Dietary Fat Manipulation Research Articles

ApoE genotype, cardiovascular risk and responsiveness to dietary fat manipulation

Cardiovascular risk is determined by the complex interactions between genetic and environmental factors. The apoE genotype represents the most-widely-studied single nucleotide polymorphism in relation to CVD risk, with >3600 publications cited in PubMed. Although originally described as a mediator of lipoprotein metabolism, the lipoprotein-independent functions of apoE are being increasingly recognised, with limited data available on the potential impact of genotype on these metabolic processes. Furthermore, although meta-analyses suggest that apoE4 carriers may have a 40-50% increased CVD risk, the associations reported in individual studies are highly heterogeneous and it is recognised that environmental factors such as smoking status and dietary fat composition influence genotype-phenotype associations. However, information is often derived from observational studies or small intervention trials in which retrospective genotyping of the cohort results in small group sizes in the rarer E2 and E4 subgroups. Either larger well-standardised intervention trials or smaller trials with prospective recruitment according to apoE genotype are needed to fully establish the impact of diet on genotype-CVD associations and to establish the potential of dietary strategies such as reduced total fat, saturated fat, or increased antioxidant intakes to counteract the increased CVD burden in apoE4 carriers.

Dietary fat and body weight control.

The global obesity epidemic has heightened the debate about dietary factors contributing to weight gain. Media stories have promulgated the notion that obesity has increased despite reductions in dietary fat intake. Some have even speculated that lower dietary fat levels may be driving the rapid rise in weight gain within the population. A close examination of the science reveals a different picture and supports the hypothesis that dietary fat, within the context of the total dietary composition consumed by many populations, promotes obesity. Hence, dietary fat control is still an important strategy as part of an overall approach to body weight management in our modern environment. Dietary fat increases the energy density of foods. Abundant evidence from preclinical and clinical studies indicates that fat promotes excess energy intake and positive energy balance. Dietary fat does not promote its own oxidation in the body and is stored efficiently, promoting a positive fat balance. Thus, both the behavioral and metabolic responses to dietary fat increase the probability of positive energy balance and body fat gain. Restoring fat balance when consuming diets rich in fat requires increasing the size of the body fat mass, increasing physical activity, or reducing dietary fat intake. Numerous epidemiologic, preclinical, and controlled clinical studies have shown that body fat is positively associated with dietary fat intake and that dietary fat manipulation leads to appropriate changes in body fat mass. Finally, data from the National Weight Control Registry, a database of > 3000 individuals who have successfully maintained a substantial weight loss, indicate that moderating dietary fat intake is a key strategy for long-term management of body weight.

Modulation of carbon tetrachloride-induced oxidative stress by dietary fat in rats

Oxidative stress is believed to be involved in the pathophysiology of a number of chronic diseases including atherosclerosis, diabetes, and cataracts and to accelerate the aging process. The aim of this study was to elucidate the role of various dietary fats in the in vivo modulation of CCl 4 induced oxidative stress using rat as a model. Rats were raised on diets enriched with saturated (Beef Tallow), n-9 (Sunola oil), n-6 (Safflower oil) or n-3 (Flaxseed oil) fatty acids and exposed to elevated oxidative stress by administration of CCl 4. Plasma concentration of 8-iso-PGF 2α, antioxidant micronutrients and antioxidant enzymes were measured to examine changes to oxidative stress subsequent to the administration of CCl 4. The fatty acid profiles of plasma and RBC membranes reflected the fats fed in the different diets. CCl 4 administration had no significant effect on fatty acid composition of plasma or RBC lipids. Plasma 8-iso-PGF 2α concentrations were elevated by CCl 4 administration regardless of the dietary fat fed. Within the induced oxidative groups the 8-iso-PGF 2α concentrations were highest in Safflower oil followed by Sunola oil, Tallow and finally Flaxseed oil. Induction of oxidative stress by CCl 4 administration was associated with a significant reduction in Vitamin A content reaching a significantly lower concentration (P <0.05) in the Tallow and Flaxseed oil groups. Vitamin E concentrations were significantly lower (p = 0.01) in the Safflower oil and the Flaxseed oil than in the Tallow diet group following CCl 4 administration. Superoxide Dismutase (SOD) and Glutathione Peroxidase (GSHPx) activities were not affected by dietary fat manipulation. The results of this study indicate that dietary fat can modulate lipid peroxidation and antioxidant defenses when exposed to a pro-oxidant challenge.

Study of Serum Leptin in Cafeteria-Diet-Overfed Rats

In a group of 15 male Wistar rats overfed with cafeteria foods (delivering a mean fat percentage of 60%) during 5 months from the age of 8 weeks and in a control group of 15 rats fed with a standard chow for the same period, serum leptin, insulin and corticosterone were measured by RIA and body composition was determined by dual-energy X-ray absorptiometry. Significantly higher fasting serum concentrations of leptin, insulin and corticosterone were found in the cafeteria-diet group. Fasting leptin concentrations were significantly higher in rats with a body fat percentage of more than 25% compared to the others, irrespective of the type of feeding. The log serum leptin correlated positively with body fat percentage and fasting insulin concentration but not with corticosterone concentration. Leptin concentration corrected for body fat mass was, however, comparable between the two diet groups, while the leptin/insulin ratio was lower in the cafeteria-diet group. In conclusion, chronic overfeeding resulting in an increased body fat percentage in rats is associated with hyperleptinemia, hyperinsulinemia and hypercorticism. Serum leptin levels appear to primarily track total body fat percentage and are unaffected by dietary fat manipulation in cafeteria-diet-induced obese rats.

Dietary fat manipulation and signal transduction in ovine skin

Protection of dietary lipids in a protein matrix prevents biohydrogenation in ruminants and increases the availability of polyunsaturated fatty acids. This alters the composition of the tissue lipids, including the membrane phospholipids, which are important substrates for signal transduction. This study investigates the effects of a diet containing protected fatty acids on the activities of key intracellular kinases in the skin. Two groups of six sheep were offered either a control diet or one containing protected cottonseed, a source of linoleic acid (C18:2), for 3 months. Skin was taken from August to October, and analysed for protein kinase C (PKC), protein kinase A (PKA), mitogen-activated protein kinase (MAPK), phosphotyrosine activity and epidermal growth factor (EGF) receptor content. Skin and wool samples were also taken to measure changes in the fibre characters and follicle function. At the end of the experiment, the mean linoleic acid content of skin phospholipids from sheep fed the protected diet was twice that of the controls. In both groups, PKC activity was significantly elevated in skin taken during September and October compared with August values. However, activities measured in the experimental sheep were higher than in controls. This coincided with a decline in wool production. PKA activity decreased significantly in both groups between August and October. MAPK activities did not alter during the experiment. Western analyses did not reveal differences in phosphotyrosine-positive or EGF receptor bands between the groups.

Comparative Effects of Dietary Fat Manipulation on Fatty Acid Composition of Rat Stomach, Jejunum, and Colon Phospholipids.

The phospholipid fatty acid composition of three parts of gastrointestinal tract (GIT) possessing different functions (stomach, jejunum, and colon) was examined to determine if these gut segments consistently respond to dietary fat. Three groups of eight weanling male Sprague-Dawley rats were fed one of three isocaloric, semi-synthetic, nutritionally adequate diets for six weeks. The fat type in the control diet was primarily beef tallow supplemented with sufficient linoleic acid (18: 2n-6) to prevent essential fatty acid deficiency, the n-6 diet contained high levels of 18:2n-6, and the n-3 diet provided high levels of eicosapentaenoic (20:5n-3) and docosahexaenoic (22:6n-3) acids with similar levels of 18:2n-6 as in the control diet. Feeding the n-3 diet resulted in the incorporation of 20:5n-3 and 22:6n-3 into all the GIT segments examined; however, the incorporation was significantly higher in the jejunum and the colon, compared with that in the stomach, phospholipids. The arachidonic acid (20:4n-6) content was lower in the stomach, jejunum, and colon phospholipids following the feeding of the n-3 diet. The 18: 2n-6 content was found to be higher following consumption of the n-3 diet compared with that found for the control diet. The 20:4n-6 content was significantly higher in the jejunum than in the colon or stomach phospholipids, whereas the 18:2n-6 content was consistently higher in all the GIT segments in animals fed the n-6 diet. This diet group also exhibited lower levels of monounsaturated fatty acids in the stomach and lower levels of saturated fatty acids in the jejunum and the colon phospholipids. Thus, dietary fat manipulations inconsistently influence the phospholipid fatty acid composition of various parts of the GIT, suggesting that the functioning of the stomach, jejunum, and colon may be affected differently by alterations in the type of dietary fat ingested.

Dietary fish oil normalize dyslipidemia and glucose intolerance with unchanged insulin levels in rats fed a high sucrose diet

The aim of this study was to investigate the relationship between the lipid-lowering effects of fish oils and concomitant consequences on glucose tolerance and insulin sensitivity in an experimental animal model of hypertriglyceridemia induced by high sucrose intake. To achieve this goal, male Wistar rats were fed a semi-synthetic sucrose rich diet (SRD) (w/w: 62.3% sucrose, 8% corn oil, 17% protein) for 90 days. At the time, a well established and permanent hypertriglyceridemia accompanied by glucose intolerance was present. After that, one half of the animals continued on the SRD up to 120 days. The other half received an SRD in which the source of fat was substituted by cod liver oil (w/w 7% CLO plus 1% corn oil) from day 90 to 120 (SRD + CLO). Control rats were fed a semi-synthetic diet (CD) (w/w: 62.5% corn starch, 8% corn oil, 17% protein) throughout the 120 days experimental period. Results obtained after the experimental period show that the hypertriglyceridemia and glucose intolerance ensuing long term feeding normal rats with a sucrose-rich diet could be completely reversed mediating no change in circulating insulin levels by shifting the source of fat in the diet from corn oil to cod liver oil. These findings suggest that manipulation of dietary fats may play a role in the management of the lipid disorders associated with glucose intolerance and insulin resistance.

Effects of dietary fat on food intake and brain uptake and oxidation of fatty acids

The present study was designed to investigate (a) whether dietary fat manipulation, quantitatively and/or qualitatively, may influence the transport of fatty acids into the brain and oxidation of fatty acids in the hypothalamus; and (b) if an inhibitor of fatty acid oxidation changed food intake on these diets. Rats were fed for 4 wk 5% or 34% corn oil or tallow diets that were isocaloric and isonitrogenous. It was found that rats fed corn oil diets had significantly higher brain uptake index of palmitate than did rats fed tallow diets. In a second experiment, rats were fed either 30% corn oil or tallow diets and injected with either saline or mercaptoacetate (MA). Both saturated fat diets and mercaptoacetate injection reduced lateral hypothalamic, but not ventromedial hypothalamic fatty acid oxidation. Mercaptoacetate increased food intake only in the corn oil fed rats. It is proposed that these uptake and metabolic changes contribute to alterations in either energy expenditure or feeding behavior.

The effect of dietary fat manipulation on the levels of enteroglucagon immunoreactivity in distal intestinal tissues of weaner and adult Wistar rats

The effect of dietary fat manipulation on the levels of enteroglucagon immunoreactivity in distal intestinal tissues of weaner and adult Wistar rats

Effect of dietary fat on diabetes-induced changes in liver microsomal fatty acid composition and glucose-6-phosphatase activity in rats.

Experimental diabetes may manifest itself in a defect in liver microsomal fatty acid desaturation and increased activity of glucose-6-phosphatase (G-6-Pase). The present study was designed to determine whether these changes could be normalized by a change in the dietary fat consumed. Control and streptozotocin-induced diabetic rats were fed nutritionally adequate diets which varied in fatty acid composition. Fatty acid analysis of liver microsomal phospholipids revealed that non-diabetic control animals fed saturated fat (beef tallow) or a diet high in omega 3 fatty acids (fish oil) exhibited a significantly higher level of 18:2 omega 6 and a lower level of 20:4 omega 6 in the phosphatidylcholine and phosphatidylethanolamine fractions compared with diabetic animals. Control and diabetic animals fed the high linoleic acid diet had similar levels of 18:2 omega 6 in the microsomal phosphatidylcholine and phosphatidylserine fractions. Microsomal G-6-Pase activity was higher in diabetic than in control animals. Activity of G-6-Pase was lower in microsomes of control animals fed the soybean oil or the fish oil diet, but was not significantly reduced in diabetic animals fed high polyunsaturated fats. Blood glucose levels were similar in control groups fed the different diets, but the plasma hemoglobin Alc level was lower in diabetic animals fed the soybean oil diet. Cholesterol and triglyceride levels were lower in diabetic animals fed the fish oil-based diet. The results suggest that dietary fat manipulation has the potential to change at least some of the abnormalities in the microsomal membrane in experimental diabetes.

Effect of Dietary Blackcurrant Seed Oil on Mouse Macrophage Subclasses of Choline and Ethanolamine Glycerophospholipids

There have been reports that dietary gamma-linolenic acid [18:3(n-6)] and alpha-linolenic acid [18:3(n-3)] are capable of regulating cellular eicosanoid biosynthesis and inflammation. Because the eicosanoid cascade is regulated in part by the distribution of arachidonic acid [20:4(n-6)] among phospholipid subclasses, the effects of feeding blackcurrant seed oil [containing 18:3(n-6) and 18:3(n-3)] on the fatty acid composition of diacyl, alkylacyl and alkenylacyl subclasses of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were studied in mouse peritoneal macrophages. After 4 wk of dietary treatment, the relative distribution (mol %) of macrophage phospholipid classes and subclasses was not altered in animals fed blackcurrant seed oil relative to those fed corn oil [containing linoleic acid, 18:2(n-6)]. Macrophages from blackcurrant seed oil-fed animals had reduced levels of PC diacyl 18:3(n-6), 18:3(n-3), 20:3(n-6), 22:5(n-3), and alkylacyl 20:3(n-6), 22:5(n-3) and 22:6(n-3). In general, dietary blackcurrant treatment produced fatty acid alterations in PE subclasses that were similar to those in PC. A major exception, however, was the reduction in 20:4(n-6) levels in all PE subclasses, whereas no effect in PC subclass 20:4(n-6) levels was noted. These findings indicate i) that pronounced differences in the polyunsaturated fatty acid (PUFA) compositions of macrophage PC and PE subclasses exist following dietary fat manipulation and ii) that 18:3(n-6) and 18:3(n-3) feeding can increase potential anti-flammatory precursor levels of 20:3(n-6) and (n-3) PUFA in the macrophage.

The Effect of Dietary Fatty Acids on Response to Pseudomonas Infection in Burned Mice

Since fatty acids influence prostaglandin synthesis, and since both fatty acids and prostaglandins modulate immune function, we investigated the hypothesis that manipulation of dietary fats would affect survival after infection in a murine burn model. Mice were fed for 2 to 3 weeks with diets containing different types and amounts of fat. They were then subjected to a 20% flame burn and infected with Pseudomonas aeruginosa. Survival in the group fed 40% of total calories as fish oil had significantly higher mortality than those fed safflower oil. This difference was not noted at lower fat levels. Similar groups of animals were sacrificed the day after injection. Splenic macrophage production of PGE2 was significantly lower in the fish-oil group, but production of LTB4 and TXB2 were not affected. In vitro tests of T- and B-cell function were not different amongst groups. We conclude that manipulation of dietary fats can alter outcome in this murine model of infection after thermal injury.

AUTHOR'S REPLY

<h3>Introduction</h3> Approximately 16,000 patients per year are left with a chronic change in bowel function and gastrointestinal symptoms following treatment for cancer. This can have a significant impact upon quality of life and even compromise on-going cancer therapy. Previous small studies focusing mainly on patients with gynaecological cancers suggest that bile acid malabsorption (BAM) may be an important cause of radiotherapy-induced diarrhoea. This retrospective study aims to elucidate the prevalence of BAM in patients referred to a specialist gastroenterology clinic which treats patients with consequences of cancer treatments. <h3>Methods</h3> Patients referred to our clinic are managed using a peer reviewed algorithm. If they report diarrhoea, defined as Bristol Stool Chart type 6–7, a routine referral for a SeHCAT (75-selenium homocholic acid taurine) scan is made to exclude BAM. BAM is diagnosed when the SeHCAT 7 day retention is &lt; 15% and is graded mild (10–15%), moderate (5–10%) and severe (&lt; 5%). <h3>Results</h3> Between 2009–2012, 262 patients were referred for a SeHCAT scan. 139 (53.1%) were male (median age 66, range 32–89) and 123 (46.9%) female (median age 61, range 20–86). 79 (37%) patients had been treated for gynaecological, 94 (44%) for urological, 41 (19%) for anorectal and 30 (11%) for upper gastrointestinal tract cancers. A further 18 (7%) were treated for other cancer types (breast, lung and haematological). BAM was diagnosed in 24 patients (25%) treated for urological cancers, with 17% (n = 4) having severe BAM. 46 patients (58%) treated for gynaecological cancers had BAM, severe in 57% (n = 26). BAM was diagnosed in 22 patients (54%) treated for anorectal cancers, with 55% having severe BAM (n = 12). In 15 patients (50%) treated for upper GI cancers, the majority (73%) had severe BAM (n = 11). For patients with other cancer types, BAM was diagnosed in 8 patients (44%) with severe BAM in 2 of these (25%). <h3>Conclusion</h3> The frequency of severe bile acid malabsorption and its impact on quality of life is poorly appreciated amongst those who treat cancer. BAM is a common problem in patients treated for a wide variety of cancers with a number of different treatment modalities. Given the effectiveness of dietary fat manipulation combined with a new generation of bile acid sequestrants, SeHCAT scanning should be a first line in investigating patients with diarrhoea after cancer therapies. <h3>Disclosure of Interest</h3> None Declared

Onset and persistence of changes in intestinal transport following dietary fat manipulation

In this study we determined the time-course for the onset and the loss of the effect of short-term feeding rats isocaloric semisynthetic diets containing a high content of saturated (HS) or polyunsaturated (HP) fatty acids on the jejunal and ileal uptake of medium- and long chain fatty acids, cholesterol and glucose. Animals were fed HP or HS for 3, 7 or 14 days; then the diet was switched to standard Purina rat chow for a further 3, 7 or 14 days. The uptake of medium chain fatty acids was unchanged. The differences between HP and HS in glucose uptake occurred within 3 days, but persisted for 14 days, whereas there were qualitative as well as quantitative changes in the pattern of lipid uptake: differences in uptake of stearic, oleic, linoleic and linolenic acids and cholesterol occurred after 7 days of feeding HP or HS. Jejunal uptake of linoleic acid was greater in HP than HS on day 7, but HS was greater than HP on day 14. The effect of diet on lipid uptake was similar in the jejunum and ileum. The altered uptake of stearic and oleic acids persisted after the rats were switched back to chow, whereas the uptake of the other nutrients became similar. Thus, changes in dietary content of saturated and polyunsaturated fatty acids have early effects on intestinal transport function; some of these changes persist even when animals are returned to feeding on chow; and glucose transport is rapidly altered by dietary changes, whereas lipid uptake changes only after 7 days.(ABSTRACT TRUNCATED AT 250 WORDS)

ラットのバター, マーガリン飼育によるリポ蛋白, 肝細胞膜, 赤血球膜の脂肪酸組成の変化について

It is well recognized that a change of fatty acid composition of plasma lipoproteins and cellular membranes alters membrane fluidity, producing significant influences on the functions of membrane-bound enzymes or lipoprotein receptors. It is important, then, to know whether or to what extent dietary fat manipulation may influence the fatty acid composition of lipoproteins and cellular membranes. We studied fatty acid composition of lipoproteins and membranes of hepatocytes and erythrocytes in rats after feeding of different fats.Wister male rats were divided into two groups which received a diet supplemented with either butter or margarine. After several feeding periods plasma levels of lipids and fatty acid composition of phospholipids in high density lipoprotein (HDL), hepatocyte membranes and erythrocyte membranes were examined. Extraction of total lipids from HDL and hepatocyte membranes was conducted by the method of Folch, and from erythrocytes by the method of Rose. Isolation of total phospholipids was done by thin layer chromatography and fatty acid composition was analyzed by gas liquid chromatography.Plasma levels of triglyceride and phospholipid after two weeks of feeding were significantly higher in the butter-fed rats than in the margarine-fed rats. The difference of cholesterol level did not reach a statistical significance.Fatty acid composition of phospholipids in HDL, hepatocyte and erythrocyte showed a characteristic response for each feeding. The level of linoleic acid in HDL, hepatocyte and erythrocyte was higher in the margarine-fed rats and the level of arachidonic in HDL and hepatocyte was also higher in the margarine-fed rats. The level of oleic acid in HDL and hepatocyte and the level of palmitic acid in hepatocyte were higher in the butter-fed rats. These results show that the fatty acid composition in lipoproteins and cellular membranes responds well to a change of dietary fats.

Dietary fat content influences uptake of hexoses and lipids into rabbit jejunum following ileal resection.

After 6 weeks' feeding on a high-fat or low-fat diet, the in vitro uptake of hexoses and lipids was measured in control rabbits with an intact intestinal tract, and in animals submitted to the surgical removal of the distal half of their small intestine. Jejunal villus height, villus surface area and mucosal surface area were higher in unresected control rabbits fed the low- as compared with the high-fat diet, whereas dietary fat content had no effect on villus morphology in resected animals. Mucosal surface area was similar in control and in resected animals fed the high-fat diet, but was lower in resected than in control animals fed the low-fat diet. The active and passive transport properties of the jejunum were influenced by dietary fat manipulation. These absorption changes were qualitatively and/or quantitatively different in animals with an ileal resection from those in animals with an intact small intestine. Dietary fat manipulation had a different effect on the uptake of each lipid probe. The effective resistance of the intestinal unstirred water layer also adapted to changes in the dietary content of fat, but the changes in uptake of hexoses, fatty acids and cholesterol cannot be simply explained by alterations in this diffusion barrier, or by changes in the villus morphology. These findings indicate the importance of dietary fat on villus structure and transport function and their adaptation to ileal resection.

Changes of arachidonic acid and n − 3 polyunsaturated fatty acids of phospholipid classes in liver, plasma and platelets during dietary fat manipulation

When rats adapted to a fat-free diet were fed a corn oil diet, endogenous n − 9 eicosatrienoic acid (the major polyunsaturated fatty acid) at the C-2 position of both phosphatidylcholine and phosphatidylethanolamine was quickly substituted by arachidonic acid in liver, plasma and platelets. Comparably, under a fish oil diet, the n − 9 was quickly substituted by n − 3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid). In both cases the n − 9 almost disappeared in 6 days. On the other hand, when the dietary process was reversed, arachidonic acid in both the phospholipid classes (especially in phosphatidylcholine) decreased more slowly than the n − 3 in the platelets and the liver mitochondria and microsomes. In platelets, even in linoleate-deficient rats, much arachidonic acid remained. However, arachidonic acid decreased similarly to the n − 3 in the plasma. These results may reveal the physiological significance of arachidonic acid in membrane phospholipids, the replacement of arachidonic acid by the n − 3 and the limitation of the replacement.

Effects of Quantity and Unsaturation of Dietary Fat on Serum Components in Normal and Diabetic Macaca nigra

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.

Studies in serum lipids, with special reference to spontaneous variations and the effect of short-term dietary changes.

Repeated measurements of the fasting and 2-hour postprandial serum lipids (cholesterol, phospholipid, and triglyceride) of "normal" [see table in the PDF file] subjects and subjects with atherosclerotic heart disease when consuming diets of high-, low-, or "normal"-fat content have been made. Triglyceride levels correlated better with the clinical diagnosis of heart disease than did cholesterol or phospholipid levels. The wide fluctuations in triglyceride levels in the same [see table in the PDF file] subject (normal or atherosclerotic) when on a "normal self-selected" diet and the unexpected findings when a short-term (3-day) period of dietary fat manipulation render the value of random triglyceride levels as an indictator of the presence or likely development of atherosclerotic heart disease of little or no value in the individual subject.