生命早期使用头孢曲松对生命后期高脂饲料负荷小鼠糖脂代谢的影响

目的探究生命早期使用抗生素对生命后期高脂饲料负荷下的小鼠血糖、血脂等糖脂代谢指标的影响。方法将48只2周龄雌性BALB/c小鼠随机分为空白对照组、抗生素组、高脂组和联合作用组,每组12只,抗生素组和联合作用组以100 mg/kg头孢曲松灌胃,其余2组灌胃等量生理盐水,持续至4周龄后停止灌胃,接着高脂组和联合作用组以高脂饲料、其余2组以普通饲料喂养12周。最后1周测定空腹血糖并进行口服糖耐量实验,实验结束后测定血脂、肝脏脂质、胰岛素和瘦素水平,并计算胰岛素抵抗指数。结果与普通饲料相比,高脂饲料引起小鼠糖耐量受损,内脏脂肪、血糖、胰岛素抵抗指数、血脂、肝脏脂质和瘦素增加(P<0.05);与空白对照组相比,抗生素组小鼠糖耐量受损,内脏脂肪、血糖和肝脏甘油三酯水平增加(P<0.05);与高脂组相比,联合作用组小鼠的糖耐量受损、血糖、胰岛素抵抗指数和肝脏总胆固醇水平增加(P<0.05)。结论生命早期使用头孢曲松增加了机体内脏脂肪、血糖、胰岛素抵抗和肝脏脂质,且加剧了高脂饲料诱导的糖脂代谢紊乱,表明生命早期使用抗生素可能会提高机体对高脂饲料诱导糖脂代谢异常的易感性。     

初断乳大鼠锌补充对成年高脂诱导肥胖后胰岛素的影响

目的 探讨初断乳大鼠锌补充对成年期高脂饮食下胰岛素水平的影响,为阐明生命早期适量补锌预防成年后胰岛素抵抗的机制提供重要依据。方法 初断乳雄性SD大鼠85只随机分为基础饲料组和高、中、低锌补充组。锌补充4周后各组均以基础饲料喂养1周,于第5周末检测大鼠血糖、胰岛素水平并计算胰岛素抵抗指数。随后将基础饲料组大鼠随机分为肥胖组和正常对照组,肥胖诱导组及3个锌补充组均喂以高脂饲料。高脂干预8周后处死所有大鼠并检测上述指标。结果 大鼠成年高脂干预后,1)3个锌补充组分别较肥胖诱导组体重明显降低(P＜0.05),高脂饲料喂养后锌补充组体重正常,而肥胖诱导组发生肥胖;2)3个锌补充组分别较肥胖诱导组血糖、胰岛素明显降低(P＜0.05),而胰岛素抵抗指数明显升高(P＜0.05),高脂饲料喂养后锌补充组胰岛素水平正常,而肥胖诱导组产生胰岛素抵抗。结论 生命早期适量补锌可持续发挥作用,在一定程度上维持成年后高脂膳食下血糖和胰岛素处于正常水平,预防胰岛素抵抗发生。     

A mixture of Salacia reticulata (Kotala himbutu) aqueous extract and cyclodextrin reduces body weight gain,visceral fat accumulation,and total cholesterol and insulin increases in male Wistar fatty rats

This study examined the effects of a mixture of an aqueous extract of Salacia reticulata (Kotala himbutu) and cyclodextrin (SRCD) on various metabolic parameters and cecal fermentation in obese fa/fa male Wistar fatty rats, a model of type 2 diabetes mellitus. Wistar fatty rats were fed 0% (control group) or 0.2% SRCD-supplemented diets and weighed weekly. The plasma glucose, triacylglycerol, total cholesterol, insulin, and adiponectin concentrations were measured at weeks 0, 2, 4, and 5. SRCD supplementation suppressed the time-dependent increase in the plasma total cholesterol and insulin concentrations. After 6 weeks of a 0.2% SRCD-supplemented diet, the body weight gain, food intake, visceral fat mass, liver mass, and liver triacylglycerol content of the rats were significantly lower, whereas the plasma adiponectin concentrations were significantly higher than those of the control group. SRCD supplementation had no significant effect on plasma glucose and triacylglycerol concentrations. SRCD supplementation significantly increased cecum mass, whereas it significantly decreased the cecal butyrate and short-chain fatty acid (sum of the acetate, butyrate, and propionate) concentrations. All of the rats were subjected to an oral glucose tolerance test at the beginning of week 6. The area under the curve for insulin was significantly smaller with SRCD supplementation and showed no change in glucose tolerance compared to that of the control group. These results suggest that bioactive compounds in SRCD may suppress the development of type 2 diabetes mellitus by influencing glucose and lipid metabolism in male Wistar fatty rats and that SRCD may influence cecal fermentation.     

Taurine alters respiratory gas exchange and nutrient metabolism in type 2 diabetic rats

OBJECTIVE: To assess the effect of taurine supplementation on respiratory gas exchange, which might reflect the improved metabolism of glucose and/or lipid in the type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. RESEARCH METHODS AND PROCEDURES: Male OLETF rats (16 weeks of age) were randomly divided into two groups: unsupplemented group and taurine-supplemented (3% in drinking water) group. After 9 weeks of treatment, indirect calorimetry and insulin tolerance tests were conducted. The amounts of visceral fat pads, tissue glycogen, the blood concentrations of glucose, triacylglycerol, taurine, and electrolytes, and the level of hematocrit were compared between groups. A nondiabetic rat strain (Long-Evans Tokushima Otsuka) was used as the age-matched normal control. RESULTS: The indirect calorimetry showed that the treatment of OLETF rats with taurine could reduce a part of postprandial glucose oxidation possibly responsible for the increase of triacylglycerol synthesis in the body. Taurine supplementation also improved hyperglycemia and insulin resistance and increased muscle glycogen content in the OLETF rats. Supplementation with taurine increased the blood concentration of taurine and electrolyte and fluid volume, all of which were considered to be related to the improvement of metabolic disturbance in OLETF rats. DISCUSSION: Taurine supplementation may be an effective treatment for glucose intolerance and fat/lipid accumulation observed in type 2 diabetes associated with obesity. These metabolic changes might be ascribed, in part, to the alteration of circulating blood profiles, where the improved hyperglycemia and/or the blood accumulation of taurine itself would play roles.     

罗格列酮及饮食干预对胰岛素抵抗大鼠骨骼肌GLUT4转位的影响

目的　探讨罗格列酮对胰岛素抵抗大鼠骨骼肌细胞葡萄糖转运蛋白 4(GLUT4)转位的影响。方法　利用高脂饲料喂养 ,使Sprague -Dawley(SD)大鼠产生胰岛素抵抗 ,用罗格列酮及饮食干预治疗 4周后 ,取骨骼肌组织 ,应用Western -bloting印迹法分析骨骼细胞膜GLUT4表达量。结果　在胰岛素刺激下 ,胰岛素抵抗大鼠骨骼肌细胞膜GLUT4表达较正常大鼠下降 5 2 72 %(P <0 0 0 1) ,罗格列酮及饮食干预组 ,细胞膜GLUT4表达较未干预胰岛素抵抗大鼠分别增加 49 5 3 %、5 0 3 4%(P <0 0 0 1)。结论　罗格列酮可促进胰岛素刺激的GLUT4转位 ,从而改善高脂喂养所引起的骨骼肌组织胰岛素抵抗     

Green tea supplementation ameliorates insulin resistance and increases glucose transporter IV content in a fructose-fed rat model

Summary.Background: Sprague-Dawley rats fed a fructose-rich diet exhibit insulin resistance and hypertension, a pathologic status resembling human type II diabetes mellitus, and are an excellent laboratory animal model for research on insulin action and the development of hypertension. Since green tea has numerous beneficial effects, we tested its effect on fructose-fed rats. Aim: The present study was therefore designed to further evaluate the effects of green tea supplementation on insulin resistance, hypertension, and the glucose transporters I and IV contents in adipose tissue in the fructose-fed rat model.Methods: The animals were divided into three groups and fed for 12 weeks with standard chow and water (control group), a high fructose diet and water (fructose group), or the same high fructose diet, but with green tea (0.5 g of lyophilized green tea powder dissolved in 100 mL of deionized distilled water) instead of water (fructose/green tea group). During the 12 weeks study period, fresh water or green tea was provided daily at 6:00 PM. Blood pressure was measured twice a week, and an oral glucose tolerance test performed after 12 weeks of diet supplementation.At the end of the experiment, plasma triglyceride (TG), free fatty acid (FFA), glucose, and insulin were assayed. The epididymal fat pads from all rats in the same group were pooled and adipocytes isolated and tested for insulin binding, glucose uptake, and their content of glucose transporters I (GLUT I) and IV (GLUT IV).Result: Compared to the control group, the fructose group developed fasting hyperglycemia, hyperinsulinemia, and elevated blood pressure. Insulin-stimulated glucose uptake and insulin binding of adipocytes were significantly reduced, and the glucose transporter IV content of adipocytes also decreased. The fructose/green tea group showed improvement in all of these metabolic defects and in insulin resistance and blood pressure.Conclusion: Based on these results, we suggest that the amelioration of insulin resistance by green tea is associated with the increased expression of GLUT IV.     

Dietary intake of medium- and long-chain triacylglycerols ameliorates insulin resistance in rats fed a high-fat diet

Objective

Excessive accumulation of visceral fat is strongly associated with insulin resistance. The present investigation examined the effects of dietary intake of medium- and long-chain triacylglycerols (MLCTs), which have been shown to induce significantly lower visceral fat accumulation in rats and humans, on high-fat diet-induced obesity and insulin resistance in rats. These effects were then compared with those observed in long-chain triacylglycerol (LCT)-fed rats.

Methods

After an 8-wk feeding of a high-fat diet, which induced severe whole-body insulin resistance, male Sprague-Dawley rats were fed a standard diet containing LCTs or MLCTs for 6 wk. After the dietary treatment, an oral glucose tolerance test was performed.

Results

Although body weight and total intra-abdominal fat mass did not differ between the two groups, mesenteric fat weight in the MLCT-fed group was significantly lower than that in the LCT group (P < 0.05). The increase in plasma insulin concentrations, but not in glucose, after glucose administration (area under the curve) was significantly smaller in the MLCT group than in the LCT group (P < 0.01) and was significantly associated with mesenteric fat weight (P < 0.05). MLCT-fed rats had significantly higher plasma adiponectin concentrations compared with LCT rats (P < 0.05). Adiponectin concentrations were negatively correlated with the area under the curve for plasma insulin (P < 0.05) and tended to be inversely related to mesenteric fat weight (P = 0.08).

Conclusion

These results suggest that dietary intake of MLCTs may improve insulin resistance in rats fed a high-fat diet, at least in part through increased adiponectin concentrations caused by a lower mesenteric fat mass.     

Impact of high-protein diets with either moderate or low carbohydrate on weight loss, body composition, blood pressure and glucose tolerance in rats

One approach to achieve weight loss and decrease both obesity and associated morbidities involves high-protein, low-carbohydrate (HPLC) diets. This study compares the impact on metabolic health of HPLC and high-protein, medium-carbohydrate (HPMC) diets offered to diet-induced obese (DIO) rats. Weanling male rats were fed either a 37 % fat diet (n 48) or stock pellets (n 12) for 22 weeks. Rats fed the 37 % fat diet accumulated more body fat (26.6 versus 14.8 % body weight, P < 0.001) compared with those on stock diet. The DIO rats had higher systolic blood pressure (+6.6 mmHg, P = 0.002), fasting insulin (+63 % P = 0.006) and areas under the glucose (+21 %, P < 0.001) and insulin (+81 %, P < 0.001) curves following an oral glucose tolerance test. DIO rats were then separated into four groups and offered for 8 weeks either: (1) the 37 % fat diet; (2) an HPLC or (3) HPMC diet; or (4) fed the 37 % fat diet to the intake of the HPMC group. Rats offered the 37 % fat or HPLC diets gained while those on HPMC lost body fat. Blood pressure was not altered by the dietary switch. Both HPLC and HPMC rats had lowered fasting insulin (P = 0.027) and improved homeostatic assessment (HOMA; P = 0.011) that was not different from those of stock animals. These improvements occurred despite differences in fat gain, and indicate that both weight loss and macronutrient intake can impact favourably on obesity-associated morbidities.     

Antihyperglycemic effect of stem bark powder from paper mulberry (Broussonetia kazinoki Sieb.) in type 2 diabetic Otsuka Long-Evans Tokushima fatty rats

The effect of stem bark powder from paper mulberry (PMSB) on serum glucose, insulin, fructosamine, and lipid concentrations, as well as enzyme activities that serve as liver injury markers, was investigated in genetically diabetic Otsuka Long-Evans Tokushima fatty (OLETF) rats. Both nondiabetic Long-Evans Tokushima Otsuka (LETO) rats and diabetic OLETF rats (30 weeks old) were fed a semisynthetic diet with or without 50 g/kg PMSB for 8 weeks and then compared. The OLETF control rats showed a high amount of daily water intake in comparison to those in the LETO group. The concentrations of glucose, fructosamine, total lipid, triglyceride, total cholesterol, and high-density lipoprotein-cholesterol and the activities of aspartate aminotransferase and alanine aminotransferase (ALT) in serum were higher in the OLETF control rats than those in the LETO control rats. However, PMSB ingestion decreased the serum levels of glucose, fructosamine, triglyceride, and total cholesterol and the activity of ALT in the OLETF rats, but not in the LETO rats. The concentration of serum insulin was also significantly increased by PMSB consumption in the OLETF rats compared to the OLETF control rats. These results suggest that PMSB might have an antihyperglycemic effect in the OLETF rat and that the increased blood insulin level would be an important regulatory factor for improving hyperglycemia in the current animal model.     

高脂饲料对OLETF大鼠糖代谢及血清磷脂脂肪酸组成的影响

目的:观察高脂饲料对自发性2型糖尿病模型OLETF大鼠糖代谢及血清磷脂脂肪酸组成的影响。方法:将20只14w雄性OLETF大鼠随机分为两组,分别以高脂及标准饲料喂饲10w,两种饲料中饱和脂肪酸、单不饱和脂肪酸、多不饱和脂肪酸占总脂肪酸的百分含量相似。大鼠第24w龄时进行口服糖耐量试验,同时测定大鼠的胰岛素水平和血清磷脂脂肪酸组成。结果:实验期间两组大鼠总进食量无统计学差异,但高脂饲料组大鼠体重明显高于标准饲料组(P<0.01);口服糖耐量试验和胰岛素水平测定结果表明,两组大鼠的糖代谢状态无统计学差异;血清磷脂脂肪酸组成中,除总n-6PUFA和18:3(n-3)的百分含量无统计学差异外,其他各脂肪酸组分在两组间的差异均具有统计学意义(P<0.01)。结论:在饲料脂肪酸组成保持可比的情况下,饲料脂肪量的增加可使OLETF大鼠的体重明显增加,而对糖代谢的影响不明显,同时对OLETF大鼠血清磷脂脂肪酸组成产生明显影响。     

不同膳食脂肪对糖耐量及胰岛素敏感性的影响

目的:比较4种膳食脂肪对大鼠糖耐量及胰岛素敏感性的影响。方法:将50只SD大鼠随机分为5组,分别为紫苏油组、葵花籽油组、橄榄油组、猪油组和基础饲料组。各膳食脂肪组大鼠的脂肪摄入量占总能量的30.4%。喂养6 w后,进行口服葡萄糖耐量试验(OGTT),测定血清胰岛素、甘油三酯、总胆固醇等指标,并计算胰岛素敏感指数(ISI)。同时分离附睾脂肪垫并称重。结果:与基础饲料组相比,猪油组大鼠葡萄糖餐后2 h血糖及胰岛素显著升高,ISI显著降低;葵花籽油组和橄榄油组大鼠的餐后2 h血糖显著低于猪油组,ISI显著高于猪油组;紫苏油组大鼠空腹及餐后2h血糖、胰岛素水平均显著低于猪油组,ISI高于猪油组,其中空腹血糖还低于葵花籽油组、橄榄油组和基础饲料组,ISI高于上述组。紫苏油组血清甘油三酯、总胆固醇水平显著低于猪油组和基础饲料组,大鼠附睾脂肪垫相对重量显著低于猪油组。结论:猪油可促使胰岛素抵抗及高血糖的发生,而紫苏油可提高大鼠胰岛素敏感性、改善糖代谢;葵花籽油和橄榄油对胰岛素敏感性和糖耐量的作用介于紫苏油和猪油之间。紫苏油对糖代谢的有利作用可能与其降低血中甘油三酯水平、减少体内脂肪堆积有关。     

Diet-induced obesity and spatial cognition in young male rats

Recent work suggests that obesity may adversely affect cognitive behavior. To examine this suggestion, the effects of feeding a standard chow diet, and either supplemental sugar or fat on the development of obesity and performance on a test of spatial learning, the Morris Water Maze (MWM), were assessed in young male Long-Evans rats. Rats given access to a sucrose solution or dietary fat in addition to the chow diet consumed approximately 10% more calories per day, gained more weight, and had larger epididymal fat pads than rats fed the chow diet alone. Moreover, rats fed the supplemental sucrose took significantly more time to find a hidden platform in the MWM than rats fed the chow diet alone or chow and supplemental fat. Additionally, when tested 10 days after the initial training trials, rats given sucrose displayed deficits in long-term spatial memory. After 6 weeks on the diets, fasting blood glucose and serum triglyceride concentrations were significantly higher in sucrose-fed rats than in rats eating only the standard diet. These results indicate that diet-induced obesity resulting from excess sucrose intake, but not fat intake, in young animals impairs spatial learning and memory. It is hypothesized that these deficits arise from metabolic insults that leave the brain vulnerable to alterations in insulin sensitivity and glucose metabolism.     

Dietary diacylglycerol reduces postprandial hyperlipidemia and ameliorates glucose intolerance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats

OBJECTIVE: The aim of the present study was to determine the effects of dietary diacylglycerol (DG) on the metabolism of lipids and glucose in type II diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats. METHODS: In experiment 1, the rats were orally administered 10 mL/kg of a triacylglycerol (TG) or DG emulsion (15% [w/v] oil), and the subsequent changes in the serum lipid levels were compared. In experiment 2, the rats were fed diets containing 15% DG or TG oil. After 22 weeks, the serum levels of lipids, glucose, and cytokines were determined. In addition, an oral glucose tolerance test (OGTT) was performed on the rats. RESULTS: Administration of an oral fat load caused marked hypertriglyceridemia with a peak at 2 h. Oral DG loading reduced the serum TG increase; the difference between the groups was significant at 4 and 6 h (P < 0.05). Diacylglycerol also markedly reduced the serum free fatty acid concentration increase due to the fat load. After 22 weeks of feeding, dietary DG reduced serum TG levels in the non-fasting state. Moreover, an OGTT revealed enhanced glucose disposal in the DG-fed rats compared with the TG-fed rats. Serum levels of adiponectin, an important insulin-sensitizing adipocytokine, were higher in the DG-fed rats than in the TG-fed rats (P < 0.05). In addition, DG-feeding reduced serum levels of C-reactive protein, a cardiovascular risk factor (P < 0.05). CONCLUSION: These results suggested that dietary DG improves lipid metabolism and glucose tolerance, and retards the progress of diabetes mellitus in OLETF rats.     

高脂膳食诱导的大鼠肥胖对小肠黏膜糖吸收功能的影响

目的探讨高脂膳食诱导肥胖的发生是否与小肠黏膜糖类消化及吸收功能的改变相关联。方法 46只雄性SD大鼠随机分为高脂组(n=31)与正常对照组(n=15),分别用高脂饲料和基础饲料饲养24周。24周后高脂饲料组大鼠根据体重分为肥胖组(n=16)及肥胖抵抗组(n=10)。测定大鼠的体重及腹腔脂肪湿重、空腹血糖水平、小肠黏膜麦芽糖酶及蔗糖酶活性。免疫组织化学法、RT-PCR法及蛋白质免疫印迹法检测大鼠小肠黏膜中Na+-依赖型葡萄糖转运蛋白(SGLT-1)的表达水平。结果肥胖组大鼠的体重、腹腔脂肪湿重、空腹血糖水平、小肠黏膜麦芽糖酶活性及SGLT-1蛋白表达量显著高于正常对照组及肥胖抵抗组(P<0.05)。3组大鼠小肠黏膜蔗糖酶活性无明显差异(P>0.05)。肥胖组大鼠小肠黏膜SGLT-1 mRNA的表达水平与正常对照组及肥胖抵抗组比较分别增加了12.5%和23%,但差异无显著性(P>0.05)。结论高脂膳食诱导的大鼠肥胖与小肠黏膜中麦芽糖酶活性增强及糖吸收的关键分子SGLT-1的表达增加相关联。     

The protective effect of neonatal oral administration of oleanolic acid against the subsequent development of fructose-induced metabolic dysfunction in male and female rats

Background

Consumption of fructose-rich diets has been implicated in the increasing global prevalence of metabolic syndrome (MetS). Interventions during periods of early ontogenic developmental plasticity can cause epigenetic changes which program metabolism for positive or negative health benefits later in life. The phytochemical oleanolic acid (OA) possesses anti-diabetic and anti-obesity effects. We investigated the potential protective effects of neonatal administration of OA on the subsequent development of high fructose diet-induced metabolic dysfunction in rats.

Method

Male and female (N?=?112) suckling rats were randomly assigned to four groups and administered orally: distilled water (DW), oleanolic acid (OA; 60 mg/kg), high-fructose solution (HF; 20% w/v) or OA?+?HF for 7 days. The rats were weaned onto normal commercial rat chow up to day 55. From day 56, half of the rats in each treatment group were continued on plain water and the rest on a high fructose solution as drinking fluid for 8 weeks. On day 110, the rats were subjected to an oral glucose tolerance test and then euthanased on day 112. Tissue and blood samples were collected to determine the effects of the treatments on visceral fat pad mass, fasting plasma levels of cholesterol, insulin, glucose, triglycerides, insulin resistance (HOMA-IR) and glucose tolerance.

Results

Rats which consumed fructose as neonates and then later as adults (HF?+?F) and those which consumed fructose only in adulthood (DW?+?F) had significant increases in terminal body mass (females only), visceral fat mass (males and females), serum triglycerides (females only), epididymal fat (males only), fasting plasma glucose (males and females), impaired glucose metabolism (females only), β-cell dysfunction and insulin resistance (males and females) compared to the other treatment groups (P?<?0.05). There were no differences in fasting serum cholesterol levels across all treatment groups in both male and female rats (P?>?0.05).

Conclusion

We conclude that neonatal oral administration of OA during the critical window of developmental plasticity protected against the development of health outcomes associated with fructose-induced metabolic disorders in the rats.

     

Evidence of a glucose-insulin imbalance and effect of dietary protein and energy level in chickens selected for high abdominal fat content

Effects of dietary protein or energy level on growth and physiological parameters were investigated in growing chickens selected for high (fat line, FL) or low (lean line, LL) abdominal fat but similar body weight. The FL birds deposited consistently more abdominal fat (about two-fold) and had poorer feed conversion, irrespective of diet. Increasing the ratio of energy to protein increased fat deposition similarly but at different levels. Body weight and feed consumption showed only minor and inconsistent differences and feed consumption following a fast and body temperature in the fed or the fasted-state showed no differences between lines. Fasting plasma glucose levels were similar for both lines at hatching but consistently lower in FL birds thereafter. This was matched by higher fasting plasma insulin levels. A similar relationship was also observed in fed FL birds at 2 weeks of age. Glucose disposal rate was faster in FL birds at 4 and 6 weeks but normal by 8 weeks. The glucose-induced insulin release was higher in FL birds at 6 and 8 weeks, indicating a normal sensitivity to insulin at a young age, with the development of a tissue insulin resistance by 8 weeks of age. The primary mechanism responsible for the fattening of FL birds appears therefore to be greater insulin release from the pancreas of the FL birds soon after hatching.     

Diet-induced obesity and spatial cognition in young male rats

Abstract

Recent work suggests that obesity may adversely affect cognitive behavior. To examine this suggestion, the effects of feeding a standard chow diet, and either supplemental sugar or fat on the development of obesity and performance on a test of spatial learning, the Morris Water Maze (MWM), were assessed in young male Long–Evans rats. Rats given access to a sucrose solution or dietary fat in addition to the chow diet consumed approximately 10% more calories per day, gained more weight, and had larger epididymal fat pads than rats fed the chow diet alone. Moreover, rats fed the supplemental sucrose took significantly more time to find a hidden platform in the MWM than rats fed the chow diet alone or chow and supplemental fat. Additionally, when tested 10 days after the initial training trials, rats given sucrose displayed deficits in long-term spatial memory. After 6 weeks on the diets, fasting blood glucose and serum triglyceride concentrations were significantly higher in sucrose-fed rats than in rats eating only the standard diet. These results indicate that diet-induced obesity resulting from excess sucrose intake, but not fat intake, in young animals impairs spatial learning and memory. It is hypothesized that these deficits arise from metabolic insults that leave the brain vulnerable to alterations in insulin sensitivity and glucose metabolism.     

Effects of whey protein and leucine supplementation on insulin resistance in non-obese insulin-resistant model rats

ObjectiveWhey protein (WP) has been reported to reduce body weight gain and improve glucose metabolism in obese individuals. This study aims to assess and compare the effects of WP and its hydrolysate-leucine (Leu) supplementation in non-obese, insulin-resistant (IR) rat models, particularly the effects on insulin sensitivity, lipid profile, and antioxidant activity.MethodsWistar rats were fed a diet consisting of 38.5% fat for 12 wk and 51.3% fat for an additional 4 wk to establish non-obese IR rats. The IR rats were then switched to regular AIN-93 diet containing 0% WP, 5% WP, 15% WP or 1.6% Leu for 8 wk. The Leu content was the same in the 15% WP and 1.6% Leu groups based on high-performance liquid chromatography. The IR rats' body weight, fasting blood glucose, fasting insulin, and homeostasis model assessment-insulin resistance were measured before and after supplementation. An oral glucose tolerance test was performed after supplementation. Body composition, plasma concentrations of the lipids profile, and antioxidant index also were analyzed.ResultsNo significant difference was observed in body weight, energy intake, and fasting blood glucose in the non-obese IR rats at the end of the experiment. Compared with the 0% WP group, the fasting insulin and homeostasis model assessment-insulin resistance significantly decreased in the 15% WP and 1.6% Leu groups. Furthermore, the blood glucose area under the curve of the oral glucose tolerance test was significantly less in the 15% WP and 1.6% Leu groups. There were no differences in the lipids profile, except for the increase in the high-density lipoprotein cholesterol in the 15% WP and 1.6% Leu groups. For the antioxidant index, the 15% WP group had significantly increased plasma levels for total antioxidation capacity, superoxide dismutase, and glutathione, and a decreased malondialdehyde concentration. The 1.6% Leu group was shown to have the same effect as the 15% WP group, except for the glutathione.ConclusionOur findings demonstrate that the supplementation of WP and Leu may improve IR and antioxidant stress without resulting in changes in body weight and energy intake in non-obese IR rats.     

乳清酸诱导的大鼠非酒精性脂肪肝与糖耐量异常和高血压关系的研究

目的研究长期摄食乳清酸诱导的大鼠脂肪肝、糖耐量及血压的变化及三者之间的关系。方法将Wistar大鼠按体重随机分为对照组和乳清酸两组,前者喂标准饲料,后者喂1%乳清酸饲料。14、30、60、90d后测体重、肝、肾周及附睾脂肪重量,肝甘油三酯(TG)、胆固醇(TC)水平和葡萄糖耐量,并在14、30、45、60、89d测血压变化。结果乳清酸组14、30、60、90 d后测,大鼠体重、体脂肪重量无明显变化,但肝重分别显著增加了46.1%(P<0.001)、35.1%(P<0.001)、40.9%(P<0.001)和42.0%(P<0.05),肝脏TG水平分别升高了383.8%(P<0.05)、301.0%(P<0.05)、538.0%(P<0.01)和1251.5%(P<0.001),肝脏TC水平也有所上升。糖耐量结果为,乳清酸组持续性异常,呈现胰岛素抵抗现象,并伴随发生高血压。结论 1%乳清酸可在短期内建立大鼠非肥胖性非酒精性脂肪肝模型,长期持续,同时伴有糖耐异常现象和高血压。该模型可用于非酒精性脂肪肝与代谢性综合征之间关系的研究。     

α-Linolenic Fatty Acid Supplementation Decreases Tumor Growth and Cachexia Parameters in Walker 256 Tumor-Bearing Rats

Fish oil (FO) has been shown to affect cancer cachexia, tumor mass, and immunity cell. n-3 PUFA, specifically α-linolenic fatty acid (ALA), has controversial effects. We investigated this in nontumor-bearing Wistar rats fed regular chow (C), fed regular chow and supplemented with FO or Oro Inca oil (OI), and Walker 256 tumor-bearing rats fed regular chow (W), fed regular chow and supplemented with FO (WFO) or OI (WOI). Rats were supplemented (1g/kg body weight/day) during 4 wk and then the groups tumor-bearing were inoculated with Walker 256 tumor cells suspension and 14 days later the animals were killed. WFO increased EPA fivefold and DHA 1.5-fold in the tumor tissue compared to W (P < 0.05). OI supplementation increased of threefold of ALA when compared to W (P < 0.05). Tumor mass in WFO and OI was of 2.3-fold lower, as well as tumor cell proliferation of 3.0-fold tumor tissue lipoperoxidation increased of 76.6% and cox-2 expression was 20% lower. Cachexia parameters were attenuate, blood glucose (25% higher), Triacylglycerolemia (50% lower), and plasma TNF-α (65% lower; P < 0.05) and IL-6 (62.5% lower). OI, rich in ALA, caused the same effect on cancer as those seen in FO.