染料木黄酮对高脂饮食喂养大鼠肝脏脂质代谢和AMPK磷酸化的影响

目的探讨染料木黄酮（Gen）对高脂饮食喂养大鼠肝脂质代谢和肝脏腺苷酸环化酶蛋白激酶（AMPK）磷酸化的影响。方法36只大鼠适应性喂养1周后随机分为4组：正常对照组（正常组）、模型对照组（模型组）、Gen高剂量干预组（Gen高组）和Gen低剂量干预组（Gen低组）。正常组大鼠给予基础饲料D12450B（脂肪供能占10％）喂养,模型组给予D12492高脂饲料（脂肪供能占60％）喂养,Gen高组给予D12492高脂饲料喂养和8mg／kgGen灌胃干预,Gen低组给予D12492高脂饲料喂养和4mg／kgGen灌胃干预。持续喂养12周后,处死所有大鼠。取血和肝组织进行相关指标的检测。全自动生化检测仪检测血清和肝组织匀浆甘油三酯（TG）、总胆固醇（TC）、高密度脂蛋白胆固醇（HDL—C）和低密度脂蛋白胆固醇（LDL—C）水平,游离脂肪酸（FFA）试剂盒检测血清和肝组织匀浆FFA水平,Westernblot法检测肝组织总AMPK和磷酸化腺苷酸环化酶蛋白激酶（pAMPK）的表达。结果与正常组比,模型组大鼠肝脏血清和肝组织TG、TC、FFA及血清LDL—C明显升高（P〈0．05或P〈0．01）,肝组织pAMPK水平显著降低（P〈0．01）。与模型组相比,Gen低组大鼠血FFA、肝FFA和TG含量明显降低（P〈0．05或P〈0．01）;Gen高组大鼠血TC、TG、LDL—C、FFA和肝TG、FFA含量明显低于模型组大鼠（P〈0．05或P〈0．01）。与模型对照组相比,低、高剂量Gen干预均能显著上调pAMPK水平（P〈0．01和P〈0．05）;但各组大鼠肝组织总AMPK水平差异无统计学意义（P〉0．05）。结论染料木黄酮能够改善12周高脂饮食诱导的大鼠肝脂肪代谢紊乱,减轻肝脏脂质沉积,其作用机制可能与其增加pAMPK水平有关。     

膳食对大鼠动脉窖蛋白-1表达的影响

目的研究膳食脂类对大鼠动脉窖蛋白-1（caveolin-1）表达的影响.方法雄性SD大鼠试验组用高脂饲料喂养15周诱导肥胖（DIO）和肥胖抵抗（DIO-R）后,将DIO组一半改用基础饲料喂养（DIO-HF/LF）,另一半继续高脂饮食（DIO-HF）;对照组（CF）一直用基础饲料喂养.第23周末用RT-PCR、免疫印迹及免疫组化方法检测动脉血管caveolin-1表达水平.结果 DIO-HF/LF组体重低于DIO-HF组而高于对照组（P＜0.05）.血管caveolin-1水平显示,DIO-HF高于DIO- HF/LF、DIO-R及CF,而其余3组之间差异无统计学意义.结论基础饮食可降低肥胖敏感大鼠体重及血管caveolin-1表达,降低心血管疾病的危险性.肥胖抵抗可能与caveolin-1维持正常表达有关.     

高脂饮食对Sprague Dawley大鼠睾丸发育的影响

目的 研究高脂饮食对青春期雄性Sprague Dawley大鼠睾丸发育过程的影响,并探究该影响是否具有可逆性。方法 将1月龄Sprague Dawley雄性大鼠60只,应用随机数字表法分为对照组（n=10）和营养性肥胖模型组(n=50),分别用普通饲料和高脂饲料喂养8周后,将10只营养性肥胖模型组大鼠和对照组大鼠处死。采用酶联免疫法检测血清睾酮和雌二醇水平,HE染色观察左侧睾丸的组织学改变,Johnsen评分评价睾丸的生精能力。剩余40只大鼠应用随机数字表法分为高脂饮食组(n=13)、正常饮食组(n=13)和减肥组(n=14),后两组大鼠均用普通饲料喂养,高脂饮食组大鼠用高脂饲料喂养,减肥组大鼠在正常饮食的基础上,每日跑步20 min,喂养6周后处死大鼠进行上述睾丸结构和功能研究。结果 高脂饮食8周后,营养性肥胖大鼠的体重明显高于对照组(O=0.006)。营养性肥胖大鼠的血清睾酮水平明显低于对照组(P=0.024),血清雌二醇水平明显高于对照组(P =0.017)。HE染色显示：与对照组比较营养性肥胖大鼠曲精小管细胞层数减少,部分曲精小管萎缩。营养性肥胖大鼠的Johnsen评分明显低于对照组(P=0.000)。高脂饮食组的睾酮水平明显低于正常饮食组(P=0.001)和减肥组(P=0.000),正常饮食组的睾酮水平也明显低于减肥组(P=0.001)。高脂饮食组的雌二醇水平明显高于正常饮食组(P=0.001)和减肥组（P=0.000）,正常饮食组的雌二醇水平也明显高于减肥组(P=0.001)。HE染色显示：高脂饮食组和正常饮食组大鼠睾丸组织的病变无进行性加重;减肥组大鼠睾丸组织的病变较轻。减肥组的Johnsen评分均明显高于其他两组（P=0.000及0.001）。相关性分析显示,Johnsen评分与大鼠体重呈负相关（r=-0.962,P=0.000）;与血清睾酮水平呈正相关(r=0.916,P=0.000)。结论 高脂饮食能导致青春期雄性Sprague Dawley大鼠营养性肥胖。营养性肥胖大鼠表现为睾丸发育不全,生精功能减弱,内分泌功能障碍,运动减肥后以上改变有所改善。肥胖程度与生精功能呈负相关。     

饮食诱导肥胖与肥胖抵抗大鼠ATP生成量的比较

目的比较饮食诱导肥胖大鼠与肥胖抵抗大鼠三磷酸腺苷（adenosinetriphosphate,ATP）生成量的差异。方法将健康雄性远交群（spraguedawley,SD）大鼠,随机分为基础饲料（control,CON）组和高脂饲料组,喂养2周后,将高脂饲料组按照体重增加量分为饮食诱导肥胖（diet—inducedobesity,DIO）组和饮食诱导抵抗（diet．in—ducedobesityresistance,DR）组。于喂养第10周末,麻醉处死动物,观察体重、摄食量、能量利用率以及肝脏、心脏、肌肉组织中ATP生成量的情况。结果DIO组的体重一直高于DR组（均有P〈0．05）。DIO组总能量摄入高于DR组和CON组（均有P〈0．001）,但DIO组与DR组能量利用率差异无统计学意义。DR组大鼠肝脏、心脏和肌肉组织中ATP生成量比DIO组分别高出12．8％,30．6％和11．6％。结论饮食诱导肥胖和肥胖抵抗大鼠的能量代谢存在差异,这种差异可能与主要能量器官中ATP的生成量有关。     

断乳后饲料构成对大鼠肝脏CPT-Ⅰ mRNA表达影响

目的研究断乳后饲料构成对大鼠肝脏肉碱棕榈酰转移酶-Ⅰ（CPT-Ⅰ）mRNA表达的影响.方法新生Wistar雄性大鼠24d断乳,按体重随机分为A、B、C、D 4组,分别喂饲高碳水化合物、高蛋白质、高不饱和脂肪酸和高饱和脂肪酸构成饲料3周后,基础饲料喂养2周,A组按体重随机再分为A1、A2 2组.A1组喂饲基础饲料作为对照组,A2和B、C、D 4组给予高脂饲料喂养6周,A2组作为高碳水化合物组.动态检测大鼠的体重、体脂含量、血糖及肝脏肉碱棕榈酰转移酶-Ⅰ mRNA水平.结果实验末期,C组大鼠体重、体脂含量和血糖均明显低于A2组（P〈0.05）;B组大鼠体重和体脂含量明显低于A2组（P〈0.05）,但血糖水平高于A2组;D组大鼠体重明显低于A2组（P〈0.05）,但血糖和体脂含量与A2组差异无统计学意义（P＞0.05）.动态观察表明,C组大鼠CPT-Ⅰ mRNA水平持续升高,且在实验末期明显高于其他组.结论断乳后进食高不饱和脂肪酸构成饲料可能通过持续增加CPT-Ⅰ基因表达,抑制大鼠肥胖形成.     

饮食控制对胰岛素抵抗大鼠骨骼肌中糖原合成酶激酶-3表达的影响

目的 观察饮食控制对高脂高糖饮食诱导的胰岛素抵抗模型大鼠骨骼肌中糖原合成酶激酶-3（GSK-3）表达的影响。方法 将30只Wistar大鼠随机分为正常组、胰岛素抵抗组和饮食治疗组，每组10只。正常组以常规饲料喂养，胰岛素抵抗组和饮食治疗组均以高糖高脂饲料喂养，4周后饮食治疗组大鼠改以常规饲料喂养，持续6周。采用Western blotting法检测各组大鼠骨骼肌中GSK-3的表达，于实验第1、5和11周分别检测其体质量、血甘油三脂和胆固醇、空腹血糖和胰岛素水平，并计算胰岛素敏感指数。结果 胰岛素抵抗组大鼠骨骼肌GSK-3的表达量较正常组增高70％（P〈0．01），饮食控制6周后饮食治疗组大鼠骨骼肌中GSK．3的表达量较胰岛素抵抗组减少23％（P〈0．01），较正常组增高31％（P〈0．05）。而饮食治疗组的胰岛素敏感指数与胰岛素抵抗组相比明显上升（P〈0．05）。结论 饮食控制可降低胰岛素抵抗大鼠骨骼肌细胞GSK-3表达水平，从而加强葡萄糖的摄取和利用，改善胰岛素抵抗。     

二陈汤对高脂饮食大鼠血脂及胰岛素抵抗的影响

目的：观察化痰方（二陈汤）对高脂饮食大鼠血脂及胰岛素抵抗的影响。方法：30只健康成年雄性大鼠按照随机数字表法分为正常组、高脂组和化痰组各10只,正常组给予正常饲料喂养,高脂组和化痰组给予高脂饲料喂养14周,化痰组第11周起给予二陈汤灌胃4周。在第14周末进行葡萄糖耐量实验（OGTT）和胰岛素耐量实验（ITT）,14周后处死大鼠,检测并比较各组血脂TC、TG的含量及第14周各组大鼠OGTT结果和ITT结果。结果：与正常组比较,高脂组大鼠血清中的TC和TG含量均明显升高（P〈0.01）;与高脂组比较,化痰组大鼠血清中的TG含量明显降低（P〈0.01）,TC有所降低,差异也有统计学意义（P〈0.05）。高脂组的空腹血糖明显高于正常组（P〈0.05）,而化痰组空腹血糖与正常组的比较差异无统计学意义（P〉0.05）;糖负荷后,高脂组的各个时间点的血糖均明显高于正常组（P〈0.05或P〈0.01）,而化痰组除了糖负荷后120 min的血糖明显高于正常组外（P〈0.01）,其余时间点与正常组的比较差异均无统计学意义（P〉0.05）。腹腔注射胰岛素后,化痰组各时间点血糖下降幅度均明显高于高脂组,30 min时高脂组血糖降低18%,而化痰组大鼠降低26%。结论：二陈汤能够降低高脂饮食大鼠血脂的含量,改善胰岛素抵抗,值得在临床上推广使用。     

饮食对下丘脑神经肽Y基因表达及肥胖影响

目的探讨高脂饮食对大鼠神经肽Y(NPY)基因表达及分泌的影响及大鼠肥胖易感性差异的机制.方法36只雌性SD大鼠按体重随机分为高脂实验组和基础对照组,分别给予高脂饲料和基础饲料喂养13周.据13周末体重从高脂饲料组选出体重最重和体重最轻者各9只为饮食诱导肥胖(DIO)和饮食诱导肥胖抵抗(DIR)组,比较各组大鼠能量摄入水平、血浆和下丘脑匀浆NPY及下丘脑NPY mRNA表达的差异.结果DIO组大鼠能量摄入量、下丘脑和血浆NPY水平之比显著高于DIR组和对照组(P＜0.01),DIO组大鼠下丘脑NPYmRNA表达显著高于DIR及对照组,而上述各指标DIR与对照组问差异均无统计学意义(P＞0.05).结论高脂饮食喂养条件下,SD大鼠表现为明显的肥胖易感性差异,这种差异与大鼠的能量摄入水平有关,下丘脑NPY高水平表达和分泌可能是导致肥胖易感大鼠多食和热能摄入过多的内在机制之一.     

“标本配穴”电针和限食干预对肥胖大鼠HPA轴及糖脂代谢的影响

目的 研究“标本配穴”电针和饮食控制对肥胖大鼠HPA轴及糖脂代谢的影响。方法 雄性Wistar大鼠随机分为5组,正常组（N）给予普通饲料喂养,模型组（M）给予高脂喂养,电针组（E）高脂喂养的同时给予“标本配穴”电针治疗,限食组（R）每只给予对照组摄食量的70%,电针+限食组（E+R）给予“标本配穴”电针结合饮食控制干预治疗,共干预8周。检测各组大鼠体重（BW）、血清糖脂（FPG、FINS、TG、TC）和ACTH、CORT水平变化,并检测下丘脑CRH含量。结果 (1) 与N组比较,M组BW及FPG、FINS、TG和TC均明显增加（P ＜0.01）,与M组比较,3个电针和饮食干预组BW及FPG、FINS、TG和TC均明显下降（P ＜0.01）,且E+R组下降程度优于E组和R组（P ＜0.05）;(2) 与N组比较,M组下丘脑CRH及血清ACTH、CORT均明显升高（P ＜0.01）,与M组比较,3个电针和饮食干预组CRH、ACTH及CORT均明显下降（P ＜0.01）,且E组效果优于R组（P ＜0.05）,而E+R组与E组比较无统计学差异（P ＞0.05）。结论 高脂饮食诱导的肥胖模型大鼠表现出HPA轴功能亢进,拮抗HPA轴亢进可能是“标本配穴”电针和饮食控制发挥减肥、改善糖脂代谢作用的途径之一。     

不同膳食构成对葡萄糖转运因子-4影响

目的探讨不同饲料构成对大鼠骨骼肌葡萄糖转运因子-4的影响。方法利用不同饲料（包括基础饲料、高蛋白、高脂肪、高能1与高能2饲料）喂养雄性Wistar大鼠9周,观察不同饲料构成对大鼠体重、脂体比、血糖及胰岛素的影响,并应用蛋白印迹法测定大鼠骨骼肌葡萄糖转运因子-4含量。结果高能饲料1组与高能饲料2组的体重、脂体比、血糖、胰岛素均显著高于基础组、高蛋白组与高脂肪组（P〈0.05）,而后3组体重、脂体比、血糖、胰岛素比较差异无统计学意义（P〉0.05）。高能饲料1组与高能饲料2组葡萄糖转运因子-4含量减少,能量相同的基础组、高蛋白组与高脂肪组含量相近。结论高能饲料可影响机体的葡萄糖代谢。     

Hydroxycitrate has long-term effects on feeding behavior,body weight regain and metabolism after body weight loss in male rats

We examined the long-term effect of hydroxycitrate (HCA) on food intake, meal patterns, body weight regain and energy conversion ratio as well as on different blood and liver variables in rats after substantial body weight loss. Rats were fed a 1% (g/100 g) fat diet (81% carbohydrate, 10% protein, 1% fat) or a 12% (g/100 g) fat diet (76% carbohydrate, 9% protein, 12% fat) in two separate experiments. Supplementing both diets with 3% HCA after 10 d of restrictive feeding reduced body weight regain over the whole subsequent period of ad libitum consumption (22 d) and decreased the energy conversion ratio [body weight regain (g)/energy intake (MJ)] at the end of the experiment. Only in rats fed the 12% fat diet, HCA had a long-term suppression of food intake. The anorectic effect occurred predominately during the light phase, and was due mainly to a reduction in numbers of meals. In rats fed the 12% fat diet, HCA had no effect on plasma beta-hydroxybutyrate (BHB), but reduced plasma triacylglycerol and increased liver fat concentration. In rats fed the 1% fat diet, HCA did not affect any metabolic variable examined. Thus, the suppressive effect of HCA on body weight regain, which was maintained for at least 3 wk, appears to be independent of the dietary fat content. Yet, the fat content of the diet seemed to be important for the long-term suppressive effect of HCA on feeding. The fact that HCA did not change plasma BHB concentration does not support a role for increased hepatic fatty acid oxidation in the anorectic effect of HCA.     

饮食诱导肥胖和肥胖抵抗大鼠脂联素水平研究

目的探讨高脂饲料对大鼠内脏脂肪中脂联素表达和血清中脂联素水平的影响及大鼠肥胖易感性差异的机制。方法 80只雄性SD大鼠,按体重随机分为两组:对照组(n=10),基础饲料喂养20w;高脂组(n=70),高脂饲料喂养12w。第12w末,根据体重将高脂组分为饮食诱导肥胖(DIO)和肥胖抵抗(DIO-R)组,继续喂养8w,观察各组大鼠体重、内脏脂肪湿重、体脂比、热能摄入量及能量利用率的差异;用Real Time PCR法测定内脏脂肪脂联素mRNA的表达水平;ELISA法测定血清脂联素水平。结果 DIO组体重、内脏脂肪湿重、体脂比、能量利用率显著高于对照组和DIO-R,而DIO-R除能量的摄入量显著低于对照组外,其他与对照组相比未见显著性差异;DIO大鼠内脏脂肪脂联素mRNA的表达水平显著低于对照组和DIO-R;DIO大鼠血清脂联素水平显著低于DIO-R。结论高脂饲料诱导下,不同肥胖易感性大鼠体内脂联素水平有明显差异性,脂联素可能在肥胖形成过程中扮演重要角色。     

A ketogenic diet increases protein phosphorylation in brain slices of rats

Ketogenic diets have been used to treat seizure disorders of children and recently it was shown to increase the drug-induced seizure threshold in rats. Protein phosphorylation is a major regulatory mechanism of signal transduction that has been implicated in modulating neuronal excitability. We investigated the basal protein phosphorylation in microslices from different brain regions (hippocampus, cerebral cortex and cerebellum) of young rats fed a ketogenic diet, and we evaluated the effect of this diet on weight development and health of these rats based on serum biochemistry. Thirty-day-old rats consumed ad libitum ketogenic (high fat) or control diets for 8 wk. Rats consuming the high fat diet had ketonemia without signs of undernutrition or illness. Microslices were incubated in media containing (32)P-phosphate, and (32)P-phosphoprotein content was analyzed by one- or two-dimensional electrophoresis followed by autoradiography. Basal protein phosphorylation was greater in brain slices from ketogenic rats. Different increments of synapsin I, GAP-43 and GFAP phosphorylation were observed in two-dimensional autoradiography. A ketogenic diet induced metabolic changes affecting the basal status of protein phosphorylation. This change could affect the mechanisms of signal transduction in neural cells involved in the increase in the seizure threshold.     

The reduced energy intake of rats fed a high-protein low-carbohydrate diet explains the lower fat deposition, but macronutrient substitution accounts for the improved glycemic control

The metabolic effect of high-protein low-carbohydrate (HP) diets on body composition and glucose homeostasis remains incompletely understood. This study assesses the respective roles of the increased protein:carbohydrate ratio (P:C) and the resulting moderate decrease in energy intake in the metabolic effects of HP diets. Rats had free access to normal (NP; 14%) or high (HP; 53%) total milk protein isoenergetic diets, or were fed the NP diet but restricted to the energy intake of HP rats (NPr), which was 89.1 +/- 9.3% that of NP rats. After 8 wk, body weight was lower in HP and NPr rats than in NP rats. In HP rats, the lower body weight was associated with a lower adipose tissue mass and a reduced proportion of large adipocytes. HP rats also had an improved oral glucose tolerance and insulin sensitivity, as assessed by the homeostatic model assessment index, compared with NPr and NP rats, and these effects were related solely to the increased P:C. These data suggest that the reduced energy intake of rats fed a high-protein, low-carbohydrate diet explains the lower fat deposition but an increased P:C per se improves glucose homeostasis.     

Effects of dietary taurine supplementation on plasma and liver lipids in OVX rats fed calcium-deficient diet

Taurine supplementation has been shown to have an effect on lowering blood lipids in ovariectomized (OVX) rats. It therefore seemed desirable to find out whether the beneficial effect of taurine on OVX rats fed calcium-deficient diet could also be reproduced. Forty female Sprague-Dawley rats were divided into two groups. One group was OVX and the other group received a sham operation (Sham). Each rat group was further divided into the control diet and the taurine supplemented (2.0 g/100 g diet) diet group. All rats were fed on calcium-deficient diet and deionized water ad libitum for 6 weeks. Plasma and liver lipids were determined by using commercial kits. LDL-cholesterol concentrations were estimated with the equation of Friedewald et al. (1972). There were no significant differences in body weight gain and food intake between the control and taurine group within Sham and OVX groups, but body weight gain, food intake, and food efficiency ratio was higher in the OVX group. Concentrations of plasma total cholesterol, triglyceride, LDL-cholesterol were significantly lower in the taurine fed group of OVX rats fed Ca deficient diet, while HDL-cholesterol concentration was increased in the taurine fed group. Therefore, in this study, we examined whether taurine also prevented hypercholesterolemia induced by ovarian hormone deficiency in ovariectomized rats when they were fed a calcium-deficient diet. These results indicate that taurine may have some beneficial effects on hypercholesterolemia and hypertriglyceridemia in OVX rats fed calcium-deficient diet.     

Behavioral and Metabolic Effects of a Calorie-Restricted Cafeteria Diet and Oleuropein Supplementation in Obese Male Rats

Diet-induced obesity models are widely used to investigate dietary interventions for treating obesity. This study was aimed to test whether a dietary intervention based on a calorie-restricted cafeteria diet (CAF-R) and a polyphenolic compound (Oleuropein, OLE) supplementation modified sucrose intake, preference, and taste reactivity in cafeteria diet (CAF)-induced obese rats. CAF diet consists of high-energy, highly palatable human foods. Male rats fed standard chow (STD) or CAF diet were compared with obese rats fed CAF-R diet, alone or supplemented with an olive tree leaves extract (25 mg/kg*day) containing a 20.1% of OLE (CAF-RO). Biometric, food consumption, and serum parameters were measured. CAF diet increased body weight, food and energy consumption and obesity-associated metabolic parameters. CAF-R and CAF-RO diets significantly attenuated body weight gain and BMI, diminished food and energy intake and improved biochemical parameters such as triacylglycerides and insulin resistance which did not differ between CAF-RO and STD groups. The three cafeteria groups diminished sucrose intake and preference compared to STD group. CAF-RO also diminished the hedonic responses for the high sucrose concentrations compared with the other groups. These results indicate that CAF-R diet may be an efficient strategy to restore obesity-associated alterations, whilst OLE supplementation seems to have an additional beneficial effect on sweet taste function.     

肥胖和肥胖抵抗大鼠神经肽Y及其受体基因表达的研究

目的:探讨高脂饲料对大鼠下丘脑神经肽Y(NPY)及其受体Y1、Y2、Y5基因表达的影响及大鼠肥胖易感性差异的机制。方法:36只雌性SD大鼠,按体重随机分为高脂组和对照组,分别给予高脂饲料和基础饲料13w。实验结束时,根据体重将高脂组分为饮食诱导肥胖(DIO)和肥胖抵抗(DIO-R)大鼠,观察各组大鼠体重、内脏脂肪湿重、脂体比、热能摄入量及能量利用率的差异;RT-PCR法测定下丘脑NPY及其受体Y1、Y2、Y5mRNA的表达水平。结果:DIO大鼠体重、内脏脂肪湿重、脂体比、热能摄入量及能量利用率显著高于对照组和DIO-R大鼠,而DIO-R大鼠与对照组相比未见显著性差异;DIO大鼠下丘脑NPY及其受体Y1、Y2、Y5mRNA的表达水平显著高于对照组和DIO-R大鼠,而DIO-R大鼠与对照组相比,除Y2受体mRNA的表达水平显著下降外,其余指标均无显著性差异。结论:高脂饲料诱导下,SD大鼠表现为明显的肥胖易感性差异,下丘脑NPY及其受体的高水平表达可能是导致DIO大鼠热能摄入过多的内在机制之一。     

Growth measurements in Sprague-Dawley rats fed diets of very low fat concentration

Young (70 g) male Sprague-Dawley rats were fed one of four diets for 28 d to determine the effects of replacing dietary fat with a noncaloric substitute. Fat contributed 17% of energy in a control diet and 36% in a high fat diet. A fat substitute was used to produce two low fat diets in which essential fatty acid was the only source of lipid. One low fat diet (low fat 1) was similar in texture to the control diet. The other low fat diet (low fat 2) was comparable to the high fat diet. Digestible energy was 92-95% of gross dietary energy in all diets. There was no effect of diet composition on energy intake of the rats. At the end of the study, animals given low fat diets weighed approximately 20 g more than those fed control or high fat diets, due to increased lean body mass. Diet had no significant effect on body fat content, gastrocnemius muscle weight or femur length. This study indicates that increasing the protein:energy ratio of the diet by replacing nonessential fat with a fat substitute may promote deposition of lean tissue rather than fat in growing animals.     

乌龙茶与绿茶减肥效果的比较研究

目的：比较乌龙茶与绿茶的减肥效果。方法：56只雄性SD大鼠随机分为4组,其中3组以高能量高脂肪饲料喂饲大鼠,同时分别予以蒸馏水或乌龙茶、绿茶1．2g／kg.bw。另1组喂以基础饲料,连续喂养30天后,测定大鼠体重、体围、肝脏重量、附睾周、肾周及肩胛间脂肪组织重量,计算Lee‘s指数、肝重／体重、脂肪重／体重,并测定血脂、下丘脑神经递质(去甲肾上腺素)含量。结果：与高脂对照组比较,乌龙茶与绿茶组大鼠体重、增重、附睾周与肾周脂肪组织重量、肾周脂肪重／体重、血清甘油三酯含量明显较低,绿茶组大鼠体围也较低,而两组间无明显差异。结论：乌龙茶与绿茶均有减肥效果,且在相同剂量下两者减肥效果相似。     

抗性淀粉对大鼠胰岛素抵抗的影响

目的探讨新型抗性淀粉Hi-maize1043对红花油饲料喂养诱导的大鼠胰岛素抵抗的影响。方法将70只大鼠随机分为7组,一组喂饲正常基础饲料(N),其余各组食用高脂饲料(HF),红花油占总能量的59%,5w后进行口服葡萄糖耐量试验(OGTT),通过计算胰岛素敏感性指数(ISI),两组间差异有统计学意义,认为高脂饲料喂饲已使大鼠产生胰岛素抵抗。将6组胰岛素抵抗大鼠随机安排进食N、HF、Hi-maize1043高(HS)、中(MS)、低(LS)和低脂(LFHS)饲料,分别为N1、HF、HS、MS、LS和LFHS组;原正常基础饲料组为N组。喂养6w后,再次进行OGTT,计算ISI,比较各组各项指标的差异。结果经过5w的高脂饲料喂养,可成功在大鼠中诱导出胰岛素抵抗。与HF、MS和LS组相比,N、N1、HS和LFHS组ISI较高(P<0.05),N1、HS和LFHS组在改善胰岛素抵抗上作用相似,且LFHS组的体重接近正常对照的N组。结论抗性淀粉(RS)可以改善大鼠中红花油诱导的胰岛素抵抗,同时有效控制体重。