Effects of fish oil and safflower oil emulsions on diet-induced hepatic steatosis in rats receiving total parenteral nutrition

This study was conducted to investigate the effects of fish oil and safflower oil emulsions in total parenteral nutrition (TPN) solutions on diet-induced hepatic steatosis. Rats were divided into a control group (C, n = 6) and four experimental groups (A, B, S, F, n = 11 approximately 14). The control group was fed a chow diet whereas the experimental groups received a high fat (15%, w/w) diet containing 0.1% (w/w) cholesterol. Group A received the high fat diet for 4 weeks, and was killed at the end of the fourth week to ensure that hepatic steatosis had occurred. Groups S and group F received TPN with safflower oil or fish oil emulsions, respectively, for 1 week following experimental diet feeding for 4 weeks. Group B was fed a limited amount of the high fat diet, without cholesterol, for 1 week following 4 weeks of experimental diet in order to maintain the same body weight and cholesterol intake as the TPN groups. Diet-induced hepatic steatosis was observed in the experimental groups. Fat deposition was reversed when the total caloric and cholesterol intake was reduced. Fish oil infusion ameliorated the severity of hepatic steatosis, whereas safflower oil had no effect on liver fat deposition. These results suggest that TPN with fish oil emulsions may be beneficial to patients with diet-induced hepatic steatosis.     

Hepatic transmethylation and blood alcohol levels

Golden Syrian hamsters that have elevated hepatic alcohol dehydrogenase activity were divided into four groups and group-fed on four different liquid diets for five weeks. Group I was fed a control diet formulated for hamsters. Group II was fed the control diet containing 20 micrograms of 4 methylpyrazole per litre. Group III was fed the hamster ethanol liquid diet (ethanol amounting to 36% of total calories). Group IV was fed the ethanol diet to which 4-methylpyrazole (20 micrograms/litre) was added. Groups I, II and III were group-fed the amount consumed by Group IV on a daily basis. Upon killing the animals, blood alcohol levels were found to be elevated in Group IV but not in Group III. Hepatic methionine synthetase (MS) was inhibited in Group IV. Betaine-homocysteine methyltransferase was induced in this group to compensate for the MS inhibition and liver betaine was lowered reflecting this induction. None of these changes were seen in Group III. Since none of the animals showed an aversion to their respective diets and gained weight normally, these data indicate that it was the elevated blood levels of ethanol rather than nutritional factors that were related to the changes in methionine metabolism.     

Effect of vitamin E on lipid components of atherogenic rats

Rats were made atherogenic by feeding a synthetic diet containing high fat (20%) and cholesterol (2%) for two, three or four weeks. For alpha-tocopherol acetate supplementation studies, the rats on atherogenic diet for two weeks received alpha-tocopherol acetate 5 mg or 20 mg/100 g body weight once daily, orally for two weeks along with the atherogenic diet. Atherogenic diet fed rats showed elevated plasma cholesterol, hepatic total lipids, triglycerides and cholesterol and the increase in the constituents paralleled the period of feeding the diet. Administration of alpha-tocopherol acetate lowered the plasma cholesterol and hepatic lipid components in a dose-dependent manner. Supplementation with alpha-tocopherol acetate reduced the elevated osmotic fragility of erythrocytes from atherogenic diet fed rats to that of control levels. Thus alpha-tocopherol acetate administration to experimental atherogenic rats could normalize the altered lipid profile of atherogenesis and thereby reduce the risk for infarction.     

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.     

Dietary taurine or glycine supplementation reduces plasma and liver cholesterol and triglyceride concentrations in rats fed a cholesterol-free diet

The effects of dietary supplementation of taurine or glycine, the two amino acids involved in bile acid conjugation in the liver, on plasma and hepatic lipid concentrations were evaluated in rats fed a cholesterol-free diet. Three groups of male rats (140150g) were fed a cholesterol-free diet (CFD), a taurine-supplemented diet (TSD; CFD + 1.5% taurine) or a glycine-supplemented diet (GSD; CFD + 1.5% glycine) for 5 weeks. There was no significant difference in organ weights and cumulative body weight gain between groups at the end of the experimental period. Plasma triglyceride level was significantly lower in rats fed the TSD (53% decrease, P<0.001) compared to those fed the CFD. Both TSD and GSD significantly lowered the plasma levels of total cholesterol (40% decrease in TSD, p<0.001 and 27% decrease in GSD, p<0.001, respectively) and LDL-plus VLDL-cholesterol (50% decrease in TSD, p<0.05 and 39% decrease in GSD, p<0.01, respectively) compared to the values for CFD. Liver cholesterol concentration was not significantly influenced by the dietary supplementation of taurine or glycine. However, both TSD and GSD showed significantly lower hepatic triglyceride concentrations (43% and 53% decreases in TSD and GSD, p<0.001, respectively), and elevated hepatic free fatty acid levels (77% increases in both groups, p<0.001) compared to the values for CFD. These results suggest the possible roles of dietary taurine or glycine as hypocholesterolemic and/or hypotriglyceridemic agents.     

Molasses increases HDL cholesterol in rats research note

Two experiments were conducted to determine whether molasses might exert effects on serum lipoproteins. In experiment 1, 24 rats were divided into two groups and fed diets containing liquid molasses from sugar beet or sucrose (7.71 g of molasses dry matter or sucrose per kg of diet). The second experiment included four groups of rats (n = l2/group) and was conducted in a bifactorial design, with the factors being molasses (non-supplementation vs. supplementation of 77.1 g of molasses dry matter per kg of diet at the expense of sucrose) and dietary cholesterol (0 vs. 5 g/kg diet). In experiment 1, the ratio of low-density lipoprotein (LDL) to high-density lipoprotein (HDL) cholesterol concentration tended to be lower in rats fed the molasses diet than in rats fed the control diet (p < 0.15). In experiment 2, rats fed the molasses diet had higher concentrations of HDL cholesterol (+ 26%) than control rats fed diets without molasses (p < 0.05). This effect was independent of the dietary cholesterol concentration. Concentrations of cholesterol in LDL, very low-density lipoprotein (VLDL), and liver as well as concentrations of triacylglycerols in plasma and liver remained unaffected by molasses in both experiments. In conclusion, the results of this study suggest that supplementation of molasses is effective at raising HDL cholesterol levels in rats.     

Hypocholesterolemic Effects of Lactic Acid-Fermented Soymilk on Rats Fed a High Cholesterol Diet

The effect of fermented soymilk on rats fed a high cholesterol diet was investigated to clarify the cholesterol-lowering function. Male Sprague-Dawley rats aged 7 weeks were fed a control diet (1% cholesterol, high cholesterol diet), high cholesterol diet containing 11.7% fermented soymilk diet (5% soy protein as final concentration, F-5), or high cholesterol diet containing 23.4% fermented soymilk diet (10% soy protein as final concentration, F-10) for 5 weeks. The liver weight and fat mass were decreased by the ingestion of fermented soymilk. The hepatic triglyceride and cholesterol levels in the F-5 and F-10 groups were significantly lowered compared to those in the control group. The plasma total cholesterol level of the F-10 group was significantly decreased. The expression of SREBP-2, a cholesterol synthesis-related gene, was significantly decreased in liver of the F-5 group, but the expression of CYP7a1, a cholesterol catabolism-related gene, was significantly increased. These results suggest that fermented soymilk can modulate the cholesterol metabolism in rats fed a high cholesterol diet.     

Consumption of Low Dose Fucoxanthin Does Not Prevent Hepatic and Adipose Inflammation and Fibrosis in Mouse Models of Diet-Induced Obesity

Fucoxanthin (FCX) is a xanthophyll carotenoid present in brown seaweed. The goal of this study was to examine whether FCX supplementation could attenuate obesity-associated metabolic abnormalities, fibrosis, and inflammation in two diet-induced obesity (DIO) mouse models. C57BL/6J mice were fed either a high-fat/high-sucrose/high-cholesterol (HFC) diet or a high-fat/high-sucrose (HFS) diet. The former induces more severe liver injury than the latter model. In the first study, male C57BL/6J mice were fed an HFC diet, or an HFC diet containing 0.015% or 0.03% (w/w) FCX powder for 12 weeks to develop obesity-induced nonalcoholic steatohepatitis (NASH). In the second study, mice were fed an HFS diet or an HFS diet containing 0.01% FCX powder for 8 weeks. FCX did not change body weight gain and serum lipid profiles compared to the HFC or HFS controls. No significant differences were present in liver triglyceride and total cholesterol, hepatic fat accumulation, and serum alanine aminotransferase levels between control and FCX-fed mice regardless of whether they were on an HFC or HFS diet. FCX did not mitigate mRNA abundance of genes involved in lipid synthesis, cholesterol metabolism, inflammation, and fibrosis in the liver and white adipose tissue, while hepatic fatty acid β-oxidation genes were significantly elevated by FCX in both HFC and HFS feeding studies. Additionally, in the soleus muscle, FCX supplementation significantly elevated genes that regulate mitochondrial biogenesis and fatty acid β-oxidation, concomitantly increasing mitochondrial DNA copy number, compared with HFC. In summary, FCX supplementation had minor effects on hepatic and white adipose inflammation and fibrosis in two different DIO mouse models.     

Reduction of plasma and hepatic triacylglycerides with whole milk-containing diets in rats

Two studies were conducted to determine the effect of diets containing milk on plasma cholesterol, triacylglycerides, apolipoproteins, and lipoprotein composition and hepatic lipid levels in rats. In the first study four groups were fed either a diet containing skim milk (SM) powder or whole milk (WM) powder or one of two control diets with casein as the protein source. The SM diet and one casein diet (SM control) each contained 5% fat by weight as corn oil. The WM diet contained 20% fat by weight, derived from the milk powder, and the second casein diet (WM control) contained 20% fat by weight from corn oil and lard. The SM group had similar plasma and hepatic lipids, as did the SM control group; plasma apolipoprotein AI, AIV and B did not differ between the groups, but the apo E level was lower in the control group. The WM group had lower plasma triacylglycerides and apo B and lower hepatic cholesterol and triacylglycerides than did the WM control group. In the second study the WM diet was fed again, and the two control diets contained casein as the protein source, 20% butter oil (so that the level of dietary fat was comparable to that of the WM diet), and either lactose or sucrose was added. The plasma apo B and triacylglycerides and the hepatic cholesterol and triacylglycerides were significantly lower in the WM group than in the casein/lactose or casein/sucrose groups. The amount of protein, cholesterol and triacylglycerides in the VLDL fraction of the plasma was lower in the WM group than in the casein/lactose or casein/sucrose groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hypocholesterolemic effect of vitamin E on cholesterol-fed rabbit

Serum cholesterol level increased sharply in rabbits fed an atherosclerosis-promoting diet containing 0.25% or 0.5% cholesterol. Oral supplementation with 2100 IU of vitamin E per week manifested a hypocholesterolemic effect only after four weeks, with 50% reduction attained on the 8th week. Changes in low density and very low density lipoprotein cholesterol levels paralleled those in the serum. Liver total cholesterol level and the ratio of free to ester forms were not different between vitamin E-supplemented and nonsupplemented rabbits, whereas a 4-5 fold increase in hepatic cholesterol-7 alpha-hydroxylase activity, elevation of bile salt concentration and improvement in bile lithogenic index were observed in the vitamin E-supplemented groups.     

Cinnamate supplementation enhances hepatic lipid metabolism and antioxidant defense systems in high cholesterol-fed rats

This study investigated the effect of cinnamate, a phenolic compound found in cinnamon bark and other plant materials, on lipid metabolism and antioxidant enzyme activities in rats fed a high cholesterol diet. Three groups of rats were given a diet containing 1 g of cholesterol/kg for 6 weeks. The control group only received the high cholesterol diet, whereas the other two groups received a diet supplemented with lovastatin or cinnamate (0.1 g/100 g of diet). The plasma high-density lipoprotein-cholesterol levels were significantly higher in the cinnamate group than in either the control or lovastatin groups, and the atherogenic index was significantly lower in rats with cinnamate supplementation. Supplementation with cinnamate resulted in significantly lower hepatic cholesterol and triglyceride levels. Accumulation of hepatic lipid droplets was higher in the control group than in the rats supplemented with either cinnamate or lovastatin. Hepatic 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase activity was significantly lower in the cinnamate group compared with the other groups, whereas only acyl-CoA:cholesterol acyltransferase activity was significantly lower in the lovastatin group compared with the control group. Cinnamate supplementation resulted in higher catalase and glutathione peroxidase activities, while hepatic thiobarbituric acid-reactive substances were significantly lower in both the cinnamate and lovastatin groups. The fecal acidic sterol was higher in the lovastatin group than in the control or cinnamate groups. These results suggest that dietary cinnamate inhibits hepatic HMG-CoA reductase activity, resulting in lower hepatic cholesterol content, and suppresses lipid peroxidation via enhancement of hepatic antioxidant enzyme activities.     

The influence of different levels of dietary fat on the incidence and growth of MNU-induced mammary carcinoma in rats

This study describes the influence of isocalorically fed diets (containing different amounts of fat) on tumor incidence and parameters of fat metabolism in female Sprague-Dawley rats. Comparisons are made between rats induced with methylnitrosourea (25 mg/kg body wt) and untreated controls (Group I). The animals received either control diets (3.9% fat by weight, Groups I and II) or fat-enriched diets (10.7%, Group III; 15.6%, Group IV; 21.4%, Group V) over a period of 180 days. At the termination of the experiment, intake of the diet containing 10.7% fat by weight (24% fat per total calories) was associated with the highest tumor incidence. Comparing the different diets, liver lipid concentrations in the individual groups increased with increasing dietary fat, whereas the total lipid in plasma decreased. During the feeding period, total lipid of the liver and plasma, and plasma cholesterol, increased in all groups, but triglycerides of plasma decreased. However, when plasma cholesterol and triglycerides were calculated as a relative amount of total lipid in plasma, cholesterol was found to be significantly decreased in Groups III and IV, and triglycerides were increased in Group III but decreased significantly in Groups I, II, and V at the end of the experiment.     

Metabolism of cholesterol is altered in the liver of C3H mice fed fats enriched with different C-18 fatty acids.

We examined whether the degree of saturation of C-18 fatty acids influenced hepatic cholesterol metabolism in C3H mice. The mice were fed diets containing 20 g/100 g fat, enriched in stearic (18:0), oleic (18:1) or linoleic acid (18:2) with or without 1 g/100 g cholesterol. Plasma total cholesterol concentration was lower in mice fed the 18:0 diet relative to those fed the 18:1- or 18:2-enriched diets (P < 0.05) regardless of dietary cholesterol supplementation. Dietary cholesterol significantly raised hepatic total cholesterol concentration (P < 0.05) in those fed the 18:1- and 18:2-enriched diets, but not in mice fed the 18:0-enriched diet. Dietary cholesterol raised biliary cholesterol concentration (P < 0. 05) in mice fed the 18:1- and 18:2-enriched diets, but not in mice fed the 18:0-enriched diet. The cholesterol saturation index was variably affected by the fat diets. Feeding diets containing cholesterol suppressed the hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) activity and induced acyl coenzyme A:cholesterol acyl transferase (ACAT) activity compared with feeding diets without cholesterol (P < 0.05), indicating that the liver was exposed to dietary cholesterol. Hepatic ACAT activity was lower in mice fed the 18:0-enriched diet compared with those fed the 18:1- or 18:2-enriched diets (P < 0.05). Addition of cholesterol to the 18:1 diet induced the largest increase of hepatic ACAT activity, and this was associated with the enrichment of VLDL with cholesterol. Varying the degree of saturation of C-18 fatty acids influences the metabolism and disposition of hepatic cholesterol.     

Carbohydrate restriction alters hepatic cholesterol metabolism in guinea pigs fed a hypercholesterolemic diet

The current study was undertaken to evaluate the effect of carbohydrate restriction on hepatic cholesterol metabolism in guinea pigs fed a hypercholesterolemic diet. Hartley male guinea pigs (n = 10 per group) were fed 1 of 3 diets: a diet with a percent energy distribution of 42:23:35 carbohydrate:protein:fat and 0.04% cholesterol (control), a diet with the same macronutrient distribution but with 0.25% cholesterol (HChol), or a carbohydrate-restricted (CR) diet with a percent energy distribution of 11:30:59 carbohydrate:protein:fat and 0.25% cholesterol for 12 wk. There was more accumulation of hepatic cholesterol and triglycerides as well as lower 3-hydroxy-3-methyl glutaryl-CoA reductase messenger RNA abundance in guinea pigs fed the high-cholesterol diets (HChol and CR) (P < 0.01). Guinea pigs fed the CR diet had lower concentrations of hepatic total cholesterol and cholesteryl ester than those fed the HChol diet (P < 0.05). There was no diet effect on hepatic LDL receptor expression. Hepatic acyl CoA cholesteryl acyltransferase (ACAT) activity was lowest in guinea pigs fed the low-cholesterol diet (9.7 +/- 4.8 pmol.min(-1).mg(-1)), intermediate in those fed the CR diet (37.3 +/- 12.4 pmol.min(-1).mg protein(-1)), and highest in guinea pigs fed the HChol diet (55.9 +/- 11.2 pmol.min(-1).mg(-1)). ACAT activity was significantly correlated with hepatic cholesterol (r = 0.715; P < 0.01) and LDL cholesterol (r = 0.59; P < 0.01) for all dietary groups, suggesting a major role of this enzyme in hepatic cholesterol homeostasis and in lipoprotein concentrations. These results indicate that dietary cholesterol increases hepatic lipid accumulation and affects hepatic cholesterol homeostasis. Carbohydrate restriction in the presence of high cholesterol is associated with lower hepatic ACAT activity and an attenuation of hepatic cholesterol accumulation.     

The influence of different levels of dietary fat on the incidence and growth of mnu‐induced mammary carcinoma in rats

This study describes the influence of isocalorically fed diets (containing different amounts of fat) on tumor incidence and parameters of fat metabolism in female Sprague‐Dawley rats. Comparisons are made between rats induced with methylnitrosourea (25 mg/kg body wt) and untreated controls (Group I). The animals received either control diets (3.9% fat by weight, Groups I and II) or fat‐enriched diets (10.7%, GroupIII; 15.6%, Group IV; 21.4%, Group V) over a period of 180 days. At the termination of the experiment, intake of the diet containing 10.7% fat by weight (24% fat per total calories) was associated with the highest tumor incidence. Comparing the different diets, liver lipid concentrations in the individual groups increased with increasing dietary fat, whereas the total lipid in plasma decreased. During the feed‐ingperiod, total lipid of the liver and plasma, and plasma cholesterol, increased in all groups, but triglycerides of plasma decreased. However, when plasma cholesterol and triglycerides were calculated as a relative amount of total lipid in plasma, cholesterol was found to be significantly decreased in Groups III and IV, and triglycerides were increased in Group III but decreased significantly in Groups I, II, and Vat the end of the experiment.     

Effects of resistant potato starch on cholesterol and bile acid metabolism in the rat

This study examines the effects of two types of resistant starch (RS), raw starch from uncooked potatoes and retrograded starch in the form of cooked and cooled potatoes, on cholesterol and bile acid metabolism in rats. Groups of 8 male Wistar rats were fed a semipurified diet containing 15% cellulose, freeze-dried raw potatoes, or freeze-dried cooked potatoes for four weeks. Serum cholesterol, liver cholesterol, and fecal steroid excretion were determined. Serum cholesterol was significantly higher and liver cholesterol was significantly lower in response to the cooked potato diet compared to the cellulose or raw potato diet. Total steroid excretion was significantly higher in rats fed the cooked potato diet (26.31 mg/d) compared to those fed the cellulose or raw potato diet (14.27 mg/d and 16.81 mg/d, respectively). Daily total bile acid excretion was significantly different among the three groups, with highest excretion seen in rats fed cooked potatoes. High daily excretion of lithocholic acid and hyodeoxycholic acid was observed in rats fed cooked potatoes. These results suggest that changes in the cecal microflora and in the production, pool size, and excretion of chenodeoxycholic acid and its derivatives may be responsible for alterations in cholesterol and bile acid metabolism observed with resistant starch feeding.     

Serum and liver lipids in rats and chicks fed with diets containing different oils

OBJECTIVES: Because dietary fat composition is determinant for serum cholesterol level, which is related to cardiovascular disease, we evaluated the effects of diets containing saturated (coconut oil) or polyunsaturated fatty acids (soybean oil) supplemented or not with dietary cholesterol on serum and liver lipid composition in two animal species. METHODS: Male Wistar rats (21 d old) were assigned to one of seven groups and fed with commercial diet or diets containing 5% or 20% soybean oil or 20% coconut oil with or without 1% cholesterol. Chicks were assigned to one of four groups and fed with diets containing 15% soybean oil or 15% coconut oil with or without 1% cholesterol. RESULTS: In rats, the accumulations of hepatic cholesterol and triacylglycerols were higher in the group fed 20% soybean oil and 1% cholesterol than in the group fed 20% coconut fat and 1% cholesterol. The highest serum levels of cholesterol and triacylglycerols were observed in the group fed coconut oil and cholesterol, compared with the group fed soybean oil and cholesterol. Triacylglycerol, high-density lipoprotein, and total cholesterol serum levels increased with diet containing coconut oil and cholesterol. In chicks, the highest hepatic cholesterol accumulation occurred in the group fed 15% coconut fat and 1% cholesterol. Total and high-density lipoprotein cholesterol levels increased with diet containing coconut oil and cholesterol, although none of these diets modified serum triacylglycerol levels. CONCLUSIONS: The type of experimental animal model and the diet composition influence lipid metabolism.     

Effects of a soluble fraction of soybean on lipid profiles in ovariectomized rats fed a cholesterolemic diet

The increases in serum lipid profiles at the onset of menopause are regarded as a risk factor for cardiovascular disease. This study was designed to clarify the effects of a dried aqueous soybean extract and ovariectomy on lipid parameters in rats fed with cholesterolemic diet. Twenty-four 9-week-old female Sprague-Dawley rats were divided into two groups of 12 each and either sham-operated or ovariectomized. The ovariectomized and sham groups were then subdivided into groups of six and fed a semipurified casein-based diet (control diet) or the same diet containing dried soybean extract (0.5%) at the expense of sucrose (experimental diet). Total isoflavone content was 4.52 mg/g of soy extract. Ovariectomized groups showed significantly greater weight gain and food intake than sham groups, while uterus weight was markedly lower in ovariectomized groups. Although ovariectomy significantly increased the concentration of serum triacylglycerol, the concentration of serum total cholesterol was not affected by the operation. Soybean extract restored the concentration of serum triacylglycerol in the ovariectomized groups to the level observed in the sham groups. On the other hand, liver cholesterol levels were significantly higher in the ovariectomized groups compared to the sham group, without effects of the diet. This study suggests that soybean extract supplementation modulates the level of serum triacylglycerol induced by ovariectomy in rats, and furthers the possibility that dietary cholesterol may be a crucial factor in determining liver cholesterol in the presence of ovarian hormone deficiency.     

Lactose protects against estrogen-induced pigment gallstones in hamsters fed nutritionally adequate purified diets

To evaluate the impact of dietary factors on gallstone induction in hamsters, male Syrian hamsters were fed for 2-8 wk purified diets that varied in type and amount of simple sugar (glucose vs. lactose, 17.5-72%), fat (2-5%), fiber (0-15%) and estrogen (0 or 300 micrograms/kg diet). Plasma and liver cholesterol and plasma triglycerides were measured, daily weight gain was determined, cecal weights were obtained, and gallbladder bile was scored by light microscopy and analyzed chemically for its lithogenicity and gallstone incidence. Lactose reduced plasma lipids, especially triglycerides, and hepatic cholesterol accumulation, and maintained a lower biliary cholesterol concentration. When fed at 30% or more, lactose reduced weight gain, increased cecal volume 2- to 4-fold and prevented gallstone formation. Diarrhea and death from 'wet tail' was associated with gallstones and was frequent in hamsters fed glucose without fiber, but its incidence was essentially eliminated by rice flour plus fiber or lactose. Under these experimental conditions of time and diet, estrogen supplementation was required for the formation of gallstones. These appeared to be pigment stones containing a minimal amount of cholesterol. In summary, pigment gallstones were induced in less than 8 wk in hamsters fed estrogen-supplemented purified diets. Lactose feeding improved lipid metabolism and reduced gallstone formation, apparently through its impact on large bowel metabolism.     

Dietary taurine alters ascorbic acid metabolism in rats fed diets containing polychlorinated biphenyls

The effect of dietary taurine on ascorbic acid metabolism and hepatic drug-metabolizing enzymes was investigated in rats fed diets containing polychlorinated biphenyls (PCB) to determine whether taurine has an adaptive and protective function in xenobiotic-treated animals. Young male Wistar rats (60 g) were fed diets containing 0 or 0.2 g/kg diet PCB with or without 30 g/kg diet of taurine for 14 d. The rats fed the PCB-containing diets had greater liver weight, higher ascorbic acid concentrations in the liver and spleen and greater hepatic cytochrome P-450 contents than control rats that were not treated with PCB (P < 0.01). In PCB-fed rats, urinary ascorbic acid excretion was enhanced, and serum cholesterol concentration (especially HDL-cholesterol) was significantly elevated compared with those in control rats. Dietary taurine significantly potentiated the increases in the urinary excretion of ascorbic acid and the rise in the levels of cytochrome P-450 which were caused by PCB treatment. On the other hand, the supplementation of taurine to control diet did not alter these variables. Taurine may enhance the hepatic drug-metabolizing systems, leading to the stimulation of the ascorbic acid metabolism in rats fed diets containing PCB.