SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
A single i.p. dose of aflatoxin B1 had no significant effect on the thrombotest clotting times of monkeys subsisting on low-fat and high-fat dietary regimens, respectively. There was a significant interaction between aflatoxin and dietary fat level.
The knowledge of the trace metal contents in dietary fats is of considerable interest from the viewpoints of food hygiene and and storage stability. In the framework of the present paper, it is dealt with the determination of the ionogenically bound heavy metals copper, iron, nickel, zinc, lead and cadmium by means of flameless atomic absorption spectrometry (AAS). Problems related to trace analysis in dietary fats are discussed. Problem-oriented surveys in the form of tables inform about:--analytical conditions of the AAS technique,--metal contents as compared to data with the approved standard method,--contents of the ionogenically bound toxic trace elements cadmium, zinc and lead in samples of various dietary fats currently used in the German Democratic Republic.
Explore the source record for details and available documents.
Of the trace elements, mercury holds an exceptional position as to its chemico-physical and toxic properties. In the light of the special analytical problem, the methods used (cold-steam AAS in combination with the addition method) are discussed. The experimental conditions required for the digestion and the cold-steam AAS of samples of emulsifiers and dietary fats are indicated. The accuracy and the reproducibility of the procedure are dealt with, and the amounts of mercury found in products of the oil and margarine industries are reported.
The influence of dietary fat on prostaglandin production and lipolysis was tested in basal and norepinephrine stimulated adipocytes isolated from the epididymal fat pads of fasted rats. Seven diets varying in fat calories and polyunsaturation were utilized. No basal differences were noted for prostaglandin E2 production or lipolysis. Norepinephrine stimulated prostaglandin E2 and F2alpha production was significantly (P less than 0.01) increased with greater polyunsaturation of fat, but not by increased fat calories. Norepinephrine stimulated lipolysis was depressed by an increase in fat calories but was unaffected by the degree of polyunsaturation of fat. This is in vitro evidence against the concept that prostaglandins play a feedback regulator role in fat cell lipolysis since no correlation could be made between the two parameters.
We studied the effect of polyunsaturated dietary fat upon the 24-hour loss of cholesterol and other sterols from the skin surface of 4 human subjects. They were fed cholesterol-free diets which provided 40% of the total caloric intake from saturated fat (cocoa butter) and then a highly polyunsaturated fat (corn oil). In both dietary fat periods, the daily loss of cholesterol through the skin was similar, 91 and 87 mg in the saturated and polyunsaturated fat periods, respectively. 87 and 89% of the total cholesterol were in the esterified form in the saturated and polyunsaturated dietary fat periods. The sterol composition of the skin surface lipid was not altered. The study suggests that the plasma cholesterol-lowering effect of dietary polyunsaturated fat was not mediated by a change in the loss of cholesterol through human skin.
One hundred and forty-four day-old chicks were allotted to six groups in a 2 x 3 factorial design involving two strains (dwarf, dw and non-dwarf, Dw+) and three levels of supplemental dietary fat (none, moderate and high). The birds were killed at four weeks of age. The overall weight gain and the total lipid content, amount of neutral lipids, glycolipids and phospholipids in the epiphyseal cartilage of the tibia were examined. Supplemental dietary fat resulted in improved weight gain, with the non-dwarfs showing a greater increase. There was no change in total lipid in epiphyseal cartilage with different levels of dietary fat. Increase in dietary fat elicited, in both strains of birds, an increase in the proportion of glycolipids and a concomitant decrease in the proportion of neutral lipids and no change in that of phospholipids. That the stimulatory effect of dietary fat on growth was exerted through an increase in glycolipids at the site of calcification is suggested.
Dietary fats have a pronounced effect on arterial thrombosis: in rats, long-chain saturated fatty acids are thrombogenic, oleic acid is neutral, and linoleic acid is anti-thrombotic. These effects are likely to be mediated, at least in part, by changes in platelet fatty acid composition and--consequently--platelet function. Blood coagulability and differences in vitamin E intake seem of no (or minor) importance. In man, dietary linoleic acid inhibits platelet aggregation and other parameters of platelet activation. Dietary fat effects on vascular prostacyclin formation have not yet been found.
The direct and indirect evidence that the fatty acid composition of dietary fat is involved in the regulation of prostaglandin biosynthesis was reviewed. Direct evidence included effects of essential fatty acid deficiencies and excesses on endogenous tissue levels and production rates of prostaglandins by several tissues. Indirect evidence included lipolytic, platelet aggregatory, hypertensive, inflammatory and immune responses. In general, composition of dietary fat did not affect prostaglandin biosynthesis unless a biochemical essential fatty acid deficiency was induced or the linoleate to saturated fatty acids ratio of the dietary fat was greater than 5. Most results were interpreted in light of changing fatty acid composition; however, very few direct measurements have been made.
The effects of various dietary fats on the activity of 3-hydroxy-3-methylglutaryl-Coenzyme A (HMG-CoA) reductase in rat liver microsomes, the rate-limiting enzyme in cholesterogenesis, were examined. A series of experiments demonstrated the dependency of the HMG-CoA reductase activity on the nature of dietary fats. When saturated fats with chain length of 12 to 18 were the dietary sources and were fed at the 10% level for 19 days, feeding fats with shorter chain fatty acids caused a lower enzyme activity compared to those with longer chain fatty acids. The activity was also regulated by the degree of unsaturation of dietary fats; when safflower oil, camellia oil or tristearin were fed at the 10% level for 18 days, the higher the unsaturation, the lower the activity. When trimyristin or tripalmitin were fed at the 10% level for 14 days, addition of essential fatty acid, at the level of minimum daily requirement (1% was replaced by safflower oil), did not affect the enzyme activity. Through the rate of incorporation of mevalonate into cholesterol in the 12,500 x g supernatant fraction of the liver was also found to be influenced by the types of dietary fats, the extent of the response appeared much smaller than that of HMG-CoA reductase. No consistent correlation between the HMG-CoA reductase activity and the content of microsomal cholesterol or cholesteryl ester and the fatty acid composition of microsomal lipids was observed.
The effects of different dietary fats on ovine adipose tissue metabolism have been investigated. Six-month old sheep were fed for 6 weeks a control diet or diets supplemented with either tallow or a mixture of sunflower seed oil and soybean oil, treated to protect the fats from hydrolysis and hydrogenation in the rumen, or with maize oil. The rates of fatty acid, glyceride glycerol, and CO2 formation were measured in perirenal and subcutaneous adipose tissue slices by following the incorporation of either 14C from labeled acetate or glucose, or 3H from tritiated water into the appropriate product. Feeding protected tallow or maize oil but not protected sunflower seed oil plus soybean oil resulted in reduced rates of fatty acid biosynthesis in both perirenal and subcutaneous adipose tissue slices and CO2 formation in perirenal adipose tissue. Feeding the fat-supplemented diets had no effect on the rate of glyceride glycerol formation. The fat-supplemented diets also resulted in reduced activities of various enzymes, thought to be involved in lipogenesis, measured in 105,000 x g supernatant fractions from adipose tissue homogenates. The results suggested that ovine adipose tissue lipogenesis is sensitive to both the amount and the nature of dietary fat.
Recent speculation concerning the relationship of dietary fat and cancer causation is challenged. Correlations between increase in per capita dietary fat intake and cancer mortality over a 60-year period show significant positive correlations for total fat and vegetable fat, and negative or no correlation for animal fat. The significant positive correlation for vegetable fat could not always be explained by the effects of total unsaturated components; individual unsaturated components, such as oleic or linoleic fatty acids; or the saturated component; but could be explained by the trans fatty acid component.
An experimental model in which adult rats underwent rapid rates of tissue repletion after dietary restriction served to explore the influence of dietary fat on cholesterol metabolism. Adult rats severely restricted in protein and energy were refed either 8 or 24 hours per day for 10 days. Refeeding diets contained approximately 0% or 20% fat by weight as safflower oil or beef tallow and 4% or 17% protein on an energy basis. Concentration or source of dietary fat did not significantly influence either serum or hepatic cholesterol concentrations. Inclusion of dietary fat increased incorporation of 3H-acetate into digitonin precipitable sterols although type of fat did not influence this parameter. Specific activities of serum and hepatic cholesterol were identical for rats fed with diets containing safflower oil and beef tallow, but an elevation in acidic 14C-steroid excretion per g diet consumed occurred with safflower oil as compared with beef tallow. The data suggest that, in the absence of exogenous cholesterol, high levels of polyunsaturated fat may influence cholesterol metabolism primarily by increasing synthesis and excretion of bile acids.
Female Sprague-Dawley rats were fed semipurified diets containing various fats, either alone or in combination, to provide different amounts of dietary fat and linoleic acid. One week before commencing the diets, each rat received an intra-gastric dose of the carcinogen 7,12-dimethylbenz[a]anthracene. Rats fed diets containing mixtures of 3% sunflower seed oil and 17% of either tallow or coconut oil developed twice as many tumors as those fed 3% sunflower seed oil or 20% of either saturated fat alone. Tumor yields in the rats fed these mixed-fat diets were comparable to those in rats fed a 20% lard diet, which provided about the same amount of linoleic acid. No further increase in tumor yield was observed in rats fed a 20% sunflower seed oil diet that contained more than five times as much linoleic acid. These results show that a certain amount of polyunsaturated fat, as well as a high level of dietary fat, is required to promote mammary carcinogenesis.
Adult male BHE rats were fed diets containing 15% of either corn oil (CO) or medium chain triglycerides (MCT) as the dietary source of fat. Further, rats were allowed to remain sedentary or were forced to exercise by swimming for 1 hour daily, for 3 weeks, followed by swimming for 2 hours daily for 3 weeks. The exercise for 3 weeks caused significant reductions in average body weight gains. After 6 weeks of exercise the lipid content of the adipose cells was reduced by about 50%. Fat cell numbers were not changed by either fat source or exercise, but fat cell size was significantly reduced after swimming daily for 6 weeks.
To examine the effect of dietary fat on lung lipids, male weanling mice (CD-1 strain) were fed purified diets containing 5% stripped lard or corn oil and kept in chambers supplied with air filtered free of airborne bacteria. Vitamin E was fed at 0, 10.5 or 105 mg dl-alpha-tocopheryl acetate/kg diet. Dietary fat and vitamin E (0 or 10.5 mg/kg) had no significant effects on the lung levels of triacylglycerol (TG) or phospholipid (PL) molecular species through 4 weeks of intake. Alterations in lung fatty acid composition were followed through 6 weeks of intake at 0, 10.5 and 105 mg vitamin E/kg diet. Vitamin E, at all levels of supplementation, had no significant effect on mouse lung fatty acid composition. Saturated fatty acids of the lung also showed little alteration by diet, but feeding the lard diet significantly elevated oleic and palmitoleic acids. In mice fed the corn oil diet the levels of linoleic acid (18:2) were twice those of lard-fed mice, and arachidonic acid (20:4) was elevated by 15.8%. The diet elevated the mean peroxidizability index (PI) on lung tissue in corn oil-fed mice.
Dietary fat affects serum lipids independently of dietary cholesterol. Normal and diabetic monkeys (Macaca nigra) were fed cereal-based, specially formulated diets with either a low fat (LF = 2.5%) or a higher fat (13.2%) content; the latter had varying concentrations of safflower and coconut oil to attain greater polyunsaturation (SFO) or saturation (CCO) in the diets. Dietary cholesterol was less than 0.01%. Serum triglyceride concentrations were greatest when monkeys consumed the LF (higher carbohydrate) diet and lowest when they consumed the SFO diet. Concentrations were greater in diabetic than in normal monkeys fed the LF and SFO diets, but both groups had similar concentrations when fed the CCO diet. Cholesterol levels in diabetic monkeys were only slightly higher than in normals regardless of diet; in both groups, levels were lowest when the LF diet was fed and highest when the CCO diet was fed. The quantity of fat had a greater effect on serum cholesterol than did the degree of polyunsaturation. In both groups, triglyceride concentrations correlated significantly with VLDL protein, and cholesterol levels correlated with LDL protein. Thus the responses of Macaca nigra to dietary fat manipulation depend upon both the diet fat content and composition as well as the normal or diabetic metabolic state of each monkey.
The time course of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase activity and lipogenesis and cholesterogenesis from 1-14C-acetate and 2-14C-mevalonate was examined in the liver of rats refed diets containing different fats at the 10% level after 48 hr fasting. Fasting caused a profound depression of the reductase activity and sterol and fatty acid synthesis. In rats refed for 30 hr, the activity of HMG-CoA reductase was restored to about one-half of the level observed in prefasting rats, irrespective of the type of dietary fats. When safflower oil and trilaurin were dietary fats, the activity remained this level until 78 hr, then declined, whereas with tristearin, activity progressively increased until 78 hr. On refeeding for 174 to 222hr, the reductase activity was significantly higher in the tristearin than in the trilaurin group. Similar patterns were demonstrated in cholesterogenesis either from acetate or mevalonate, though extents of activation after refeeding were markedly different in these precursors. Dietary fat dependent changes in the content of hepatic cholesterol and in the concentration of plasma cholesterol were also observed.