半饥饿状态下高脂喂养对大鼠肉毒碱及脂类代谢的影响

目的探讨高脂饲料喂养半饥饿状态下大鼠肉碱及脂肪代谢的变化.方法用限食的方法造成半饥饿大鼠模型,观察给予普通饲料的半饥饿对照组与给予高脂饲料的实验组血浆肉碱浓度、附睾脂肪垫重量,肝游离氨基酸和脂肪含量,血中甘油三酯、游离脂肪酸以及游离氨基酸浓度等指标的变化.结果给予高脂饲料的实验组动物血浆游离肉碱浓度显著低于正常组和实验前水平(P＜0.05);肝脂肪含量、血游离脂肪酸浓度均显著高于半饥饿对照组(P＜0.05);两组半饥饿动物血和肝脏中大部分游离氨基酸浓度显著低于正常组,半饥饿对照组其浓度降低更显著,同时合成肉碱的赖氨酸和蛋氨酸浓度也显著降低.结论高脂饲料喂养半饥饿状态下,游离肉碱浓度降低,脂类代谢负担加重,提示在高脂半饥饿状态下需补充外源性肉碱.     

Oxidative stress and antioxidant status in rat blood, liver and muscle: effect of dietary lipid, carnitine and exercise

The purpose of this study was to determine the effect of dietary fat, carnitine supplementation, and exercise on oxidative damage and antioxidant status. Male Wistar rats (60 days old) were fed diets containing either hydrogenated fat (HF) or peanut oil (PO) with or without 0.5 mg % (of dry diet) carnitine. The rats were given exercise, i.e. swimming for 60 minutes, for 6 days/week for 6 months under each dietary condition. The blood malondialdehyde (MDA) level was higher in PO-fed rats, more so in exercising ones, while the same was not altered in carnitine-supplemented rats irrespective of the dietary fat or physical activity. The MDA level was significantly decreased in muscle, while increased in liver, of carnitine-fed rats. The blood glutathione (GSH) level also significantly increased in exercising rats as compared to sedentary ones, while carnitine supplementation elevated it in all the groups. Exercise and carnitine supplementation significantly lowered GSH levels in liver while increasing it in muscle. The glutathione peroxidase (GPX) activity was significantly increased in blood and muscle from PO-fed exercising rats as compared to sedentary ones, while carnitine supplementation elevated GPX activity in all the groups. The liver and muscle catalase (CAT) activities were significantly increased in PO-fed exercising rats, while carnitine did not have any effect. The pro-oxidative effect of the monounsaturated fatty acid (MUFA)-rich PO diet and prolonged regular exercise was less pronounced due to augmented antioxidant enzymes, GPX and CAT, induced by training to protect against the oxidative stress, while carnitine supplementation could help to counter lipid peroxidation due to exercise through redistribution of GSH from liver to blood and muscle.     

Effects of L-carnitine on obesity, diabetes, and as an ergogenic aid

Data on the functionalities of L-carnitine on obesity, diabetes, and as an ergogenic aid are summarized as follows: Obesity: Total lipid, triglyceride, and total protein increased during the 3T3-L1 cell differentiation. However, nonesterified carnitine (NEC), acid-soluble acylcarnitine (ASAC), and acid-insoluble acylcarnitine (AIAC) concentrations were lower in the differentiated 3T3-L1 cells. In addition, the exogenously added carnitine inhibited the increases in triglyceride and total lipid levels. In an animal study, L-carnitine supplementation reduced serum leptin and abdominal fat weight caused by high-fat diet in C57BL/6J mice. Diabetes: In an animal study, streptozptpcin-induced diabetic rats had markedly lower IGFBP-3 than normal rats, and IGFBP-3 was increased by L-carnitine treatment, demonstrating that L-carnitine treatment of diabetic rats modulates the IGFs/IGFBPs axis. A study of Korean diabetics indicated that there is a remarkable abnormality in lipid and carnitine metabolism in Korean diabetic patients. Ergogenic aids: We investigated the separate and combined effects of L-carnitine and antioxidant supplementation on carnitine and lipid concentrations in trained and non-trained animal and humans. Supplementation of L-carnitine and antioxidants improve lipid profiles and exercise ability in exercise-trained rats. Also, both exercise training and supplementation of carnitine and antioxidants improved lipid profiles and carnitine metabolism in humans, suggesting that carnitine and antioxidant supplementation may improve exercise performance.     

Creatine supplementation prevents the accumulation of fat in the livers of rats fed a high-fat diet

The aim of the present study was to examine the effects of creatine supplementation on liver fat accumulation induced by a high-fat diet in rats. Rats were fed 1 of 3 different diets for 3 wk: a control liquid diet (C), a high-fat liquid diet (HF), or a high-fat liquid diet supplemented with creatine (HFC). The C and HF diets contained, respectively, 35 and 71% of energy derived from fat. Creatine supplementation involved the addition of 1% (wt:v) of creatine monohydrate to the liquid diet. The HF diet increased total liver fat concentration, liver TG, and liver TBARS and decreased the hepatic S-adenosylmethionine (SAM) concentration. Creatine supplementation normalized all of these perturbations. Creatine supplementation significantly decreased the renal activity of l-arginine:glycine amidinotransferase and plasma guanidinoacetate and prevented the decrease in hepatic SAM concentration in rats fed the HF diet. However, there was no change in either the phosphatidylcholine:phosphatidylethanolamine (PE) ratio or PE N-methyltransferase activity. The HF diet decreased mRNA for PPARα as well as 2 of its targets, carnitine palmitoyltransferase and long-chain acylCoA dehydrogenase. Creatine supplementation normalized these mRNA levels. In conclusion, creatine supplementation prevented the fatty liver induced by feeding rats a HF diet, probably by normalization of the expression of key genes of β-oxidation.     

Dietary L-carnitine supplementation in obese cats alters carnitine metabolism and decreases ketosis during fasting and induced hepatic lipidosis

This study was designed to determine whether dietary carnitine supplement could protect cats from ketosis and improve carnitine and lipid metabolism in experimental feline hepatic lipidosis (FHL). Lean spayed queens received a diet containing 40 (CL group, n = 7) or 1000 (CH group, n = 4) mg/kg of L-carnitine during obesity development. Plasma fatty acid, beta-hydroxybutyrate and carnitine, and liver and muscle carnitine concentrations were measured during experimental induction of FHL and after treatment. In control cats (CL group), fasting and FHL increased the plasma concentrations of fatty acids two- to threefold (P < 0.0001) and beta-hydroxybutyrate > 10-fold (from a basal 0.22 +/- 0.03 to 1.70 +/- 0.73 after 3 wk fasting and 3.13 +/- 0.49 mmol/L during FHL). In carnitine-supplemented cats, these variables increased significantly (P < 0.0001) only during FHL (beta-hydroxybutyrate, 1.42 +/- 0.17 mmol/L). L-Carnitine supplementation significantly increased plasma, muscle and liver carnitine concentrations. Liver carnitine concentration increased dramatically from the obese state to FHL in nonsupplemented cats, but not in supplemented cats, which suggests de novo synthesis of carnitine from endogenous amino acids in control cats and reversible storage in supplemented cats. These results demonstrate the protective effect of a dietary L-carnitine supplement against fasting ketosis during obesity induction. Increasing the L-carnitine level of diets in cats with low energy requirements, such as after neutering, and a high risk of obesity could therefore be recommended.     

Fish Oil Enriched n-3 Polyunsaturated Fatty Acids Improve Ketogenic Low-Carbohydrate/High-Fat Diet-Caused Dyslipidemia,Excessive Fat Accumulation,and Weight Control in Rats

Low-carbohydrate and high-fat diets have been used for body weight (BW) control, but their adverse effects on lipid profiles have raised concern. Fish oil (FO), rich in omega-3 polyunsaturated fatty acids, has profound effects on lipid metabolism. We hypothesized that FO supplementation might improve the lipid metabolic disturbance elicited by low-carbohydrate and high-fat diets. Male SD rats were randomized into normal control diet (NC), high-fat diet (HF), and low-carbohydrate/high-fat diet (LC) groups in experiment 1, and NC, LC, LC + 5% FO (5CF), and LC + 10% FO diet (10CF) groups in experiment 2. The experimental duration was 11 weeks. In the LC group, a ketotic state was induced, and food intake was decreased; however, it did not result in BW loss compared to either the HF or NC groups. In the 5CF group, rats lost significant BW. Dyslipidemia, perirenal and epididymal fat accumulation, hepatic steatosis, and increases in triglyceride and plasma leptin levels were observed in the LC group but were attenuated by FO supplementation. These findings suggest that a ketogenic low-carbohydrate/high-fat diet with no favorable effect on body weight causes visceral and liver lipid accumulation. FO supplementation not only aids in body weight control but also improves lipid metabolism in low-carbohydrate/high-fat diet-fed rats.     

饲料中丙酸和丁酸对肥胖小鼠脂肪代谢的影响

目的 探讨外源性短链脂肪酸对高脂诱导的肥胖小鼠脂肪代谢的影响。方法 将40只3~4周龄C57BL/6J雄性小鼠分成4组,分别给予正常饲料、高脂饲料以及分别添加丙酸和丁酸的高脂饲料喂养4个月。喂养过程结束后,心脏采血,取性腺周围脂肪、肩胛骨下脂肪和肝脏。检测血浆甘油三酯(TG)、总胆固醇(TCH)等浓度,观察脂肪和肝脏组织细胞形态变化,同时检测甘油三酯脂肪酶(atgl)、激素敏感脂肪酶(hsl)、二酯酰甘油酰基转移酶2(dgat2)、肉碱脂酰转移酶(cpt)及解偶联蛋白1(ucp1)等基因mRNA表达水平。结果 与正常饲料喂养组相比,高脂饲料组小鼠体重、血浆TG和TCH水平、肝脏脂肪聚集均显著增加(P<0.05);而高脂饲料中添加丙酸和丁酸则抑制了小鼠体重的增加和肝脏脂滴聚集,同时降低了血浆TG和TCH水平(P<0.05)。脂肪代谢相关基因表达检测显示,与正常饲料组小鼠相比,高脂饲料组小鼠性腺周围脂肪组织和肝脏中atgl、hsl、cpt1c基因mRNA的表达量均显著性降低,而dgat2基因mRNA的表达量明显升高(P<0.05);而高脂饲料中添加丙酸和丁酸提升了性腺周围脂肪组织和肝脏中agtl、hsl、cpt1c基因mRNA的表达,而抑制了dgat2的表达(P<0.05)。肩胛骨下脂肪中上述基因的表达几乎未受到饲料丙酸和丁酸添加的影响(P>0.05)。结论 丙酸和丁酸可能通过促进脂肪分解和氧化对高脂饲料诱导肥胖小鼠的体重增加发挥抑制作用。     

Plasma lipoprotein cholesterol in rats fed a diet enriched in chitosan and cholesterol

To investigate the effect of dietary chitosan on plasma lipoprotein cholesterol metabolism, male Sprague-Dawley (SD) rats fed a cholesterol-enriched diet containing cellulose (CE) or chitosan (CS) were studied for 2 wk. Lower plasma total cholesterol, low-density lipoprotein (LDL) cholesterol and very-low-density lipoprotein (VLDL) cholesterol were observed in rats fed a diet containing chitosan. In addition, significantly higher high-density lipoprotein (HDL) cholesterol and HDL2 cholesterol were observed in rats after 2 wk of chitosan feeding. Rats fed the chitosan diet had increased triacylglycerol percentages and decreased free cholesterol, cholesteryl ester and phospholipid percentages in VLDL lipid composition. Chitosan significantly decreased the surface lipid proportions and increased the core lipid proportions in VLDL particles. In addition, the ratios of surface lipids to core lipids of the VLDL particles in rats fed a diet containing chitosan were significantly decreased. A significantly lower plasma apolipoprotein B (Apo B) concentration was observed in rats fed the chitosan diet as compared to those fed the cellulose diet. No significant difference in plasma triacylglycerols or glucose levels was observed between the two dietary groups. Results from this study suggest that chitosan may alter the VLDL particle size and also play an important role in the regulation of lipoprotein metabolism in rats.     

Effect of diet on plasma carnitine levels and urinary carnitine excretion in humans

This investigation determines the effect of two isocaloric diet regimens on plasma carnitine and urinary carnitine excretion in man. Seven healthy men were served a high-carbohydrate, low-fat (C) or a low-carbohydrate, high-fat (F) diet for 2 wk, ie, one diet regimen for 4 d followed by a 3-d break and concluded with 4 d more on the other diet regimen. The two regimens contained the same amount of carnitine-rich food. Plasma free carnitine rose significantly from the initial value on F diet and was significantly higher from day 3 than C diet. Plasma acyl carnitine increased on both diets. Urinary excretion of carnitine increased only on F diet. Renal clearance of both free and acyl carnitine was significantly greater on F diet than on C diet. Results showed that composition of a diet with constant carnitine content influenced carnitine metabolism in man.     

Enzymatically synthesized glycogen reduces lipid accumulation in diet-induced obese rats

Based on a recent study indicating that enzymatically synthesized glycogen (ESG) possesses a dietary, fiber-like action, we hypothesized that ESG can reduce the risk of obesity. In this study, the antiobesity effects of ESG were investigated in a model of diet-induced obesity. Male Sprague-Dawley rats were divided into 4 groups and fed a normal or high-fat diet, with or without 20% ESG, for 4 weeks. Body weight, food intake, lipid deposition in the white adipose tissues and liver, fecal lipid excretion, and plasma lipid profiles were measured. At week 3, the body fat mass was measured using an x-ray computed tomography system, which showed that ESG significantly suppressed the high-fat diet–induced lipid accumulation. Similar results were observed in the weight of the adipose tissue after the experiment. Moreover, ESG significantly suppressed the lipid accumulation in the liver but increased fecal lipid excretion. The plasma concentrations of triacylglycerol and nonesterified fatty acid were lowered after a high-fat diet, whereas the total bile acid concentration was increased by ESG. However, the hepatic messenger RNA (mRNA) levels of enzymes related to lipid metabolism were not affected by ESG. Conversely, the mRNA levels of long-chain acyl-CoA dehydrogenase and medium-chain acyl-CoA dehydrogenase were up-regulated by ESG in the muscle. These results suggest that the combined effects of increased fecal lipid excretion, increased mRNA levels of enzymes that oxidize fatty acids in the muscle, and increased total bile acid concentration in the plasma mediate the inhibitory effect of ESG on lipid accumulation.     

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。     

Effects of high-fat diet intake on glucose uptake in central and peripheral tissues of non-obese rats

We previously demonstrated that plasma glucose concentration was higher while plasma insulin concentration was lower in rats fed a high-fat diet. In the present study, we examined the effects of high-fat diet on glucose uptake in central and peripheral tissues in non-obese rats. Forty male Sprague-Dawley rats were fed high- or low-fat diets for 4 wk. Body weight and body fat accumulation were not different between the two diet groups after 4 wk. Glucose uptake in the skeletal muscles and adipose tissues, estimated by the 2-deoxy-D-glucose method, was lower in the rats fed the high-fat diet than that in the rats fed the low-fat diet, whereas uptake in the liver and pancreas did not differ between the two groups. Glucose uptake in the hypothalamus and cortex was higher in the high-fat diet group as compared with that in the low-fat diet group. These results suggest that increased plasma glucose levels in rats fed the high-fat diet were caused by a decrease in glucose uptake in the skeletal muscles and adipose tissues. Reduced plasma insulin level in the high fat diet group with no difference in glucose uptake in the pancreas may be due to increased sympathetic activity in the pancreas resulting from the increased glucose uptake in the brain regions involved in autonomic functions.     

High hydrostatic pressure extract of garlic increases the HDL-cholesterol level via up-regulation of apolipoprotein A-I gene expression in rats fed a high-fat diet

ABSTRACT: BACKGROUND: Cardiovascular disease (CVD) is the number one cause of mortality worldwide and a low high-density lipoprotein cholesterol (HDL-C) level is an important marker of CVD risk. Garlic (Allium sativum) has been widely used in the clinic for treatment of CVD and regulation of lipid metabolism. This study investigated the effects of a high hydrostatic pressure extract of garlic (HEG) on HDL-C level and regulation of hepatic apolipoprotein A-I (apoA-I) gene expression. METHODS: Male Sprague-Dawley rats were divided into two groups and maintained on a high-fat control diet (CON) or high-fat control diet supplemented with high hydrostatic pressure extract of garlic (HEG) for 5 weeks. Changes in the expression of genes related to HDL-C metabolism were analyzed in liver, together with biometric and blood parameters. RESULTS: In the HEG group, the plasma levels of triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) were significantly decreased by 19% and 24%, respectively, relative to the control group. The plasma HDL-C level was increased by 59% (P < 0.05). The HEG-supplemented diet lowered the atherogenic index (AI) by 45% as compared to the CON group. Hepatic TG and total cholesterol (TC) levels were reduced by 35% and 43%, respectively in comparison with the CON group. The HEG supplementation increased hepatic mRNA levels of apoA-I, which is one of primarily proteins of HDL-C particle (P < 0.05). The gene expression of ATP-binding cassette transporter A1 (ABCA1) and lecithin:cholesterol acyltransferase (LCAT), importantly involved in the biogenesis in HDL, were also up-regulated by dietary HEG. CONCLUSIONS: These results suggest that HEG ameliorates plasma lipid profiles and attenuates hepatic lipid accumulation in the high-fat fed rats. Our findings provides that the effects of HEG on the increase of the plasma HDL-C level was at least partially mediated by up-regulation of hepatic genes expression such as apoA-I, ABCA1, and LCAT in rats fed a high-fat diet.     

Reduced adiposity in bitter melon (Momordica charantia) fed rats is associated with lower tissue triglyceride and higher plasma catecholamines

Slower weight gain and less visceral fat had been observed when rats fed a high-fat diet were supplemented with freeze-dried bitter melon (BM) juice; the metabolic consequences and possible mechanism(s) were further explored in the present study. In a 4-week experiment, rats were fed a low-fat (70 g/kg) or a high-fat (300 g/kg) diet with or without BM (7.5 g/kg or 0.75%). BM-supplemented rats had lower energy efficiency, visceral fat mass, plasma glucose and hepatic triacylglycerol, but higher serum free fatty acids and plasma catecholamines. In the second experiment, 7-week BM supplementation in high-fat diet rats led to a lowering of hepatic triacylglycerol (P<0.05) and steatosis score (P<0.05) similar to those in rats fed a low-fat diet. BM supplementation did not affect serum and hepatic cholesterol. However, plasma epinephrine and serum free fatty acid concentrations were increased (P<0.05). In the third experiment, BM(7.5 and 15 g/kg) and 1.5 % BM lowered triacylglycerol concentration in red gastrocnemius and tibialis anterior (P<0.05) muscle, but a dose-response effect was not observed. These data suggest that chronic BM feeding leads to a general decrease in tissue fat accumulation and that such an effect is mediated in part by enhanced sympathetic activity and lipolysis. BM or its bioactive ingredient(s) could be used as a dietary adjunct in the control of body weight and blood glucose.     

The effect of taurine on plasma cholesterol concentration in genetic type 2 diabetic GK rats

The purpose of this study is to investigate the effect of taurine on the plasma cholesterol concentration in genetic type 2 diabetic rats fed cholesterol-free or high-cholesterol diets. Diabetic rats (GK male rats) and normal rats (Wistar male rats) were fed either a cholesterol-free or cholesterol-enriched (1% cholesterol + 0.25% sodium cholate) diet supplemented with or without 3% taurine for 21 or 14 d. Compared to the normal rats, diabetic rats showed a high glucose concentration in their blood and plasma, but it was not affected by taurine feeding. The plasma insulin concentration was higher in the diabetic rats than in the normal rats. At the start of the experiment, the plasma cholesterol concentration was significantly higher in the diabetic rats than in the normal rats. Taurine did not affect the plasma cholesterol level in rats fed the cholesterol-free diet. However, taurine feeding significantly increased the plasma HDL-cholesterol concentration in the diabetic rats fed the cholesterol-free diet. In both the diabetic and normal rats fed the cholesterol diet, the plasma cholesterol concentration was significantly lower in rats fed the diet supplemented with taurine than in the rats fed the control diet. It was concluded that taurine has a hypocholesterolemic effect in both diabetic and normal rats fed diets containing cholesterol. Moreover, these results suggest that taurine seems to affect the HDL-cholesterol metabolism in diabetic rats fed a cholesterol-free diet.     

The effect of a high fat diet on the carnitine content of skeletal and cardiac muscle from streptozotocin-diabetic and control rats

Streptozotocin-diabetic (SZ) and control rats were maintained on high fat (HF) or on low fat (LF) diets for a period of two weeks. Skeletal and cardiac muscle were assayed for free fatty acids and for free, short-chain, and long-chain carnitine. The free fatty acid content of both skeletal and cardiac muscle was increased in SZ rats fed the LF diet and was not augmented appreciably by HF feeding. The level of free carnitine was decreased in muscles from diabetic animals maintained on the LF regimen and was unaffected by the HF diet. The amount of long-chain carnitine esters was increased in both skeletal and cardiac muscle from LF-fed SZ rats and decreased in heart from HF-fed diabetic animals. The absolute amounts of free and long-chain carnitine measured in tissue from the LF fed control rats did not differ consistently from those in muscles from HF-fed control rats. However, the long-chain carnitine/free carnitine ratio was elevated significantly in both skeletal and cardiac muscle from the HF-fed control animals, but was not increased in SZ rats maintained on the HF regimen. Together, these data suggest that high fat feeding results in increased lipid utilization in control but not in diabetic rats.     

Dose-dependent lipotropic effect of carnitine in chronic alcoholic rats

The objective of this study was to determine if the lipotropic effect of supplementary DL-carnitine was dose dependent. Male Sprague-Dawley rats were fed for 45 d a liquid ethanol diet in which 36% of the total energy was derived from ethanol. The ethanol diet, containing 1.27 g L-carnitine per g of the diet, was fed as such or was supplemented with 0.1%, 0.4%, 0.8%, 1.2%, or 1.6% (wt/wt) DL-carnitine. Results showed a definite inverse relationship between the concentrations of lipids and those of carnitine fractions in both plasma and liver. The concentrations of total lipids and triglycerides were significantly lower with increasing levels of supplementary carnitine, whereas those of carnitine fractions were significantly higher than in controls up to 0.8% supplemental carnitine. The changes in the plasma and hepatic concentrations of various classes of lipid and carnitine were inversely related and were found to be progressive up to 0.8% DL-carnitine supplementation. Therefore, it was concluded that the lipotropic effect of dietary carnitine is dose dependent, and that the optimal supplementary level is 0.8% DL-carnitine.     

Grape skin improves antioxidant capacity in rats fed a high fat diet

This study was conducted to investigate the effect of dietary grape skin on lipid peroxidation and antioxidant defense system in rats fed high fat diet. The Sprague-Dawley rats were fed either control (5% fat) diet or high fat (25% fat) diet which was based on AIN-93 diet for 2 weeks, and then they were grouped as control group (C), control + 5% grape skin group (CS), high-fat group (HF), high fat + 5% grape skin group (HFS) with 10 rats each and fed corresponding diets for 4 weeks. The hepatic thiobarbituric acid reacting substances (TBARS) were increased in high fat group as compared with control group, but reduced by grape skin. The serum total antioxidant status, and activities of hepatic catalase and superoxide dismutase, xanthine oxidase and glucose-6-phosphatase were increased by supplementation of grape skin. Glutathione peroxidase activity was significantly higher in CS group than in C group. Grape skin feeding tended to increase the concentration of total glutathione, especially in control group. The ratio of reduced glutathione to oxidized glutathione was lower in high fat groups than in control groups. The ratio was increased by dietary supplementation of grape skin in control group. These results suggest that dietary supplementation of grape skin would be effective on protection of oxidative damage by lipid peroxidation through improvement of antioxidant defense system in rats fed high fat diet as well as rats with low fat diet.     

Anti-obesity and hypolipidemic effects of a proprietary herb and fiber combination (S&S PWH) in rats fed high-fat diets

The objective of this study was to investigate the effects of S&S PWH, a proprietary herb and fiber combination (Bionutrigen Inc., Daejon, Republic of Korea), on body weight and lipid metabolism in rats fed with a high-fat diet. Three groups of male Sprague-Dawley rats were fed different diets for a 6-week period: normal control diet containing 5% (wt/wt) corn oil (NC group), high-fat diet containing 10% (wt/wt) lard plus 5% (wt/wt) corn oil (HF group), and high-fat diet supplemented with powdered 5% (wt/wt) S&S PWH (S&S PWH group). The body weights and relative weights of the epididymal and perirenal white adipose tissue were significantly lower in the S&S PWH group than in the HF group. S&S PWH supplementation significantly lowered plasma total cholesterol and triglyceride concentrations, whereas it elevated the ratio of high density lipoprotein-cholesterol/total-cholesterol and improved the atherogenic index. The accumulation of hepatic lipid droplets and the epididymal white adipocyte size were less in the S&S PWH group than in the HF group. Hepatic hydroxyl-3-methylglutaryl-coenzyme A reductase and acyl-coenzyme A:cholesterol acyltransferase activities were significantly lower, while adipocyte lipoprotein lipase activity was significantly higher, in the S&S PWH group than in the HF group. These beneficial effects may be due to the combined properties of the phenolic compounds present in high concentrations (1.89 g/100 g) in the S&S PWH. In conclusion, these results suggest that S&S PWH can be considered as an anti-obesity functional formula that is effective for suppressing body weight gain and enhancing lipid profile.