膳食蛋白质对大鼠脂联素及其受体基因表达影响

目的 探讨不同膳食蛋白质摄入对大鼠脂联素及其受体表达的影响。方法 将36只雄性成年Wistar大鼠按体重随机分为酪蛋白组、大豆蛋白组和谷豆蛋白混合组,喂养12周,观察各组大鼠血脂水平及脂肪组织脂联素、骨骼肌组织脂联素受体1(Adipo R1)和肝脏组织脂联素受体2(Adipo R2)mRNA表达水平。结果 大豆蛋白组和谷豆蛋白混合组大鼠脂联素mRNA水平分别为(1.17±0.05)和(1.46±0.02),均高于酪蛋白组(0.79±0.06),AdipoR1 mRNA水平分别为(1.14±0.02)和(1.26±0.05),均高于酪蛋白组(0.89±0.06),谷豆混合蛋白组大鼠脂联素mRNA水平高于大豆蛋白组,差异均有统计学意义(P<0.05);脂联素mRNA水平与血清甘油三脂(TG)水平呈负相关(r=-0.64,P<0.05)。结论 膳食蛋白质可影响大鼠脂联素和脂联素受体的表达,大豆蛋白和谷豆混合蛋白相对酪蛋白可上调脂联素及其受体的表达,且谷豆混合蛋白的作用更强。     

能量限制对大鼠脂联素及PPARγ基因表达的影响

目的探讨限制能量摄入对大鼠内脏脂肪中脂联素(adiponectin)和PPARγ基因表达的影响。方法选用36只雄性Wistar大鼠,按体重随机分为基础组、限能1组和限能2组,单笼喂养12w,检测大鼠在自由摄食、80%和60%限能水平下空腹血糖、血脂和血胰岛素水平的变化;取内脏脂肪组织采用RT-PCR法检测脂联素和PPARγ基因表达水平。结果限能组TG水平显著低于基础组(P<0.05),HDL-C水平显著高于基础组(P<0.05),空腹血糖水平与基础组比较差异无统计学意义,限能2组TC水平显著高于基础组(P<0.05);限能组大鼠内脏脂肪中脂联素及其PPARγ基因表达水平均显著高于基础组(P<0.05),60%限能组又显著高于80%限能组(P<0.05)。结论限制能量摄入增高脂联素及PPARγ基因表达水平且均与限能程度有关;能量限制可能通过激活PPARγ诱导脂联素基因表达。     

等能量摄食条件下不同膳食脂肪供能比对大鼠血糖、血脂的影响

目的探讨等能量摄食条件下不同膳食脂肪供能比对大鼠血糖和血脂等指标的影响。方法将40只雄性SD大鼠按随机区组法分为低脂饲料、普通饲料、中脂饲料和高脂饲料组4组,等能量饲喂脂肪供能比分别为5%、15%、25%、40%的饲料10周。每周测大鼠体重和体长,第0、5和10周取尾血测空腹血糖、血脂和胰岛素水平,第10周末取肾周及附睾周脂肪称重,计算体脂比。结果实验第5、10周,大鼠体重、Lee's指数、体脂比、血清胰岛素和低密度脂蛋白胆固醇水平在各组间差异无统计学意义;第10周,高脂组血糖与低脂组相比显著升高(P0.01);高脂组总胆固醇、甘油三酯、高密度脂蛋白胆固醇与低脂组相比显著降低(P0.01);第10周,高脂组血糖与0周相比升高(P0.05),高脂组总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇与0周相比降低(P0.01)。结论在等能量摄食、正常生长条件下,高脂肪供能比饲料不会引起大鼠肥胖,但可能会导致大鼠糖脂水平的改变。     

不同脂肪酸构成比膳食对大鼠脂联素及其受体表达的影响

目的探讨不同脂肪酸构成比膳食对大鼠脂联素及其受体表达的影响。方法将72只Wistar大鼠随机分为对照组和5个实验组(A～E),实验组分别设膳食中饱和脂肪酸(SFA)/单不饱和脂肪酸(MUFA)/多不饱和脂肪酸比值(PUFA)(S/M/P)为1:1.7:1.2、1:1:1、2:1:1、1:2:1和1:1:2,喂养12w,测定脂肪组织脂联素(adiponectin,ADPN)、骨骼肌组织脂联素受体1(AdipoR1)、肝脏组织脂联素受体2(AdipoR2)mRNA的表达水平。结果与基础组相比,1:1.7:1.2组和1:1:1组的两种脂肪组织和2:1:1组的皮下脂肪组织脂联素mRNA表达显著降低(P<0.05),其中1:1.7:1.2组下降程度较高(P<0.001)。与1:1.7:1.2组比较,其余各实验组脂联素表达水平均显著升高(P<0.05),以1:1:2组的升高程度最高(P<0.001)。各实验组AdipoR的表达水平与基础对照组并无明显差别(P>0.05)。结论高脂饮食降低脂肪组织脂联素mRNA表达水平,不饱和脂肪酸对促进脂联素基因表达和分泌有明显作用,其中PUFA的作用较MUFA显著。     

脂联素、瘦素与白细胞介素在急性脑梗死中的临床意义

目的研究血清瘦素（Leptin）、脂联素（Adiponectin）与白细胞介素-1（interleukin，IL-1）、6、8水平变化在急性脑梗死的临床诊断、治疗、病情转归和判断预后的应用价值。方法以ELISA法分别检测急性脑梗死患者治疗前后以及正常对照组血清瘦素、脂联素及IL-1、6、8含量，并探讨各指标与神经功能缺损的关系。结果急性脑梗死患者治疗前、后血清瘦素及IL-1、6、8含量较对照组明显升高（P〈0．01），脑梗死治疗后以上各指标明显下降；而血清脂联素结果在治疗前较对照组明显降低（P〈0.01），治疗后升高程度与治疗前及对照组差异显著（P〈0．01）。脑梗死组神经功能缺损程度与各指标变化均无显著差异（P〉0．05）。结论血清瘦素、脂联素及IL-1、6、8含量水平的变化与脑梗死的临床变化有较密切的关系，可以作为脑梗死病情变化的监测指标和预后判断指标，同时也为在脑梗死发病早期使用生物因子（如抗粘附分子抗体）及药物治疗提供临床实验依据。     

驻岛礁人员脂肪摄入及血脂、体脂调查

西沙、南沙的地理位置特殊，环境条件艰苦，供给困难且周期长。为了解驻礁人员的膳食中脂肪摄入、血脂及体脂情况，自2001年9月-2003年4月，对驻岛礁人员进行了膳食营养、血脂及体脂情况调查。现报告如下。     

慢性阻塞性肺疾病患者血脂水平、瘦素和脂联素的变化

目的分析研究慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者血脂水平、瘦素和脂联素的变化及意义。方法选择2014年2—8月在本院呼吸内科住院治疗的106例COPD患者为观察组,选择同期健康体检者100例为对照组,比较观察组和对照组的TC、TG、HDL-C、LDL-C、载脂蛋白A1(apolipoprotein A1,APo A1)、载脂蛋白B(apolipoprotein B,APo B)、瘦素和脂联素水平。计量资料采用t检验,P0.05为差异有统计学意义。结果观察组血清TC[(4.22±0.50)mmol/L]、TG[(1.29±0.31)mmol/L]均低于对照组[(4.80±0.37)、(1.60±0.23)mmol/L],组间比较差异均有统计学意义(P0.05);观察组Apo B水平[(0.68±0.20)g/L]比对照组[(0.95±0.77)g/L]降低,差异有统计学意义(P0.05)。观察组瘦素水平为[(0.38±0.07)mg/ml]低于对照组[(0.50±0.04)mg/ml],差异有统计学意义(t=14.988,P0.05);观察组脂联素水平为[(0.53±0.17)mg/L]高于对照组[(0.42±0.05)mg/L],差异有统计学意义(t=6.221,P0.05)。结论血清瘦素和脂联素对COPD患者的诊断有重要的参考价值。血脂相关指标与COPD患者病情发展有相关性,因此在此类人群中进行血脂等指标检查十分必要。     

不同程度非酒精性脂肪肝患者血清瘦素和脂联素的变化

目的分析不同程度非酒精性脂肪肝患者血清瘦素和脂联素的变化,探讨非酒精性脂肪肝病理发展过程。方法轻度脂肪肝组(A组)、中重度脂肪肝组(B组)、正常对照组(C组)各50人,检测收缩压、舒张压、体重指数(BMI)、腰臀比(WHR)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、空腹血糖(FPG)、瘦素(LEP)和脂联素(ADPN),并进行比较。结果 A、B组BMI、WHR较C组明显升高(p<0.05),B组BMI、WHR较A组明显升高(p<0.05)。A、B组TC、TG、LDL-C、LEP较C组明显升高(p<0.05),A、B组HDL-C、ADPN较C组明显降低(p<0.05);B组TG、LEP较A组升高(p<0.05),B组ADPN较A组降低(p<0.05)。LEP与TG呈正相关,ADPN与TG呈负相关。结论 LEP、ADPN在不同程度NAFLD中均有表达;随着NAFLD程度的加重,LEP升高和ADPN降低更明显。     

中老年冠心病患者血清瘦素与脂联素水平的关系

目的 探讨中老年冠心病患者血清瘦素和脂联素的表达及相关性.方法 选取88例年龄≥55岁行冠状动脉造影的患者,根据造影结果分为冠心病组52例和对照组36例,采用酶联免疫吸附试验法测定血清瘦素和脂联素水平.结果 冠心病组患者血清瘦素水平高于对照组[(9.38±3.51) μg/L比(7.27±3.25) μg/L,P＜0.05],脂联素水平低于对照组[(11.08±3.87) mg/L比(13.34±4.94) mg/L,P＜0.05],Logistic多元回归分析显示仅有血清瘦素水平是中老年冠心病的独立危险因素.Spearman相关分析显示,血清脂联素与瘦素水平呈负相关(r=-0.320,P=0.002).结论 中老年冠心病患者血清脂联素水平的降低与瘦素水平的升高相关,血清瘦素水平的升高是冠心病的独立危险因素,而血清脂联素水平降低并不是冠心病的独立危险因素.     

2型糖尿病患者血清内脂素、脂联素和瘦素水平的变化

目的研究2型糖尿病(T2DM)患者血清中内脂素、脂联素和瘦素水平,为阐明T2DM的发病机制提供基础。方法将220例新诊T2DM患者和214例年龄、性别与体重指数(BMI)相匹配的健康对照组,按BMI≥25kg/m2或25kg/m2分为肥胖亚组和非肥胖亚组,采用酶联免疫吸附法(ELISA)和放射免疫法(RIA)检测其血清内脂素、脂联素和瘦素水平,并同时采用生化和化学发光法检测空腹血糖(FPG)、甘油三酯(TG)、胆固醇(Chol)以及空腹胰岛素(FINS)等。结果1.T2DM组血清内脂素、FPG、FINS、胰岛素抵抗指数(HOMA-IR)、TG、Chol水平均高于健康对照组(P0.05～0.001),而脂联素水平低于健康对照组(P0.001),瘦素在两组人群中差异无统计学意义(P0.05);2.无论是T2DM组还是健康对照组中,其肥胖亚组中的内脂素、瘦素、FINS、HOMA-IR、TG、Chol水平均高于非肥胖亚组(P0.05～0.001),而脂联素低于非肥胖亚组(P0.01～0.001);3.消除BMI因素影响的偏相关分析显示,T2DM患者血清内脂素水平仅与FPG、FINS、HOMA-IR呈正相关(r=0.267～0.443,P0.05～0.01),与脂联素呈负相关(r=-0.312,P0.05)。结论内脂素和脂联素参与了肥胖、胰岛素抵抗以及T2DM发生过程,而瘦素可能仅与肥胖状况有关,未能以独立因子作用直接参与T2DM的发生。     

Effects of dietary protein, fat and restriction on body composition and energy balance in lactating rats

Isoenergetic diets formulated at three levels of dietary protein using 12,24 and 40% casein and at two levels of fat using 2.26 and 13.82% corn oil were fed at five levels of intake, ad libitum, 75, 62.5, 50 and 37.5% of average ad libitum intake, to 90 lactating rats from d 7 to 14 of lactation. Regression equations developed from lactating rats killed on d 7 of lactation were used to calculate initial body composition and energy of rats killed on d 14 of lactation. Changes in body weight and body water were significantly (P less than 0.05) affected by dietary fat and protein, but change in dry lean body mass was affected only by level of dietary fat, whereas body nitrogen and fat and lean body energy were not affected by level of dietary fat or protein. However, restricted intake significantly increased loss of all these. Likewise, restricted intake decreased milk production. Changes in weights of heart and liver were not affected by diet or intake, whereas intestinal weight decreased with intake restriction. Liver enzyme activities were markedly affected by intake restriction, whereas responses to dietary protein and fat were marginal.     

葡多酚对高脂膳大鼠血脂与脂质过氧化的影向

目的　观察葡多酚 (GPC)对饲以高脂膳食、乙醇等不同膳食的大鼠血脂及脂质过氧化的影响。方法　将大鼠随机分为正常对照组、高脂膳组、高脂乙醇组、高脂GPC组、高脂乙醇GPC(高、低剂量 )组、高脂乙醇VE组 7个组 ,喂养 6周 ,测定血清甘油三脂 (TG)、总胆固醇 (TC)、高密度脂蛋白胆固醇 (HDL -C)、低密度脂蛋白胆固醇 (LDL -C)、活性氧 (ROS)、丙二醛 (MDA)水平及超氧化物歧化酶 (SOD)活性等指标。结果　高脂组、高脂乙醇组的血清TG、TC、ROS、MDA水平均较实验前显著性升高 ;同高脂乙醇组比较 ,高脂乙醇高GPC组的血清TC、MDA水平均显著性降低 ,SOD活性显著性升高 (P <0 0 5 )。结论　GPC对乙醇与高脂膳食引起的血脂水平升高和脂质过氧化均有一定的抑制作用。     

Food intake, energy balance and serum leptin concentrations in rats fed low-protein diets

Studies examining the effects of low-protein diets on food intake and body weight have shown varied results. Many researchers have found low dietary protein to increase food intake, while others have found no effect or even a decrease. In 63 male Sprague-Dawley rats, we examined several low levels of dietary protein (2%, 5%, 8%, 10%, 15% vs. 20% casein) to determine the dose-response relationships between low dietary protein and food intake, body composition, energy balance and serum leptin concentrations. Food intake, over the range of low dietary protein, showed a quasi bell-shaped response curve with peak intake occurring in rats fed 8-10% casein. Peak feeding occurred at or just below the estimated protein requirement of the rats (10-12.5% casein). Compared to the 20% casein controls, food intake was severely reduced in rats fed 2% casein, while it was greater in the other low-protein groups. The amount of body fat steadily increased between the 15% casein group and the 8% casein group, and sharply declined between the 5% casein group and 2% casein group. The change in body fat reflected both the change in food intake and altered energy partitioning. Serum leptin concentrations were greater in rats fed the 5 and 8% casein diets than in control rats fed 20% casein. Serum leptin concentrations were positively associated with body fat content (r(2) = 0.763, P < 0.001). Increased serum leptin concentrations in the presence of increased food intake is suggestive of a state of leptin resistance. This animal model may provide important insights into diet-induced obesity.     

Smoking status: effects on the dietary intake, physical activity, and body fat of adult men

This investigation evaluated the relationship between smoking status and body fatness, dietary intake, and physical activity in adults. Subjects were 210 males who were either regular cigarette smokers (n = 35) or nonsmokers (n = 175). Estimated body fat and waist-to-hip (girth) measurements were carefully obtained. Additionally, a sensitive assessment of long-term dietary intake and a multifactorial approach to the assessment of physical activity were made. Results indicated that smokers had lower estimated body fat as calculated by multiple skinfold thickness assessments. In contrast, smokers reported the same total energy intakes as nonsmokers and their levels of physical activity were significantly lower than those of nonsmokers. The differences in intake and expenditure in smokers and the role of metabolism as a possible determinant of the body fat differences in smokers vs nonsmokers are discussed.     

Impact of dietary fat content and fat oxidation on energy intake in humans

Three studies were performed to assess the effects of a high-fat diet and exercise-induced changes in fat oxidation on energy intake in humans. In the first study the short-term effect of a high-fat diet on spontaneous energy intake was investigated. The second study evaluated the long-term effect of a high-fat diet on adiposity and the third study evaluated the effect of exercise-induced changes in fat oxidation on short-term regulation of energy intake when subjects were consuming a high-fat diet. The results of these studies indicate that a high-fat diet induces a short-term hyperphagia, a high percentage of lipids in the usual diet is associated with a higher adiposity, and exercise may attenuate or amplify the high-fat, diet-induced hyperphagia, depending on the magnitude of the exercise-induced increase in fat oxidation.     

Effect of dietary fat on serum and tissue lipids of adult rats.

The effect of 3 types of fat: 1) Ghee, 2) Corn oil, 3) Subsidized vegetable oil (SVO) on serum and tissue lipids was studied by using adult albino male rats mean weight 114 g. Rats fed diet containing SVO had the highest serum cholesterol and LDL-cholesterol concentrations than those fed diet containing ghee or corn oil. Serum high density lipoprotein-cholesterol (HDL) concentration was highest in animals fed the ghee and lowest with those fed the SVO diet. On the other hand phospholipids values tend to be lower when feeding diets containing oils. Also serum triglycerides levels were higher on saturated fat diet than on the unsaturated fat diets. The same trends were found for liver cholesterol as in serum cholesterol. SVO diet gave the highest liver cholesterol concentration. Also SVO gave the highest heart phospholipids values.     

Feeding a liquid diet increases energy intake, weight gain and body fat in rats

Studies were undertaken to analyze the role of moisture content of foods in producing dietary obesity. Female CD rats consumed more energy when offered a sucrose solution and plain water to drink than when they were only given plain water, regardless of the sugar content of their diet (0-65%). This suggested that the overeating that commonly occurs when sucrose solutions are offered may not be due to sucrose per se. In subsequent experiments, rats were fed modified AIN-76 diets high in sucrose, starch or fat for 28-42 d. For some rats, the diet was liquefied by adding water to make a 32% suspension. Plain drinking water was always available. Rats fed high carbohydrate liquid diets, with or without solid diet, consumed 8-15% more energy than rats fed solid diet only. Rats fed liquid diets also gained 43-206% more weight than did rats fed solid diets. Analysis of carcass composition revealed that the liquid diets increased body fat. For high fat diets, the results were more complicated. Addition of water to a low cellulose, high fat diet did not increase adiposity, whereas addition of water to a high cellulose, high fat diet did increase adiposity. These results suggest that the obesity-inducing effects of feeding sugar solutions or cafeteria diets may be due, in part, to the high water content of these foods.     

Effect of energy intake on the promotion of mammary carcinogenesis by dietary fat

The effect of low-fat and high-fat diets on the induction of mammary carcinomas by 1-methyl-1-nitrosourea (MNU) was studied in female Sprague-Dawley rats. All rats were given MNU (25 mg/kg body wt) at 50 days of age. For the first 17 weeks after carcinogen administration, they were fed a purified diet containing either 5 or 20% fat incorporated into agar gel. Food intake was restricted, so that the amounts fed provided the same amount of net utilizable energy each day for both groups, regardless of the fat content of the diets. From 17 to 32 weeks, the diets were fed ad libitum. During the restricted feeding period, there was no significant difference in tumor incidence or in the number of tumors detected between the groups. During the weeks in which animals were fed ad libitum, significantly more tumors appeared in the high-fat group than in the low-fat group. The data provide support for the hypothesis that consumption of a high-fat diet can lead to an enhancement of mammary carcinogenesis. It appears, however, that diets must be consumed ad libitum for the stimulatory effect on tumor occurrence to be exhibited.     

Effect of energy intake on the promotion of mammary carcinogenesis by dietary fat

The effect of low‐fat and high‐fat diets on the induction of mammary carcinomas by 1‐methyl‐1‐nitrosourea (MNU) was studied in female Sprague‐Dawley rats. All rats were given MNU (25 mg/kg body wt) at 50 days of age. For the first 17 weeks after carcinogen administration, they were fed a purified diet containing either 5 or 20% fat incorporated into agar gel. Food intake was restricted, so that the amounts fed provided the same amount of net utilizable energy each day for both groups, regardless of the fat content of the diets. From 17 to 32 weeks, the diets were fed ad libitum. During the restricted feeding period, there was no significant difference in tumor incidence or in the number Of tumors detected between the groups. During the weeks in which animals were fed ad libitum, significantly more tumors appeared in the high‐fat group than in the low‐fat group. The data provide support for the hypothesis that consumption of a high‐fat diet can lead to an enhancement of mammary carcinogenesis. It appears, however, that diets must be consumed ad libitum for the stimulatory effect on tumor occurrence to be exhibited.