基地的建设。     

医学本科生营养与食品卫生学实验课教学改革探讨

营养与食品卫生学是预防医学范畴中的一门主干课程,营养学实验和食品卫生学实验对于培养实践型营养与食品卫生学人才十分重要。本文针对营养与食品卫生学实验教学中存在的问题和弊端,改变传统的教学模式,采取多种教学方式,积极开展综合性、设计性实验,改善考核方式,为今后培养营养与食品卫生学实践性人才和进一步进行实验教学改革打下了一定的基础。     

高脂肪膳食对肥胖大鼠学习记忆能力影响

目的 探讨高脂肪膳食诱导的肥胖大鼠学习记忆能力变化.方法 健康雄性SD大鼠50只,随机选取10只,通过皮下注射D-半乳糖,建立大鼠学习记忆损伤模型,喂基础饲料(阳性对照组),其余动物高脂肪饲料连续喂养2周后,根据体重筛选出基础组大鼠10只,喂基础饲料,其余大鼠继续喂高脂肪饲料,10周后,再根据体重筛选出肥胖大鼠10只,采用Morris水迷宫方法检测大鼠学习记忆能力,处死动物后,测量体脂肪含量,收集血清,检测血脂指标.结果 肥胖大鼠体重、肾周脂肪、睾周脂肪、网膜脂肪、体脂肪含量均明显高于基础组大鼠,血脂水平无明显变化;阳性对照组大鼠第3象限平均逃避潜伏期(18.54±2.73)s和总路程(298.60±48.18) cm明显高于基础组[分别为(8.27±1.82)s、(124.85 ±29.17) cm] (P ＜0.05);与基础组比较,肥胖组大鼠第3象限平均逃避潜伏期和总路程[分别为(9.72±2.t9)s、(166.31±37.12) cm]具有升高趋势.各组大鼠穿越平台次数差异无统计学意义.结论 高脂肪膳食诱导的肥胖大鼠可能存在学习能力损伤.     

饮食诱导肥胖易感和肥胖抵抗大鼠HSL和LPL基因表达的研究

目的探讨高脂饮食诱导肥胖易感(OP)大鼠和肥胖抵抗(OR)大鼠,激素敏感性脂肪酶(HSL)和脂蛋白脂肪酶(LPL)基因表达的差别。方法健康雄性SD大鼠80只,高脂饲料喂饲5周后,筛选出OP大鼠和OR大鼠,再将所有大鼠转为基础饲料喂饲10周后,处死动物,收集血清和白色脂肪组织,应用RT-PCR方法比较白色脂肪组织HSL和LPL基因的表达。结果高脂饲料喂饲5周后,OP大鼠白色脂肪组织HSL基因表达显著低于OR大鼠,而LPL基因表达显著高于OR大鼠;而转成基础饲料喂饲10后,OP大鼠HSL基因表达与OR大鼠无显著差异,但LPL基因表达仍显著高于OR大鼠。结论HSL基因表达水平下降和LPL基因表达水平升高,通过抑制脂肪分解促进脂肪合成,导致高脂饮食诱导肥胖易感大鼠的形成。HSL基因高表达更多是由高脂饮食诱导产生的,而LPL基因表达升高才是肥胖大鼠的特征性基因表达改变。     

Effects of genistein and folic acid on neuronal membrane and mitochondrial membrane damaged by β-amyloid peptides 31-35

Objective To observe the neuro-protective effects of genistein (Gen) and folic acid (FA) on neurons membrane and mitochondrial membrane damaged by β-amyloid peptides 31-35 (Aβ31-35).Methods The primary cultured rat cerebral cortical neurons were randomly divided into DMEM(control) ,Aβ31-35 (25 μmol/L) ,Gen( Gen 27 μg/ml) ,FA( FA 40 μg/ml) and Gen + FA( Gen 27 μg/ml + FA 40 μg/ml).Gen and/or FA were added two hours before Aβ31-35 addition.After twenty four hours, MTT assay was performed to measure the viability of cultured neurons.Fluorescence polarization was performed to observe the neuron cell membrane fluidity.The mitochondrial membrane potential(MMP) was determined to investigate the alteration of mitochondrial structure and function of neurons by laser scanning confocal microscope and a flow cytometer was used to investigate the activation of mitochondrial permeability transition pore (MPTP).Each experiment was repeated three times.Results Compared with group Aβ31-35 (0.845 ± 0.050, F = 4.931, P ＜ 0.05 ＝, the absorbance was significantly higher in group Gen (0.982 ± 0.110, t=3.523,P＜0.01＝,FA (0.947 ±0.061,t=2.745,P＜0.01＝ and Gen+ FA (0.996 ± 0.090, t = 3.966, P ＜ 0.01 ＝.The viscosity of cell neuron membrane in group Gen ( 1.75 ± 0.28,t=2.085,P＜0.05＝,FA (1.66±0.37,t=2.357,P＜0.05＝ andGen + FA (1.50±0.20,t=3.784,P ＜ 0.05 ＝ was significantly lower than that in group Aβ31-35 (2.11 ± 0.44, F = 5.529, P ＜ 0.01 ＝, which indicated the cell membrane fluidity was significantly higher in group Gen and/or FA than that in group Aβ31-35.MMP was significantly decreased by Aβ31-35 (3.364 ± 1.140, t= 3.949, P＜ 0.01 ＝ when comparing to control group (6.383 ± 1.683) ,while it was significantly increased by Gen (5.286 ± 1.792,t=2.406,P＜0.05＝,FA (5.884±2.022,t=2.887,P＜0.01＝ and Gen + FA (6.120 ±2.124,t=3.304,P ＜ 0.01 ＝ when comparing to group Aβ31-35 ( F = 7.585, P ＜ 0.01 ＝.MPTP was activated by Aβ31-35 and Gen and/or FA could reverse this progress.Conclusion Gen and/or FA could protect the neuronal and mitochondrial membrane from the impairment induced by Aβ31-35.     

中国已注册改善营养性贫血保健食品现状分析

目的 了解中国已注册改善营养性贫血保健食品现状,为企业研发和政府监管提供参考依据.方法 收集1996年3月-2021年2月国家食品药品监督管理总局网站"数据查询"栏目和国家市场监督管理总局网站"特殊食品信息查询"公布的228个中国已注册改善营养性贫血保健食品相关数据,应用Ucinet 6和SPSS 22.0统计软件对其...     

高脂饮食诱导肥胖与肥胖抵抗动物模型建立

目的建立高脂饮食诱导肥胖易感（OP）大鼠和肥胖抵抗（OR）大鼠动物模型。方法高脂饲料喂饲健康雄性SD大鼠8周后,筛选出OP大鼠和OR大鼠。实验结束后,处死动物,测量体脂肪含量,并收集血清,以检测血糖与血脂水平。结果OP大鼠肾周脂肪、睾周脂肪、网膜脂肪、体脂肪含量均显著高于OR大鼠,OP大鼠血糖、甘油三酯水平显著高于OR大鼠,而高密度脂蛋白水平显著低于OR大鼠。结论使用高脂饲料建立饮食诱导肥胖与肥胖抵抗动物模型,方法可靠,模型成功。     

《营养与食品卫生学》设计性实践教学的改革与体会

在以学生为主体的教学模式的改革中,本学系在《营养与食品卫生学》教学工作中开展了设计性实践教学,通过指导学生进行选题、查阅文献、课题设计与实施以及论文写作与交流等系统的科研实践活动.激发了学生的学习兴趣,培养了学生发现问题、分析问题和解决问题的能力以及严谨求实的科学精神,提高了学生组织协调、团结协作、人际交流等综合素质.     

Effects of genistein and folic acid on neuronal membrane and mitochondrial membrane damaged by β-amyloid peptides 31-35

Objective To observe the neuro-protective effects of genistein (Gen) and folic acid (FA) on neurons membrane and mitochondrial membrane damaged by β-amyloid peptides 31-35 (Aβ31-35).Methods The primary cultured rat cerebral cortical neurons were randomly divided into DMEM(control) ,Aβ31-35 (25 μmol/L) ,Gen( Gen 27 μg/ml) ,FA( FA 40 μg/ml) and Gen + FA( Gen 27 μg/ml + FA 40 μg/ml).Gen and/or FA were added two hours before Aβ31-35 addition.After twenty four hours, MTT assay was performed to measure the viability of cultured neurons.Fluorescence polarization was performed to observe the neuron cell membrane fluidity.The mitochondrial membrane potential(MMP) was determined to investigate the alteration of mitochondrial structure and function of neurons by laser scanning confocal microscope and a flow cytometer was used to investigate the activation of mitochondrial permeability transition pore (MPTP).Each experiment was repeated three times.Results Compared with group Aβ31-35 (0.845 ± 0.050, F = 4.931, P ＜ 0.05 ＝, the absorbance was significantly higher in group Gen (0.982 ± 0.110, t=3.523,P＜0.01＝,FA (0.947 ±0.061,t=2.745,P＜0.01＝ and Gen+ FA (0.996 ± 0.090, t = 3.966, P ＜ 0.01 ＝.The viscosity of cell neuron membrane in group Gen ( 1.75 ± 0.28,t=2.085,P＜0.05＝,FA (1.66±0.37,t=2.357,P＜0.05＝ andGen + FA (1.50±0.20,t=3.784,P ＜ 0.05 ＝ was significantly lower than that in group Aβ31-35 (2.11 ± 0.44, F = 5.529, P ＜ 0.01 ＝, which indicated the cell membrane fluidity was significantly higher in group Gen and/or FA than that in group Aβ31-35.MMP was significantly decreased by Aβ31-35 (3.364 ± 1.140, t= 3.949, P＜ 0.01 ＝ when comparing to control group (6.383 ± 1.683) ,while it was significantly increased by Gen (5.286 ± 1.792,t=2.406,P＜0.05＝,FA (5.884±2.022,t=2.887,P＜0.01＝ and Gen + FA (6.120 ±2.124,t=3.304,P ＜ 0.01 ＝ when comparing to group Aβ31-35 ( F = 7.585, P ＜ 0.01 ＝.MPTP was activated by Aβ31-35 and Gen and/or FA could reverse this progress.Conclusion Gen and/or FA could protect the neuronal and mitochondrial membrane from the impairment induced by Aβ31-35.