Protein, carbohydrate, and ethanol consumption: interactions in AA and ANA rats

Female rats of the alcohol-preferring AA line were given a choice between protein, carbohydrate, and fat sources. Subsequent free access to alcohol decreased their intake of carbohydrate but not of protein or fat. The individual alcohol intakes were negatively correlated with the carbohydrate intakes (-0.76) and with the alcohol-induced changes in carbohydrate intake (-0.83), but positively correlated with the concurrent protein intakes (0.78). The alcohol consumption and ethanol elimination rate of AA rats were subsequently found to vary directly with the protein content (5, 10, 20 and 40% by energy) of the premixed diet given to them--they drank more than 9 times more ethanol on the 40% than on the 5% protein diet--but the alcohol intake of the alcohol-avoiding ANA rats was not affected by protein intake. The results clearly indicate that the three macronutrients are related to alcohol consumption in different ways, suggesting that protein intake affects the selection of alcohol of AA rats through a factor correlated to ethanol elimination (but not through a ceiling effect from the rate of elimination) and that the alcohol in turn reduces carbohydrate consumption.     

Liver fat and plasma ethanol are sharply lower in rats fed ethanol in conjunction with high carbohydrate compared with high fat diets

The effects of high fat and high carbohydrate diets on alcohol metabolism were studied on blood alcohol and liver fat concentration. In Experiment 1, rats consumed an alcohol-containing liquid diet. Blood was collected for ethanol, glucose and lactate analyses and livers were excised for lipid determination. Blood ethanol and liver fat were lower when rats consumed the high carbohydrate diet. Glucose concentrations were lower in rats fed the high fat diet compared with those fed the high carbohydrate diet when ethanol was consumed. In Experiment 2, rats consumed a high fat, ethanol-containing diet for 13 d. Half of the rats were switched to a high carbohydrate, ethanol-containing diet for an additional 11 d. The same analyses were carried out as for Experiment 1. Switching the high fat-fed rats to the high carbohydrate diet reversed the high blood ethanol and high liver fat values, even though the rats consumed significantly more alcohol with the high carbohydrate diet. In Experiment 3 the same high fat and high carbohydrate diets without ethanol were consumed for 2 wk, at which time ethanol was administered acutely, intraperitoneally, at 2 g/kg. Blood was analyzed for ethanol, glucose and lactate 30, 60 and 120 min after injection. Rats fed the high carbohydrate diet had lower blood ethanol but higher lactate at 120 min compared with those fed the high fat diet. The results suggest that the rate of ethanol elimination is slower in rats fed high fat than in those fed high carbohydrate diets, resulting in elevated blood ethanol and liver fat levels for the former.     

A high-fat meal or injection of lipids stimulates ethanol intake.

Findings of earlier studies support the idea of a possible relation between dietary fat and ethanol intake, but it is unclear whether acute exposure to fat can increase ethanol consumption directly. In the current series of experiments, we examined whether daily overeating of fat, a single high-fat meal, or the injection of fat can increase ethanol intake. In Experiment 1, adult Sprague-Dawley rats were maintained on a high-fat diet (50% fat) for 7 days and switched subsequently to a laboratory chow diet while being trained to drink 9% ethanol. Rats that had eaten the greatest amount of the high-fat diet subsequently drank the most ethanol. In Experiment 2, a 1-h meal of the high-fat diet (50% fat) produced a significant increase in 7% ethanol consumption in comparison with what occurred after consumption of an equicaloric, low-fat (10% fat) meal. In Experiment 3, the orosensory effect of fat was eliminated with an intraperitoneal injection of a fat emulsion, Intralipid (20% fat, 5.0 ml). The injection of Intralipid, in comparison with saline, increased the ingestion of 9% ethanol. This finding is in contrast to what occurred with injection of an equicaloric, 50% glucose solution, which suppressed ethanol intake. These findings provide new evidence to support a positive relation between dietary fat and the consumption of ethanol.     

Zinc and ethanol: dietary interrelationships in pregnant rats

Pregnant rats were fed three different liquid diets with ethanol providing 33.3, 35.6 and 50.8% of the total calories. The 35.6 and 50.8% ethanol diets, containing egg white as a source of protein, were zinc deficient and were fed to two groups of rats without zinc supplementation. At each level of ethanol, one additional group was supplemented with a moderate level of zinc and another group with a high level of zinc. The 33.3% ethanol diet contained casein as a source of protein and had a high level of zinc. Each rat in the ethanol group was yoked with another rat fed a diet in which the ethanol was replaced by an isocaloric amount of carbohydrate. Records were kept of food consumed, weight gained or lost, number of pups delivered, total weight of litter, and weights of each pup. Maternal and neonatal tissues were taken for zinc and copper analyses. The rats fed ethanol diets were found to ingest the same amount of ethanol-derived calories per day regardless of diet or concentration of ethanol. On the higher level of ethanol (50.8%), the rats, therefore, ingested fewer total calories and lost weight. No pups were delivered from this group of dams. Their respective pair-fed groups, although restricted in weight gain, delivered live pups at all levels of zinc. The pups from dams fed zinc-deficient diets had lower total body zinc levels and lower liver zinc levels. Sufficient dietary zinc improved the condition of the pregnant rats and their progeny, but there were no indications that higher levels of dietary zinc resulted in further improvement.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of dietary composition on hepatic lipid accumulation of rats with chronic ethanol intake

Diets higher in carbohydrate, fat or protein (diets 1, 2, and 3, respectively) were formulated isoenergetically with or without ethanol to study their effects on the accumulation of hepatic total lipids in rats fed for a period of 8 weeks. Ethanol ingestion did not affect body weight gain of rats fed diet 1, but diets 2 and 3 resulted in decreased weight gain as compared to the pair-fed controls. These body weight changes between control and ethanol groups were significant 2 weeks after beginning the treatment. Ethanol administration did not change hepatic weights of rats fed diet 1, but increased hepatic weights of rats fed diets 2 and 3. Higher protein alone in the diet increased liver weight. Ethanol intake increased the hepatic total lipid content of rats fed diets 2 and 3, but did not affect those fed diet 1 compared to their pair-fed controls. Hepatic cholesterol content increased in rats fed both the higher protein and higher fat diets. Both weight gain, liver weight, and hepatic total lipids consistently showed that the rats consuming 39% wheat starch as carbohydrate were not adversely affected by ethanol ingestion while those groups fed higher fat or higher protein with ethanol were adversely affected. Possible mechanisms are discussed.     

断乳后不同饲料构成对高脂膳食大鼠肥胖发生的影响

目的研究断乳后不同饲料构成对高脂膳食大鼠肥胖发生的影响。方法雄性Wistar大鼠出生后24天断乳,按体重随机分为A、B、C三组,分别给予高碳水化合物供能的基础饲料、高蛋白质供能饲料和高不饱和脂肪供能饲料。3周后均转为基础饲料。2周后再按体重将A组分为A1、A2两组,A1组继续基础饲料,A2、B、C组则转为以猪油为主的高脂膳食,6周后结束实验。分别在不同处理期末每组随机处死8只动物,称重、留取脂肪组织,计算脂体比,采血检测血糖、血脂和激素指标。结果断乳后喂饲高不饱和脂肪饲料可以显著降低高脂膳食大鼠的体重、体脂肪含量和脂体比(P<0.05),显著降低胰岛素水平、提高胰岛素敏感性(P<0.05),显著增加胰高血糖素、甲状腺激素等促脂解激素的水平(P<0.05),增加瘦素敏感性(P<0.05),改善高脂膳食大鼠的瘦素抵抗。早期喂饲高蛋白质饲料也有一定的降低体重、体脂肪含量和促脂解作用趋势,但是该组的血糖值高于A2组。结论断乳后给予高不饱和脂肪饲料可以显著抑制高脂膳食大鼠的肥胖发生。     

Thyroid and growth responses of young Zucker obese and lean rats to a low protein-high carbohydrate diet

Experiments were conducted to study the effects of a low protein-high carbohydrate diet on growth and thyroid function in obese and lean male and female Zucker rats. The nine feeding regimens included animals ad libitum fed either a 22% casein and 59% carbohydrate diet (control) or an 8% casein and 73% carbohydrate diet (low protein) and appropriate pair-fed groups to control for the lean rats eating less than the obese rats and the rats fed the low-protein diet eating less than those fed the control diet. The rats were 4 weeks old at the start of the experiment which lasted 7 weeks. Final body size, tibia length and nonfat dry mass of the lean rats were dependent primarily on the amount of protein consumed, whereas growth of the obese rats was related to total energy intake rather than to protein intake. The relative hyperphagia, decreased efficiency of energy utilization and increased oxygen consumption and serum T3 concentrations in the lean rats fed the low-protein diet were consistent with the development of an adaptive thermogenesis, allowing the excess non-protein energy to be dissipated through excess heat production. There was no evidence for such an adaptive thermogenesis in the obese rats. The suggestion that the obese rats were already overeating for protein and storing the excess energy as fat and that the decreased thyroid response might be part of a protective mechanism against overheating was discussed.     

Place conditioning with ethanol in rats bred for high (UChB) and low (UChA) voluntary alcohol drinking

The main goal of this study was to investigate the ability of an ethanol dose (1 g/kg) administered intraperitoneally to induce conditioned place preference (CPP) and/or conditioned place aversion (CPA) in two lines of rats selectively bred for their high (UChB) or low (UChA) voluntary ethanol intake. It was found that five pairings with ethanol induced CPA in ethanol-naïve rats of both lines, but the magnitude of avoidance was lower in the UChB relative to the UChA rats, indicating that ethanol was less aversive to naïve rats bred for high alcohol drinking. After 2 months of high voluntary ethanol drinking (∼6–7 g/kg/day), in free choice between 10% ethanol and water, ethanol produced CPP in UChB rats, reflecting that ethanol had become rewarding to these rats. By contrast, the low voluntary ethanol intake (<1 g/kg/day) displayed by UChA rats preexposed for 2 months in free choice did not change ethanol-induced CPA. However, preexposure of UChA rats to forced ethanol drinking (∼5.7 g/kg/day) and the later inhibition of ethanol-derived acetaldehyde by 4-methylpyrazole (10 mg/kg intraperitoneal), an inhibitor of the enzyme alcohol dehydrogenase, not only increased their voluntary ethanol intake in free choice, but also had a facilitating effect on the development of CPP. Taken together, these results show that the expression of the reinforcing effects of ethanol required a period of voluntary ethanol intake in UChB rats, whereas in UChA rats, both prior exposure to forced ethanol drinking and reduction of high blood ethanol-derived acetaldehyde were required.     

Influence of chronic ethanol intake on obesity, liver steatosis and hyperlipidaemia in the Zucker fa/fa rat

The effect of chronic alcohol intoxication on metabolic disturbances and fatty infiltration and degeneration was studied in genetically obese, hyperlipoproteinaemic, fa/fa Zucker rats. Sixteen obese Zucker (fa/fa) rats, sixteen lean Zucker rats (Fa/-) and sixteen Wistar rats, all male rats aged 7-8 weeks, were given either a control (C) diet (13% of energy from protein, 37% from fat, 50% from carbohydrate) or an ethanol (E) diet (13% of energy from protein, 37% from fat, 14% from carbohydrate, 36% from ethanol) for 4 weeks. The fa/fa rats given diet E consumed more energy than those given diet C, but after 4 weeks the weight gains and degrees of obesity were similar for both groups. With both diets, the developed hyperlipidaemia could be explained by the hyperinsulinaemia. Both hypertriglyceridaemia and hypercholesterolaemia were lower in fa/fa rats eating diet E than in those given diet C. Fatty infiltration of the liver, as assessed by hepatic triacyglycerol and cholesterol contents, was observed with both diets, but for fa/fa rats it was less extreme in those given diet E.     

断乳后不同饲料构成对大鼠体重、体脂含量及激素敏感性脂肪酶基因表达的影响

目的研究断乳后不同饲料构成对高脂膳食大鼠体脂含量及脂肪组织中激素敏感性脂肪酶(HSL)基因表达的影响。方法新生Wistar雄性大鼠24天断乳,按体重随机分为A、B、C、D四组,分别给予高碳水化合物构成的基础饲料、高蛋白质构成饲料、高不饱和脂肪酸和高饱和脂肪酸构成饲料喂养3周。然后均转为基础饲料喂养2周后,按体重将A组随机分为A1、A2两组。A1组继续喂饲基础饲料作为对照组,A2和B、C、D四组给予高脂饲料喂养6周,结束实验;A2组则为高碳水化合物组。动态观察大鼠的体重、体脂含量、血糖变化及白色脂肪组织HSLmRNA水平。结果实验末期,断乳后喂饲高不饱和脂肪酸构成饲料的C组,体重、体脂含量和血糖均显著低于高碳水化合物组A2(P<0·05);断乳后喂饲高蛋白质的B组体重和体脂含量明显低于A2组(P<0·05),但血糖水平高于A2(P>0·05);断乳后摄取高饱和脂肪酸饲料的D组,尽管体重明显低于A2(P<0·05),但血糖和体脂含量与A2组无差异(P>0·05)。动态观察表明,断乳后喂饲高不饱和脂肪酸的C组大鼠,白色脂肪组织HSL基因表达水平持续升高。结论断乳后喂饲高不饱和脂肪酸饲料不仅可以降低高脂膳食大鼠的体重、体脂含量,还可明显改善血糖异常,抑制肥胖形成;对基因表达的调控可能参与早期饮食对后续肥胖的程序性影响。     

Soymilk products affect ethanol absorption and metabolism in rats during acute and chronic ethanol intake

In this study we evaluated the effects of soy products on ethanol metabolism during periods of acute and chronic consumption in rats. Gastric ethanol content and blood ethanol and acetaldehyde concentrations were investigated after the oral administration of ethanol (34 mmol/kg) plus soy products such as soymilk (SM) or fermented soymilk (FSM). The gastric ethanol concentration of the FSM group was greater than that of the control group, whereas portal and aortal blood ethanol concentrations of the FSM group were lower than in controls. The aortal acetaldehyde concentration in the FSM group was lower than that of the control group. The direct effect of isoflavones on liver function was investigated by using hepatocytes isolated from untreated rats. Genistein (5 micromol/L) decreased ethanol (P = 0.045) and tended to decrease acetaldehyde (P = 0.10) concentrations in the culture filtrate. Some variables of ethanol metabolism in the liver were investigated after chronic ethanol exposure for 25 d. Rats consumed a 5% ethanol fluid plus the SM diet, the FSM diet or a control diet. Microsomal ethanol oxidizing activity was significantly lower in the FSM group than the control group. Furthermore, cytosolic glutathione S-transferase activity was higher in the SM and FSM groups than in the control group. Acetaldehyde dehydrogenase activity (low K(m)) in the FSM group (P = 0.15), but not in the SM group (P = 0.31), tended to be greater than in the control group. The amount of thiobarbituric acid reacting substances in the liver of the SM and FSM groups tended to be less than that of the control group (P = 0.18 and 0.10, respectively). These results demonstrate that soymilk products inhibit ethanol absorption and enhance ethanol metabolism in rats.     

The frequency of daily ethanol consumption influences the effect of ethanol on insulin sensitivity in rats fed a high-fat diet

The different effects of ethanol on insulin sensitivity may be due to complex reasons. Here, we focus on the various daily ethanol consumption frequencies in rats fed a high-fat (HF) diet and explore the possible mechanism mediated by adiponectin and AMP-activated protein kinase (AMPK). A total of thirty-six male Wistar rats were fed a HF diet and were randomly divided into three groups: those that received tap water (C); those that received ethanol via a gastric tube twice per d (E1); those that received free access to ethanol for drinking (E2). The total daily ethanol dosage in groups E1 and E2 were the same (5 g/kg per d). At the end of 18 weeks, insulin sensitivity was evaluated. Adiponectin AMPK and GLUT4 levels were determined. We found that the different administration frequencies led to markedly different plasma ethanol concentrations and there were intimate relationships between plasma ethanol concentration and insulin sensitivity. Insulin resistance was markedly improved in group E1, whereas only a slight improvement was observed in group E2. Accordingly, adiponectin, phosphorylated AMPK and GLUT4 levels were significantly increased in group E1. Based on these findings, we propose that ethanol concentration might be the major influencing factor mediating the effect of ethanol on insulin sensitivity. At a total daily dosage of 5 g/kg per d, twice daily administration of ethanol was more beneficial than continuous drinking. The protective effect of ethanol might be mediated by increased adiponectin levels, which subsequently improve the activation of AMPKα and GLUT4 expression in adipose tissue.     

The effect of a high-fat diet and sucrose drinking option on the development of obesity in spontaneously hypertensive rats

1. Energy intakes, body-weights, body fat index, total body fat and interscapular brown adipose tissue (IBAT) were examined in adult male, spontaneously hypertensive, stroke-prone (SHR-SP) rats and normotensive Wistar/Kyoto (WKY) controls given one of four diets for 33 d: (a) a starch diet, (b) a starch diet and a sucrose solution drinking option, (c) an 80% energy from fat (F80) diet, (d) the F80 diet and a sucrose drinking option. 2. The SHR-SP rats showed a complete resistance to obesity on all four diets. For the high-fat diet the WKY animals became markedly obese with approximately two-fold increases in body-weight gain and body fat index when compared with the SHR-SP rats. The gain in total body fat was also significantly greater. IBAT as a percentage of total body-weight did not differ between the WKY and SHR-SP groups. 3. Compared with the WKY animals, the SHR-SP rats showed a reduced food intake but had the same potential to gain weight from the high-fat diet. 4. It is concluded that the resistance to obesity by the hypertensive animals is the result of a diminished energy intake.     

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.     

Serum leptin and insulin levels in lactating protein-restricted rats: implications for energy balance

The present study analysed the effect of protein restriction on serum insulin and leptin levels and their relationship with energy balance during lactation. Four groups of rats received isocaloric diets containing 170 g protein/kg or 60 g protein/kg from pregnancy until the 14th day of lactation: control non-lactating, control lactating (both fed a control diet), low-protein non-lactating and low-protein lactating. Energy intake, body composition, energy balance, serum insulin and leptin concentrations and the relationship between these hormones and several factors related to obesity were analysed. Low-protein-intake lactating rats exhibited hypoinsulinaemia, hyperleptinaemia, hypophagia and decreased energy expenditure compared with control lactating rats. The protein level in the carcasses was lower in the low-protein lactating group than in the control lactating group, resulting in a higher fat content in the first group compared with the latter. Body fat correlated inversely with serum insulin and positively with serum leptin level. There was a significant negative correlation between serum leptin and energy intake, and a positive relationship between energy intake and serum insulin level in lactating rats and in the combined data from both groups. Energy expenditure was correlated positively with serum insulin and negatively with serum leptin in lactating rats and when data from control non-lactating and lactating rats were pooled. Lactating rats submitted to protein restriction, compared with lactating control rats, showed that maternal reserves were preserved owing to less severe negative energy balance. This metabolic adaptation was obtained, at least in part, by hypoinsulinaemia that resulted in increased insulin sensitivity favouring enhanced fat deposition, hyperleptinaemia and hypophagia.     

Changes in women's plasma lipid and lipoprotein concentrations due to moderate consumption of alcohol are affected by dietary fat level.

We studied the impact of substituting ethanol for dietary carbohydrate, in high- and low-fat diets, on plasma lipids and lipoprotein concentrations. During a 12-wk, weight maintaining, controlled feeding study, women consumed only food and beverage provided by the Human Studies Facility of the USDA Beltsville Human Nutrition Research Center. Twenty-six women (age 41-59 y) consumed either a high-fat diet (38% of energy from fat) or a low-fat diet (18% of energy from fat) for 12 wk. The 12-wk feeding period was divided into two 6-wk periods in a cross-over design during which either ethanol or carbohydrate was added to the diet (5% of total daily energy intake). When the women consuming the high-fat diet had ethanol added to their diet, they had 6% lower plasma cholesterol (P = 0.003), 11% lower LDL cholesterol (P = 0.001) and 3% higher HDL cholesterol (P = 0.06) than when they had an equal amount (% energy) of carbohydrate added to their diet. The greater HDL cholesterol concentration was due to a 21% greater the HDL(2) subfraction (P = 0. 001). The ratio of LDL to HDL cholesterol was 14% lower. No significant differences existed in plasma lipids in women consuming the low-fat diet between the periods in which they had ethanol or carbohydrate added to their diet. This study suggests that the decreases in cardiovascular disease risk factors typically seen with moderate alcohol consumption may not be evident in individuals consuming a diet low in fat. Therefore changes in the risk factors associated with a low-fat diet and moderate alcohol consumption do not appear to be additive.     

高糖高脂饲料对Wistar大鼠生长和糖脂代谢的影响

目的观察高糖高脂饲料对Wistar大鼠生长及糖脂代谢的影响。方法雄性Wistar大鼠20只,按体重和空腹血糖随机分为2组(n=10):对照组和实验组,分别以普通饲料和高糖高脂饲料喂养6周,观察大鼠的生长曲线、食物利用率,测定大鼠的糖脂代谢指标。结果喂养6周后,实验组大鼠的体重、食物利用率、内脏脂肪占体重百分比、血清总胆固醇和低密度脂蛋白胆固醇均显著高于对照组(P<0.05),血清高密度脂蛋白胆固醇显著低于对照组(P<0.01)。两组的空腹血糖(FPG)无显著差异。实验组大鼠的糖耐量降低,葡萄糖曲线下面积显著高于对照组。结论正常血糖状态下,高糖高脂饲料可引起Wistar大鼠中心型积聚的体脂增加,血清总胆固醇增加,导致葡萄糖耐量能力减退,为2型糖尿病进程中的重要危险因素。     

Concurrent physical activity increases fat oxidation during the shift to a high-fat diet

BACKGROUND: It takes several days to adapt to a high-fat diet. In an earlier study, we observed a large degree of interindividual variation in the capacity to adapt to a high-fat diet. We hypothesized that concurrent physical activity would accelerate fat oxidation during an isoenergetic high-fat diet. OBJECTIVE: The objective of this study was to determine the effect of increased physical activity on the ability of young healthy men to increase fat oxidation during the shift to a high-fat diet. DESIGN: Six young healthy men participated in a randomized, single-blind crossover study. The volunteers consumed a diet contributing 37% of energy as fat, 14% as protein, and 49% as carbohydrate for 4 d. Energy expenditure and macronutrient balance were then measured in a respiration chamber as the energy content of the isoenergetic diet was changed to 50% fat, 14% protein, and 36% carbohydrate. Treadmill walking, as the physical activity, was used to increase total daily energy expenditure to 1.8 times the resting metabolic rate during 1 of 2 stays in the metabolic chamber. Total daily energy expenditure was maintained at 1.4 times the resting metabolic rate for the other stay. RESULTS: Energy balance was not significantly different between the 2 conditions. The 24-h respiratory quotient decreased more rapidly and to a greater extent under conditions of increased energy expenditure. Further, there was a decrease in the interindividual variability in the response of the respiratory quotient to a high-fat diet with increased energy expenditure (physical activity). Cumulative carbohydrate and protein balances were greater under conditions of increased physical activity. Conversely, cumulative fat balance was greater under sedentary conditions. CONCLUSION: Concurrent physical activity increases fat oxidation during the shift to a high-fat diet.     

EFFECTS OF DIETS DECREASING ETHANOL CONSUMPTION ON ACETALDEHYDE METABOLISM IN UChA AND UChB RATS

It has previously been reported that the introduction of a newissue (D1) of a stock diet (D0) caused a significant decreasein voluntary ethanol consumption in rats of our UChA (low ethanolconsumer) and UChB (high ethanol consumer) strains, and that,after changing to a diet lacking in animal products (D3), ethanolconsumption reached the previous level attained in UChB ratsand exhibited a bimodal distribution in UChA rats in such away that about one-third of these consumed more than 2 ml ofa 10% (v/v) ethanol solution per 100 g of body weight, as didUChB rats. When UChA rats exhibiting high ethanol consumptionand also UChB rats were fed on the D3 diet with a brewer's yeastsupplement, a significant decrease in ethanol intake was observed.Since significant correlations of voluntary ethanol intake toblood acetaldehyde levels, and to hepatic and brain aldehydedehydrogenase (AldDH) activities, have been reported, the effectson these parameters of diet D1 and of supplements of brewer'syeast or disulfiram were studied. Results showed that rats ofboth strains fed on a D1 diet exhibited a significant increasein blood acetaldehyde level after ethanol administration, concomitantwith an inhibition of hepatic and brain AldDH activities anda significant decrease in ethanol intake. Thus, this effectcould be related to a disulfiram-hke activity. The decreasein ethanol intake induced by brewer's yeast was not accompaniedby changes of blood acetaldehyde level after ethanol, nor byinhibition of hepatic AldDH activity in either strain. Nevertheless,a significant inhibition of brain AldDH activity in UChB, butnot in UChA, rats was observed. Thus, the effect of brewer'syeast on ethanol consumption could not be ascribed to a disulfiram-likeactivity of this supplement.the beginning of pregnancy, couldbe toxic for the human placenta and development of the fetus.     

饮食诱导肥胖抵抗和饮食诱导肥胖大鼠的对比研究

目的 探讨饮食诱导肥胖抵抗(DIO—R)大鼠和饮食诱导肥胖(DIO)大鼠的肥胖相关指标的变化。方法 采用50只健康雄性别大鼠，随机分为对照组和高脂组，分别用基础饲料和高脂饲料喂养13周，然后根据体重筛选出DIO—R和DIO组，观察能量摄入和体脂含量的变化；试纸法测定血糖；应用酶法测定大鼠总胆固醇(CHO)、甘油三脂(TG)、高密度胆固醇(HDL—C)；放免法测血清瘦素(1eptin)含量。结果 在前5周时，DIO—R大鼠与DIO大鼠摄入的总能量无显性差异；在实验终期，DIO—R大鼠明显低于DIO大鼠(P＜0．05)。DIO—R大鼠体脂含员、血糖、TG、CHO均明显低于DIO大鼠(P＜0．05)，DIO—R和DIO大鼠的HDL—C无明显差别。高脂饲料使大鼠血清(1eptin)水平明显增加(P＜0．05)，但DIO—R与DIO大鼠间无明显差别。结论 高脂饲料能够诱导别大鼠发生肥胖和肥胖抵抗，血清leptin水平增加在大鼠肥胖抵抗的发生中起部分作用。