Dietary corn oil does not suppress the fructose induced increase in hepatic fatty acid synthesis

The effect of dietary glucose and fructose on hepatic and whole body fatty acid synthesis in the presence and absence of added corn oil in the diet was examined in mice. Fructose-fed mice have higher rates of hepatic but not extra-hepatic fatty acid synthesis invivo than do those fed glucose. In addition, fructose based diets elicit higher hepatic activities of fatty acid synthetase (FAS) ATP citrate lyase (CL), malic enzyme (ME) and glucose-6-phosphate dehydrogenase (G6PD) than do glucose based diets. Glucokinase (GK) was higher in glucose fed than fructose fed mice. Acetyl CoA carboxylase (AcCx) was the same on both diets. Inclusion of 5% corn oil in the diets decreased the activities of hepatic AcCx, FAS, ME, G6PD and invivo hepatic and extra hepatic fatty acid synthesis in glucose fed mice but did not inhibit these in fructose fed mice except for G6PD where the inhibition was less than in glucose fed mice. Thus fructose feeding lead to higher rates of fat synthesis and less sensitivity to inhibition by dietary fat than does glucose feeding.     

Response of rat hepatic fatty acid synthesis and activities of related enzymes to changes in level of dietary fat.

The rate of in vivo fatty acid synthesis as well as the levels of glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), malic enzyme (ME), citrate cleavage enzyme (CCE), acetyl-CoA carboxylase (ACX) and fatty acid synthetase (FAS) activities, have been studied in the liver of rats fed a fat-free diet for 7 days, followed by diets containing different amounts of soybean oil (0 to 24.79 kcal%) for 7 days. The dietary fat depressed activities of G6PD, 6PGD, ME, CCE, and FAS significantly at 1.24 or 2.48 kcal%. On the other hand, AC activity and the rate of fatty acid synthesis were decreased when the level of dietary fat was 12.39 kcal% or greater. These findings, as well as the pattern of decrement of enzyme activities and of lipogenesis, suggest a close correlation of fat feeding to ACX activity and fatty acid synthesis. The results also suggest that changes of G6PD, 6PGD, ME, CCE, and FAS activities may be largely independent of those modifications which occur in the substrate flux, concomitantly with the decrease of lipogenesis caused by the inclusion of fat in the diet.     

Dietary sea cucumber cerebroside alleviates orotic acid-induced excess hepatic adipopexis in rats

ABSTRACT: BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a prevalent chronic liver disease in industrialized countries. The present study was undertaken to explore the preventive effect of dietary sea cucumber cerebroside (SCC) extracted from Acaudina molpadioides in fatty liver rats. METHODS: Male Wistar rats were randomly divided into four groups including normal control group, NAFLD model group, and two SCC-treated groups with SCC at 0.006% and 0.03% respectively. The fatty liver model was established by administration of 1% orotic acid (OA) to the rats. After 10d, serum and hepatic lipid levels were detected. And the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were also determined. Besides, to gain the potential mechanism, the changes of key enzymes and gene expressions related to the hepatic lipid metabolism were measured. RESULTS: Dietary SCC at the level of 0.006% and 0.03% ameliorated the hepatic lipid accumulation in fatty liver rats. SCC administration elevated the serum triglyceride (TG) level and the ALT, AST activities in OA-fed rats. The activities of hepatic lipogenic enzymes including fatty acid synthase (FAS), malic enzyme (ME) and glucose-6-phosphatedehydrogenase (G6PDH) were inhibited by SCC treatment. And the gene expressions of FAS, ME, G6PDH and sterol-regulatory element binding protein (SREBP-1c) were also reduced in rats fed SCC. However, dietary SCC didn't affect the activity and mRNA expression of carnitine palmitoyltransferase (CPT) in liver. Besides, suppression of microsomal triglyceride transfer protein (MTP) activity was observed in SCC-feeding rats. CONCLUSIONS: These results suggested that dietary SCC could attenuate hepatic steatosis due to its inhibition of hepatic lipogenic gene expression and enzyme activity and the enhancement of TG secretion from liver.     

Dietary fatty acids on the control of glucose-6-phosphate dehydrogenase and malic enzyme in the starved-refed rat.

The role of dietary unsaturated fat in the control of hepatic glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) and malic enzyme (ME) (EC 1.1.1.40) was studied in rats subjected to one or two cycles of starvation-refeeding. Rats starved and refed a control (5% corn oil) diet showed a threefold increase in G6PD activity and a twofold increase in ME activity compared to ad libitum-fed rats. After a second cycle of starvation-refeeding G6PD and ME activities showed fourfold and threefold increases, respectively, as compared to ad libitum-fed rats. Feeding rats diets containing 8% linoleic acid (as triglycerides) prevented the increase in G6PD and ME activities upon starvation-refeeding, diets with oleic, palmitic, and stearic acis when fed did not prevent this increase. Feeding rats various combinations of linoleic, linolenic and oleic acids following starvation prevented the additional increase in G6PD and ME activities after a second starvation-refeeding cycle; however, linoleic acid fed alone during the first refeeding prevented the additional increase in ME activity but not in G6PD activity. It is suggested that the dietary control of these enzymes involves one or more specific polyunsaturated fatty acids.     

胆固醇影响大鼠脂肪代谢的机制研究

目的:研究胆固醇影响大鼠脂肪代谢的机制。方法:以添加1%胆固醇的AIN76合成饲料喂食Wistar大鼠4w,对照组不添加胆固醇。分别测血清甘油三酯(TG)、总胆固醇(TC)、磷脂(PL)、高密度脂蛋白(HDL-C)、血糖、游离脂肪酸(NEFA)浓度;测肝脏TG、TC、PL浓度以及苹果酸酶(ME)、葡萄糖6磷酸脱氢酶(G6PDH)、脂肪酸合成酶(FAS)、磷脂酸磷酸酶(PAP)和肉毒碱棕榈酰转移酶(CPT)活性、酰基辅酶A-胆固醇酰基转移酶(ACAT)、胆固醇7a-羟化酶(CYP7A)和羟甲基戊二酸单酰辅酶A还原酶(HMG-CoA reductase)mRNA。结果:胆固醇显著增加大鼠血液TC和非HDL-C浓度、降低HDL-C和TG浓度,使肝脏TC和TG浓度分别提高了20和4倍。胆固醇组大鼠肝脏ME活性降低40%、G6PDH活性降低70%、FAS活性降低50%,PAP活性降低15%,CPT的活性降低25%,肝脏FAS的mRNA量降低35%,CPT1和CPT2的mRNA量分别降低30%和50%。HMG-CoA还原酶mRNA量降低25%,而CYP7A和ACAT mRNA量分别增加了6.5和1.6倍。结论:高胆固醇饮食引起肝脏TG蓄积,但并不增加肝脏TG合成相关酶的活性和基因表达。     

Short-term modulation of lipogenesis by macronutrients in rainbow trout (Oncorhynchus mykiss) hepatocytes

Rainbow trout (Oncorhynchus mykiss) hepatocytes were cultured under simulated conditions of varying nutritional status to explore the short-term modulation by dietary substrates of the main lipogenic enzymes: glucose-6-phosphate dehydrogenase (G6PD), malic enzyme (ME), ATP-citrate lyase (ACL), acetyl-CoA carboxylase (ACoAC) and fatty acid synthetase (FAS). Primary cultures were individually exposed to varying amounts of glucose, hydrolysed casein and long-chain polyunsaturated fatty acids (PUFA) for 12 h. A second set of experiments was designed to evaluate the effects of mixing different relative amounts of these macronutrients in the culture medium. Glucose concentrations of up to 20-25 mm showed a stimulatory effect on G6PD, ME, ACL and ACoAC activity while an earlier inhibitory effect on FAS was observed at 10-20 mm glucose The use of hydrolysed casein as a nutritional source of amino acids inhibited the activity of FAS and ME and stimulated G6PD, ACoAC and ACL activity Low levels of linolenic acid exerted a stimulatory effect on all the lipogenic enzymes assayed with the exception of FAS, and increased amounts showed some inhibition of lipogenic activities Eicosapentaenoic acid and docosahexaenoic acid showed a similar effect, although the former strongly inhibited FAS activity while the latter showed greater potential to inhibit ACoAC and G6PD. A complete change in the relative levels of glucose, hydrolysed casein and PUFA in turn led to changes in the enzyme activity patterns observed. The present study shows the feasibility of exploring the direct regulation of lipogenesis in isolated fish cells by varying the relative amounts of main macronutrients, mimicking in vivo dietary conditions. It is felt that such an approach may serve to investigate the macronutrient regulation of other metabolic pathways.     

Effect of dietary fat and sucrose on the activities of several rat hepatic enzymes and their diurnal response to a meal.

Regulation of the cytoplasmic enzymes, pyruvate kinase (PK), glucokinase (GK), phosphoenolpy ruvate carboxykinase (PEPCK), fructose-1,6-diphosphatase (FDP), ATP citrate-lyase (ATP-CL), NAD-malate dehydrogenase (NAD-MD), NADP-malate dehydrogenase (NADP-MD), glutamic-pyruvic transaminase (GPT), glucose-6-phosphate dehydrogenase (G6PD), and 6-phosphogluconate dehydrogenase (6PGD), in rat liver by dietary fat (F diet) and dietary sucrose (S diet) was investigated. Mealfeeding the S diet to adult rats for 5 and 9 months resulted in a diurnal dietary response (i.e., food response) variation of FDP, GK, ATP-CL, 6PGD, and PK, while meal-feeding the S diet to young rats resulted in diurnal dietary response variation of ATP-CL, G6PD, NADP-MD, 6PGD, GPT, and PK. Meal-feeding the fat diet results in essentially no diurnal variation in enzyme activity. The overall effect of meal-feeding, as compared with ad libitum feeding, of the S diet was to increase the levels of G6PD, ATP-CL, and NADP-MD and to decrease the level of PEck in the meal-fed rats. Young rats meal-fed the two diets have higher enzyme activities than meal-fed adult rats for the observed enzymes (except for GPT and NAD-MD). In general, hepatic levels of the enzymes studied are low in the F diet-fed animals and markedly higher for the S diet-fed animals. These results suggest that dietary carbohydrate specifically induces those enzymes involved in carbohydrate metabolism, whereas dietary fat does not affect their levels. On the basis of prior evidence for an early requirement of RNA synthesis for sucrose induction of G6PD, this widespread induction of liver enzymes by carbohydrate must indicate either increased synthesis of ribosomal RNA with later regulation of synthesis specifically of these enzymes or increased synthesis of a rather large group of specific messenger RNAs i.e., coordinate genetic control of a number of these enzyme messenger RNAs.     

Effect of corn gluten and its hydrolysate consumptions on weight reduction in rats fed a high-fat diet

This study examined the effects of corn gluten (CG) and its hydrolysate consumptions on weight reduction in rats fed a high-fat diet. Eight-month-old male Sprague-Dawley rats (n=40) were fed a high-fat diet (40% calorie as fat) for 4 weeks. They were then randomly divided into four groups and fed the isocaloric diets with different protein sources for 8 weeks. The protein sources were casein (control group), intact CG (CG group), CG hydrolysate A (CGHA group, 30% of protein as peptides and 70% as free amino acids) and CG hydrolysate P (CGHP group, 93% of protein as peptides and 7% as free amino acids). Body weight gain, adipose tissue weights, nitrogen balance, absorptions of energy, protein and fat, lipid profiles in plasma, liver and feces and hepatic activities of carnitine palmitoyl transferase (CPT), fatty acid synthase (FAS), malic enzyme (ME) and glucose-6-phosphate dehydrogenase (G6PDH) were assessed. The CGHA diet had the highest amount of BCAAs, especially leucine, and most of them existed as free amino acid forms. The CGHA group showed significant weight reduction and negative nitrogen balance. Protein absorption and apparent protein digestibility in the CGHA group were significantly lower than those in other groups. Adipose tissue weights were the lowest in the CGHA group. Activity of CPT tended to be higher in the CGHA group than in other groups and those of FAS, ME and G6PDH were significantly lower in the CGHA group than in other groups. In conclusion, the CGHA diet which had relatively high amounts of free amino acids and BCAAs, especially leucine, had a weight reduction effect by lowering adipose tissue weight and the activities of FAS, ME and G6PDH in experimental animals, but it seemed to be a negative result induced by lowering protein absorption, increasing urinary nitrogen excretion and protein catabolism.     

Gender-linked differences in dietary induction of hepatic glucose-6 phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and malic enzyme in the rat

The objective of these studies was to determine how alterations in dietary carbohydrate affect hepatic glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH) and malic enzyme (ME) activities in adult female rats. Rats were either starved 2 d and then refed a nonpurified diet or a purified 65% carbohydrate diet (glucose, sucrose, fructose or cornstarch) for 3 d, or switched from nonpurified to purified diets for 3 d. Liver G6PDH, 6PGDH and ME activities were determined. In males, enzyme activities were 8- to 12-fold and 3-fold higher when starved and refed purified diets and nonpurified diets, respectively, whereas in females, activities were 2- to 3-fold higher only when refed purified diets. Both genders had higher enzyme activities when shifted to purified diets. Females responded less dramatically than males. Of the higher enzyme activities observed during starvation-refeeding studies, in females 58-65% of the change is a function of switching rats from nonpurified to purified diets. In contrast, in males only 24-40% of the higher activities could be attributed to diet shifting. Results of these studies indicate that the effects of dietary carbohydrates on hepatic G6PDH, 6PGDH and ME activities are gender dependent.     

Absence of a generalized disaccharide effect in adult female rats

Adult female Sprague-Dawley rats were either prefed ground nonpurified diet, starved 48 h, then refed a purified carbohydrate diet for 72 h or shifted from ground nonpurified diet directly to a purified carbohydrate diet for 72 h. Diets were formulated to contain 65% carbohydrate either as the disaccharides maltose or sucrose or as their respective monosaccharide equivalents glucose and invert sugar (glucose: fructose, 1:1). Alternations in hepatic glucose 6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH) and malic enzyme (ME) activities, relative liver size and food efficiency were determined. Rats starved and refed invert sugar had higher levels of G6PDH and ME than those red glucose, indicating a positive fructose effect. The greatest changes in hepatic enzyme activities were observed in rats consuming diets containing sucrose. Positive fructose and disaccharide effects were obtained with sucrose for all enzymes studied in both dietary shift and starve-refeed studies. No disaccharide effect was observed with maltose. In conclusion, females did not display a generalized disaccharide effect with either dietary shifting or starvation refeeding.     

Relationship of level and type of dietary fat to fetal and maternal rat lipogenesis and lipid deposition

Pregnant rats were pair-fed isoenergetic diets with varying fat content and varying fatty acid compositions to determine if manipulation of the maternal diet would affect fetal lipid metabolism. A mixture of tallow and lard replaced cornstarch on an equal-energy basis so that fat supplied 5 to 65% of the metabolizable energy. Fat content of the maternal diet did not affect fetal weight or fetal body composition. No differences in fetal liver fatty acid synthetase (FAS), glucose-6-phosphate dehydrogenase (G6PD) activities or rate of in vivo fatty acid synthesis were noted. In vivo fatty acid synthesis was greater in fetal liver than maternal liver. Dietary manipulation did not affect in vivo fatty acid synthesis in either fetal or maternal liver. Maternal liver FAS and G6PD activities were generally greater than fetal liver FAS and G6PD activities. These enzyme activities were decreased in maternal livers when the high-fat diet was fed. A sudden decrease in food consumption 24 hours before killing may explain the apparent inconsistencies in enzyme activities and fatty acid synthesis rates. The results of this study indicate that the level of fat in the maternal diet has no effect on the amount of lipid accumulated in fetal tissues or fetal lipogenesis.     

Demonstration of a specific metabolic effect of dietary disaccharides in the rat.

Male Wistar rats were starved and refed diets containing either 40% carbohydrate as monosaccharides (glucose, fructose, invert sugar) or disaccharides (maltose, sucrose), or 42.2% carbohydrate as glucose. Induction of various liver enzymes and changes in total liver lipid levels by the different dietary sugars were studied. Liver enzymes measured included glucose-6-phosphate dehydrogenase (g6pd), 6-phosphogluconate dehydrogenase (6PGD), malic enzyme (ME), phosphofructokinase (PFK), L-alpha-glycerol phosphate dehydrogenase (LalphaGPD), pyruvate kinase (PK), citrate cleavage enzyme (CCE), acetyl CoA carboxylase (AcCoAC), and fatty acid synthetase (FAS). The responses in enzyme activity to diets containing glucose or invert sugar were used as the basal response. Enzyme responses to refeeding the carbohydrate diets fell into three categories: (1) enzyme activity increased both by the disaccharide configuration of the carbohydrate and by fructose (G6PD, PK, CCE, AcCoAC, FAS); (2) enzyme activity increased only by the disaccharide configuration of the carbohydrate (6PGD, ME); and (3) enzyme activity increased only by fructose (PFK, LalphaGPD). Total liver lipid level was increased both by the disaccharide configuration of the carbohydrate and by fructose. Refeeding diets containing equal molar amounts of glucose or maltose did not abolish the disaccharide effect. The data indicate that the disaccharide configuration of maltose and sucrose may have an effect at the gastrointestinal level, which causes an increased induction of certain enzymes in the liver.     

The effect of biotin deficiency and dietary protein content on lipogenesis, gluconeogenesis and related enzyme activities in chick liver

Chicks were given biotin-deficient diets containing either suboptimal (low) or supraoptimal (high) concentrations of protein from 1-d-old until they were used during their fourth week of life. The low-protein diet predisposed chicks to develop fatty liver and kidney syndrome and the high-protein diet to develop classical biotin deficiency signs. Two other groups, as controls, received biotin-supplemented rations. Low dietary protein increased lipogenesis by isolated hepatocytes but had little effect on gluconeogenesis compared to high dietary protein. Low dietary protein decreased activities of hepatic isocitrate dehydrogenase (EC 1.1.1.42), fructose-1,6-bisphosphatase (EC 3.1.3.11) and glucose-6-phosphatase (EC 3.1.3.9; GP) and increased activities of fatty acid synthase (FAS), citrate cleavage enzyme (EC 4.1.3.8; CCE) and malate dehydrogenase (decarboxylating) (EC 1.1.1.39). When biotin deficiency was superimposed, the rate of lipogenesis by isolated hepatocytes (from fed birds) was decreased. Gluconeogenesis from lactate and glycerol was also depressed. Activity of GP was further decreased by biotin deficiency on the low-protein regimen and FAS and CCE were further increased. PK activity was increased by biotin deficiency.     

Regulation of glucose-6-phosphate dehydrogenase and malic enzyme in liver and adipose tissue: effect of dietary trilinolein level in starved-refed and ad libitum-fed rats.

The responses of glucose-6-phosphate dehydrogenase (G6PD) (EC 1.1.1.49) and malic enzyme (ME) (EC 1.1.1.40) were studied in liver and adipose tissue of rats fed for 2 days a high glucose diet containing levels of synthetic trilinolein ranging from 0 to 25% (w/w) of the diet (trilinolein was substituted for glucose). One group of rats was starved for 2 days before the trilinolein-containing diets were fed (starved-refed); a second group of rats was fed a fat-free diet for 7 days before the trilinolein-containing diets were fed (ad libitum). Liver G6PD activity decreased exponentially and liver ME activity decreased linearly with increasing dietary trilinolein in starved-refed rats, but did not decrease significantly in ad libitum fed rats. Total liver lipid decreased exponentially with increasing trilinolein in starved-refed rats, but increased exponentially in ad libitum fed rats. Adipose tissue G6PD and ME activities decreased slightly with increasing trilinolein in starved-refed rats, but did not decrease in ad libitum fed rats. When the data were adjusted by analysis of covariance for differences in glucose intake, the liver responses in starved-refed rats were still significant but the adipose tissue responses were not, indicating that the responses of adipose tissue (but not of liver) may have resulted from decreased glucose intake rather than from increased trilinolein intake. The results suggest that dietary trilinolein inhibits the characteristic increase in liver G6PD, ME and total lipids upon starvation-refeeding. However, after the levels of these parameters have been increased by feeding a fat-free diet they cannot be decreased by dietary trilinolein in 2 days.     

Effect of dietary seal and fish oils on triacylglycerol metabolism in rats

Eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids were distributed mainly in the sn-1 and 3 positions of seal oil triacylglycerol and in the sn-2 position of fish oil triacylglycerol. Seal oil or fish oil-rich fats having constant polyunsaturated/monounsaturated/saturated fatty acids and n-6/n-3 polyunsaturated fatty acid (PUFA) ratios were fed to rats for 3 wk. Control rats were fed on a fat containing linoleic acid as the sole PUFA. Seal oil more effectively lowered serum and liver triacylglycerol concentrations than fish oil. The activities of fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH) and hepatic triacylglycerol lipase (HTGL) were significantly lower in the seal oil group than in the control group, whereas the activity of HTGL was significantly lower and the hepatic peroxisomal beta-oxidation and activity of lipoprotein lipase (LPL) in adipose tissue were significantly higher in the fish oil group than in the control group. These observations suggest that the predominant hypotriacylglycerolemic effect of seal oil is caused by the suppression of fatty acid synthesis.     

Repression of pentose phosphate pathway dehydrogenase synthesis and mRNA by dietary fat in rats

We have studied the effects of polyunsaturated fatty acid and its metabolism on the activity, relative synthesis and mRNA levels for rat hepatic glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD). Rats were meal-fed high carbohydrate diets containing either no fat, 5% safflower oil or 5% safflower oil + eicosa-5,8,11,14-tetraynoic acid (TYA). Hepatocytes were isolated and used as a source of RNA, de novo radiolabeled protein and postmitochondrial supernatant for enzyme assay. Dietary safflower oil, as a source of linoleic acid, repressed G6PD activity, synthesis and mRNA levels two- to threefold without significantly changing the amount of carbohydrate consumed. Similar but smaller changes were observed for 6PGD. Dietary fat + TYA (an analogue of arachidonate that inhibits normal metabolism of linoleic acid) prevented the fat-dependent lowering of G6PD and 6PGD activity, synthesis and mRNA levels. Our results suggest that a metabolite of linoleic acid regulates the activity of two lipogenic enzymes, G6PD and 6PGD, by lowering gene expression or mRNA processing or stability.     

下丘脑腹内侧核损伤性肥胖大鼠急性期脂肪代谢相关酶活性研究

目的 :　观察下丘脑腹内侧核损伤性肥胖大鼠在自由进食状态下脂肪合成与分解代谢的变化。方法 :　雌性 SD大鼠分为下丘脑腹内侧核损伤肥胖组 (VMH)和下丘脑腹内侧核非损伤对照组 (假手术 ) ,于下丘脑腹内侧核手术 1 w后 ,留取血样、肝脏、皮下脂肪、子宫外周和肠系膜脂肪组织以及腓肠肌分别测定生化指标、脂肪合成酶和分解酶活性。结果 :　在自由进食状态下VMH血清胰岛素水平显著高于对照组 ,而血浆游离脂肪酸显著低于对照组。大鼠肝脏微粒体甘油三酯转运蛋白 (MTP)、肝脏磷脂酰磷酸水解酶 (PAP)、苹果酸酶 (ME)、葡萄糖 - 6-磷酸脱氢酶(G6PDH)以及子宫外周脂肪组织 ME和肠系膜脂肪组织 ME、G6PDH的活性均高于对照组。与对照组相比 ,VMH组子宫外周、肠系膜脂肪组织和腓肠肌激素敏感脂酶 (HSL)活性没有变化 ,皮下脂肪组织的 HSL活性升高。在 VMH组 ,皮下脂肪组织、子宫外周脂肪组织、肠系膜脂肪组织以及腓肠肌中的脂蛋白脂酶活性均显著升高。结论 :　下丘脑腹内侧核损伤性肥胖大鼠自由进食状态下肝脏合成和转运甘油三酯能力增强 ,脂肪组织如子宫外周和肠系膜脂肪组织的脂质合成和储存增多 ;而外周组织如肌肉组织和皮下脂肪组织的脂肪分解和动员也增加     

Effect of dietary cholesterol and fat levels on lipid peroxidation and the activities of antioxidant enzymes in rats

The aim of this study was to investigate the effect of dietary fat levels, with or without cholesterol, on lipid peroxidation and the activities of antioxidant enzymes in rats. Thirty-two Wistar rats aged 4 weeks were divided into 4 groups and fed high (20%; HF) or low (5%; LF) fat, with or without 1% cholesterol, for 6 weeks. Cholesterol feeding resulted in significantly higher concentrations of serum cholesterol, but lowered serum triacylglycerol levels. Cholesterol feeding also led to markedly decreased levels of hepatic thiobarbituric acid reactive substances (TBARS) and lower activities of hepatic superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase, and glucose-6-phosphate dehydrogenase (G6PDH) when compared with cholesterol-free counterparts in both HF and LF diets. On the other hand, rats fed high-fat diets showed increased serum and liver TBARS, but decreased hepatic GSH-Px, SOD, and G6PDH activities. Hepatic catalase activity was lower in rats fed cholesterol-containing diets, but higher in rats fed high-fat diets, and interaction existed between cholesterol and fat feeding. These results suggested that dietary cholesterol might delay lipid peroxidation and decrease the activities of the hepatic antioxidant enzymes. The degree of lipid peroxidation was also influenced by dietary fat levels.     

Interrelationships in rats among dietary vitamin B6, glycine and hydroxyproline. Effects of oxalate, glyoxylate, glycolate, and glycine on liver enzymes.

Urinary endogenous oxalate was increased by feeding vitamin B6-deficient or control rats with 5.2% hydroxyproline, or 3% glycine plus 5.2% hydroxyproline. The activities of liver lactic dehydrogenase (LDH), glucose-6-phosphate dehydrogenase (G6PD) , malic enzyme (ME), and ATP citrate lyase were decreased in vitamin B6-DEFICIENT RATS, AND THEIR LIVEr G6PD was further decreased by the addition of glycine and hydroxyproline to their diets. Supplementing control diets with the two amino acids decreased the activities of rat liver LDH, G6PD, and ATP citrate lyase. The effects of glycine and hydroxyproline feeding on the enzymes studied did not appear related to alterations in insulin availability. Since in vitamin B6-deficient rats, there are increases in urinary levels of oxalic and glycolic acids, and glycine, and increases in tissue levels of glyoxylic acid and glycine, the effects of these metabolites on the activities of the above mentioned enzymes were measured. Oxalic acid inhibited the activities of LDH, G6PD, and ME. Glyoxylic acid inhibited LDH and ME, but not G6PD. Glycolic acid inhibited G6PD and ME, but not LDH. ATP citrate lyase was not affected by these substances. Glycine had no effect on the enzymes studied. Diets which increased oxalate excretion generally reduced or did not alter liver and kidney levels of oxalate, glycolate, and glyoxylate. However, the feeding of glycine and hydroxyproline increased kidney oxalate, and liver and kidney glyoxylate in vitamin B6-deficient rats.