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PubMed1992

Development of dietary obesity in rats: influence of amount and composition of dietary fat.

This study was conducted to examine long-term effects of amount and type of dietary fat on body weight and body composition. Adult male Wistar rats were fed high fat (HF; 60% of calories) or low fat (LF; 20% of calories) diets for 28 weeks. Half of the rats in each condition received diets with saturated fat (lard) (S) and the remainder received diets with polyunsaturated fat (corn oil) (U). From 28-39 weeks, HF rats were switched to LF diets (fat type remained constant). From 40-50 weeks, previously HF fed rats were weight-matched to rats in the LF fed groups. HF rats became fatter than LF rats during weeks 1-28 and remained heavier and fatter from weeks 28-39. During weeks 1-28, type of dietary fat had no effect on total body fat in either HF or LF rats, but during period 2 (weeks 28-39), U rats were heavier and fatter than S rats. There was some indication that U diets were associated with greater accumulation of fat in subcutaneous adipose tissue depots than S diets. From 40-50 weeks, rats previously fed the HF diet required less food to maintain their body weight than did LF diet rats. In summary, these results suggest that although both amount and type of dietary fat can affect body weight and body composition, the effects of the type of fat are less than those of amount of dietary fat.

Adipose Tissue↗
PubMed1992

Effects of high and low dietary fat and indomethacin on tumour growth, hormone receptor status and growth factor expression in DMBA-induced rat breast cancer.

The effects of high and low dietary fat (20% vs. 0.5% corn oil), and of the prostaglandin synthetase inhibitor indomethacin (0.005% w/w), on tumour incidence, tumour growth, hormone-receptor status and growth-factor expression were examined in dimethylbenzanthracene (DMBA)-induced rat breast cancer. The high dietary-fat group showed a significantly higher tumour incidence, larger tumour size and larger number of bromodeoxyuridine(BrdU)-positive cells of tumours as compared with those in the low dietary-fat group. Indomethacin reduced tumour incidence significantly, but conversely increased the tumour size and the number of BrdU-positive cells in both the high and the low dietary-fat groups. No significant difference was noted in the hormone-receptor status of the tumours. Growth factors (TGF-alpha and IGF-II) were somewhat highly expressed in the high dietary-fat group as compared with the low dietary-fat group, but indomethacin rather reduced the growth-factor expression. It is concluded that high dietary fat stimulates tumour incidence and tumour proliferation, while indomethacin has dual effects: a stimulating effect on tumour proliferation, but an inhibiting effect on tumour incidence. It is also suggested that hormone-receptor status and growth-factor expression do not play an important role in their stimulating effects on tumour proliferation.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2003

Dietary fat and cardiovascular disease risk: quantity or quality?

When considering dietary fat quantity, there are two main factors to consider, impact on body weight and plasma lipoprotein profiles. Data supporting a major role of dietary fat quantity in determining body weight are weak and may be confounded by differences in energy density, dietary fiber, and dietary protein. With respect to plasma lipoprotein profiles, relatively consistent evidence indicates that under isoweight conditions, decreasing the total fat content of the diet causes an increase in triglyceride and decrease in high-density lipoprotein (HDL) cholesterol levels. When considering dietary fat quality, current evidence suggests that saturated fatty acids tend to increase low-density lipoprotein (LDL) cholesterol levels, whereas monounsaturated and polyunsaturated fatty acids tend to decrease LDL cholesterol levels. Long-chain omega-3 fatty acids, eicosapentaenoic acid (EPA) (20:5n-3) and docosahexaenoic acid (DHA) (22:6n-3), are associated with decreased triglyceride levels in hypertriglyceridemic patients and decreased risk of developing coronary heart disease (CHD). Dietary trans-fatty acids are associated with increased LDL cholesterol levels. Hence, a diet low in saturated and trans-fatty acids, with adequate amounts of monounsaturated and polyunsaturated fatty acids, especially long-chain omega-3 fatty acids, would be recommended to reduce the risk of developing CHD. Additionally, the current data suggest it is necessary to go beyond dietary fat, regardless of whether the emphasis is on quantity or quality, and consider lifestyle. This would include encouraging abstinence from smoking, habitual physical activity, avoidance of weight gain with age, and responsible limited alcohol intake (one drink for females and two drinks for males per day).

Cardiovascular Diseases↗
PubMed1991

Gastric lipase: evidence of an adaptive response to dietary fat in the rabbit.

In the rabbit, the stomach is the only source of preduodenal lipase, and in humans, it is quantitatively the most important. Thus, the adaptive response of gastric and pancreatic lipases to dietary fat was studied in the adult rabbit. Effect of duration was studied by feeding rabbits 12% dietary fat for 1, 2, or 4 weeks or 2.7% for 2 weeks (control). To study the effects of the amount of fat, rabbits were fed the control diet (2.7% fat) or 6% and 12% dietary fat for 2 weeks. The influence of sunflower oil and butter was compared by feeding rabbits 12% dietary fat for 2 weeks. Approximately doubling (6% vs. 2.7%) the usual amount of dietary fat was sufficient to induce a maximum increase in gastric lipase activity in the fundus [+ 66.3% (units per gram tissue) or + 85.2% (units per milligram protein)] and the total stomach mucosa [+ 84.5% (units per mucosa)], whereas pancreatic lipase activity only significantly increased when rabbits were fed 12% dietary fat. A full adaptive response was observed for both gastric and pancreatic lipases after 2 weeks of diet. Triglyceride composition did not noticeably change the adaptive response of both lipolytic enzymes. The present results agree closely with those concerning lingual lipase in the rat and evidence that gastric lipase shows an adaptive response to moderate fat intake. The implications of these findings concerning humans are discussed.

Adaptation, Physiological↗
PubMed1984

Colon cancer and dietary fat, phosphate, and calcium: a hypothesis.

Increased dietary fat was suggested to promote colon cancer by increasing the levels of free ionized fatty acids and bile acids in the colon contents. In the presence of calcium ions the irritating and toxic effects of the free acids on colon epithelial cells could be reduced by being converted to insoluble calcium soaps. The level of supplementary dietary calcium to supply adequate calcium and thus reduce the potential toxicity of dietary fat was considered.

Bile Acids and Salts↗
PubMed1984

Reversal of the promotional effect of high-fat diet on mammary tumorigenesis by subsequent lowering of dietary fat.

Female Sprague-Dawley rats were given 7,12-dimethylbenz(a)anthracene at 50 days of age to induce mammary tumors, and beginning one week later were fed a high-fat, semipurified diet containing 20% sunflowerseed oil to promote tumor development. After another 7 weeks, when one third of the rats had palpable mammary tumors, the rats were randomly assigned to five groups of 31 animals each, with the same number of tumor-bearers in each group. One group was continued on the high-fat diet, another was given a fat-free diet, and the three remaining groups were fed diets containing 10% lard, butter, or coconut oil, respectively. During the next 29 weeks, rats fed the diets containing 0% or 10% fat developed significantly fewer tumors than those continued on the 20% fat diet. The diets containing 10% fat suppressed tumorigenesis at least as effectively as the fat-free diet. Rats fed the 10% butter and 10% lard diets had growth rates comparable to those fed the 20% sunflowerseed-oil diet throughout, and evidence of essential fatty acid deficiency was seen only in rats on the fat-free diet. These results provide additional evidence that high-fat diets promote development of mammary cancer and suggest that reducing the level of dietary fat might help to prevent the development and recurrence of breast cancer in humans.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1983

Effect of dietary fat supplement on lipid metabolism of Holstein Heifers.

Twenty Holstein heifers were fed four rations containing 0, 10, 20, and 30% whole sunflower seed as a source of dietary fat. All rations consisted of alfalfa hay, sunflower hulls, and grain mixtures and were isonitrogenous at 12% crude protein and isocaloric at 2.6 Mcal metabolizable energy per kilogram dry matter. Average body weight gains were not different among treatment groups. Heifers fed sunflower seed (fat) diets consumed less total dry matter, significantly improving growth efficiency (gain/feed). Concentration of total lipid and urea nitrogen in blood serum were increased whereas glucose was depressed with higher amounts of dietary fat. High fat diets (20 and 30%) elevated total lipid, triglyceride, and nonesterified fatty acids in the blood. Total and free cholesterol in blood also were increased, but high density lipoprotein-cholesterol remained unchanged with increasing concentration of dietary fat. Dietary fat was correlated positively with lipid components of blood serum and negatively with glucose.

Animals↗
PubMed1999

Meta-analysis: dietary fat intake, serum estrogen levels, and the risk of breast cancer.

BACKGROUND: There is compelling evidence that estrogens influence breast cancer risk. Since the mid-1980s, dietary fat intervention studies have been conducted to investigate the effect of fat intake on endogenous estrogen levels. To further our understanding of the possible relationship between dietary fat and breast cancer, we conducted a meta-analysis of dietary fat intervention studies that investigated serum estradiol levels, and we reviewed the nature of the evidence provided by prospective analytic studies of fat consumption and breast cancer risk. METHODS: A computerized search of the English language literature on estrogen/estradiol and dietary fat intervention studies published from January 1966 through June 1998 was conducted using the MEDLINE database. Pooled estimates were derived from the change in estradiol levels associated with fat reduction from 13 studies. Analyses were conducted separately for premenopausal and postmenopausal women and in both groups combined. RESULTS AND CONCLUSIONS: Statistically significant reductions in serum estradiol levels of -7.4% (95% confidence interval [CI] = -11.7% to -2.9%) among premenopausal women and -23.0% (95% CI = -27.7% to -18.1%) among postmenopausal women were observed, with an overall -13.4% (95% CI = -16.6% to -10.1%) reduction observed. The greatest reductions occurred in two studies in which dietary fat was reduced to 10%-12% of calories compared with 18%-25% of calories in the other studies. A statistically significant reduction in estradiol levels of -6.6% (95% CI = -10.3% to -2.7%) remained after exclusion of these two studies. Review of prospective analytic epidemiologic studies that allowed for dietary measurement error suggests that the possibility that reducing fat consumption below 20% of calories will reduce breast cancer risk cannot be excluded. IMPLICATIONS: Dietary fat reduction can result in a lowering of serum estradiol levels and such dietary modification may still offer an approach to breast cancer prevention.

Adult↗
PubMed1996

Dietary fat in relation to body fat and intraabdominal adipose tissue: a cross-sectional analysis.

Numerous studies report positive links between dietary fat and adiposity. However, the relation between fat intake and intraabdominal adipose tissue (IAAT), a risk factor for cardiovascular disease and diabetes, is not known. We therefore evaluated the association between dietary fat and adipose tissue stores in 135 white men aged 44 +/- 10 y (mean+/- SD: weight, 86 +/- 14 kg; body fat, 23 +/- 8%) and in 214 white women aged 45 +/- 14 y (weight, 64 +/- 12 kg; body fat, 33 +/- 10%). Dietary intake was estimated from 3-d food records, body composition from hydrostatic weighing, IAAT and subcutaneous abdominal adipose tissue (SCAAT) by computed tomography, and physical activity by using the Baecke Questionnaire. After adjustment for fat-free mass, sex, age, physical activity, and nonfat energy intake, fat intake was weakly correlated with fat mass, explaining only 2% of the variance (partial R2 = 0.018, P < 0.01). In a separate model that evaluated type of fat, saturated fat was positively related (partial R2 = 0.025, P < 0.01) to fat mass after adjustment for fat-free mass, sex, age, physical activity, and nonfat energy intake whereas polyunsaturated fat intake was negatively related (partial R2 = 0.007, P = 0.056). On the basis of partial correlation analyses, dietary fat was also associated with SCAAT adjusted for nonfat energy intake and IAAT (partial R2 = 0.014, P < 0.01), but not IAAT adjusted for nonfat energy intake and SCAAT. However, the association between dietary fat and adjusted SCAAT was not significant after further adjustment for sex, age, and physical activity. Thus, results of this cross-sectional analysis suggest that dietary fat independently plays a very minor role in increasing overall adiposity and does not specifically influence fat accretion in the intraabdominal region.

Adipose Tissue↗
PubMed1980

Effect of dietary fat on the fluidity of platelet membranes.

Dietary fat type was reflected in the phospholipid fatty acid composition of the plasma membrane of rabbit platelets and apparently controlled the fluidity of these membranes. Rabbits were maintained for 6 months on diets that varied in stearic and polyunsaturated fatty acids and thus had different potentials for thrombosis. Microviscosities at 37 C, calculated from the arisotropy of fluorescence from the probe 1,6-diphenyl-1,3,5-hexatriene, were 3.5, 3.4, 2.8 and 2.2 poise for platelet membranes isolated from rabbits whose only source of dietary fat was cocoa butter, milkfat, coconut oil, or corn oil, respectively. The relative findings of the membrane isolates were correlated with the polyunsaturated fatty acid contents of the membrane phospholipids.

Animals↗
PubMed1987

Influence of dietary fat and selenium in initiation and promotion of aflatoxin B1-induced preneoplastic foci in rat liver.

Aflatoxin B1-induced hepatic gamma-glutamyl transpeptidase-positive foci were quantified in rats fed different levels of fat and selenium during either initiation or early promotion. Male Sprague-Dawley rats were divided into 12 groups. One of six experimental diets were fed to groups 1-6 prior to and during aflatoxin B1 exposure (initiation, weeks 1-4.5) and to groups 7-12 during weeks 4.5-15 (promotion). The six experimental diets contained 2 or 20% corn oil, each with either less than 0.02, 0.15 or 2.5 (or 1.9) p.p.m. selenium. When not fed the experimental diets, rats were fed a modified AIN-76A diet. In groups 1-6, 0.03% phenobarbital was added as a promoter to the AIN-76A diet. Individual and interactive effects of selenium and fat were dependent on the stage of carcinogenesis. High dietary fat fed with either less than 0.02 or 0.15 p.p.m. selenium during initiation resulted in a significant increase in the number and size of foci when compared with low fat groups. In rats fed 20% fat and 2.5 p.p.m. selenium during initiation, preneoplastic development was reduced below all low fat groups. In contrast, selenium status but not dietary fat level influenced focal formation during promotion. Rats fed less than 0.02 p.p.m. selenium had a significantly greater percentage of liver section occupied by foci than rats fed either 0.15 or 1.9 p.p.m. selenium. Feeding 1.9 p.p.m. selenium during promotion did not afford greater protection above the 0.15 p.p.m. level. Hepatic glutathione peroxidase activity at week 15 was significantly diminished in animals fed less than 0.02 p.p.m. selenium during promotion. Feeding 1.9 p.p.m. selenium when compared with 0.15 p.p.m. did not result in a consistent increase in enzyme activity. Although differences were observed in growth due to dietary treatment, there were no significant correlations between preneoplastic foci and body weight, food consumption or food efficiency. These findings indicate an interaction between dietary fat and selenium during initiation, but not during early promotion. Furthermore, dietary selenium and fat may function by different mechanisms at different stages of carcinogenesis.

Aflatoxin B1↗
PubMed2002

Changes in the chemical composition of surfactant-like particles secreted by rat small intestine in response to different dietary fats.

Consumption of dietary oil, viz., corn, fish, coconut, or olive, induced the secretion of surfactant-like particles (SLP) in rat intestine. These lipoprotein particles differ in (i) levels of alkaline phosphatase activity, (ii) lipid composition, and (iii) FA composition in response to feeding of different oils. The secreted particles had similar buoyancy (1.07-1.08 g/mL) and cholesterol/phospholipid molar ratios (0.61-0.72) except that feeding coconut oil to rats produced SLP with a low (0.18) cholesterol/phospholipid molar ratio compared to control animals. It is concluded from these observations that feeding different oils induces the secretion of lipoprotein particles in rat intestine with different chemical compositions.

Alkaline Phosphatase↗
PubMed1995

Body fat distribution is a determinant of the high-density lipoprotein response to dietary fat and cholesterol in women.

We have conducted a dietary trial that addressed the factors influencing the variability in plasma lipids in response to dietary fat and cholesterol with a focus on the effects of gender and body fat distribution. Sixty-seven women and 53 men were selected so that overall men and women had a similar mean age, LDL cholesterol, and body mass index. After a 2-week low-fat period subjects were given two liquid supplements for 3 weeks each, one that contained 31 to 40 g fat and 650 to 845 mg cholesterol, and one that was fat free. Measurements included plasma lipids and lipoproteins, glucose, insulin, hepatic triglyceride lipase activity, apolipoprotein E polymorphism, and three indexes of body fat (body mass index, waist girth, and waist-hip ratio). In response to dietary fat and cholesterol supplementation only the changes in HDL cholesterol, especially in HDL2, differed between the sexes. Although on univariate analysis lipoprotein changes were predicted by baseline lipoprotein levels, body mass index, waist girth, waist-hip ratio, hepatic triglyceride lipase activity, and insulin, multiple regression showed only waist-hip ratio to predict changes in HDL2 cholesterol in women and body mass index and baseline HDL2 cholesterol in men. Changes in LDL were predicted by baseline LDL cholesterol in women and apolipoprotein E phenotype and age in men. These studies explain much of the variability that individuals show in lipoprotein changes, especially in the more desirable changes in cholesterol transport in HDL2, in response to eating saturated fat and cholesterol.

Adipose Tissue↗
PubMed2004

Lipoprotein(a) as a marker of coronary artery disease and its association with dietary fat.

OBJECTIVE: The main objectives of the study were to evaluate the effect of dietary fat on plasma lipoprotein(a) [Lp(a)] levels and to study the potential of Lp(a) as a more reliable marker for CAD compared to other lipids and lipoproteins. METHODS: Twenty CAD patients and 20 healthy controls were recruited for the study. Their fasting plasma Lp(a) levels and complete lipid profile were assayed. The fat intake was calculated using 24 hours dietary recall method. The patients and controls were each divided into two subgroups: Group A consuming dietary fat > 30% and Group B consuming dietary fat < or = 30% of the total kilo-calories/day. RESULTS: Results indicated that plasma Lp(a), total serum cholesterol (TC), tryglyceride (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C) and LDL-C/HDL-C ratio of CAD patients were significantly higher than the controls. High fat intake was found to be associated with higher plasma Lp(a) levels (p<0.05) in patients only. No significant correlation was found between Lp(a) levels and other conventional lipoproteins. CONCLUSION: The lack of correlation between Lp(a) and other lipoproteins indicates its potential as an independent risk factor for CAD. High fat intake led to higher plasma Lp(a) levels in patients; hence it would be worthwhile to evaluate the effect of quality and quantity of fat intake on plasma Lp(a) levels in a larger sample size.

Adult↗
PubMed1979

Effect of different dietary fats on daily loss of sterols from the skin of man.

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.

Adult↗
PubMed1969

Effects of dietary fats on plasma lipids and lipoproteins: an hypothesis for the lipid-lowering effect of unsaturated fatty acids.

Several aspects of the effects of dietary fat on plasma lipids and lipoproteins were investigated in 12 subjects during the long-term feeding of formulas containing 40% of their calories as either saturated or unsaturated fats. The changes in fatty acid composition of plasma lipids, shown previously to occur after prolonged feedings of a dietary fat, required 10-14 days to be complete and were synchronous with the effect of the fat on plasma lipid concentrations. The change in lipid concentration occurred in low but not in high density lipoproteins. The effects on lipid levels of the low density lipoproteins were found to occur with little or no effect on the concentration of the protein moiety of these lipoproteins; as a result, cholesterol- and phospholipid to protein ratios in low density lipoproteins fell during unsaturated fat feeding. The effects of dietary fat on plasma phospholipids were studied in detail: the relative amounts of phosphatidylcholine, phosphatidylethanolamine, sphingomyelin, and lysophosphatidylcholine were unaffected by the type of dietary fat. However, the molecular species of phosphatidylcholine were markedly affected. More than 90% of the fatty acids at the alpha-position were saturated during both saturated and unsaturated feedings. In contrast, during unsaturated feedings, linoleate at the beta-position outnumbered oleate by approximately 4:1, whereas during saturated feedings these two types of fatty acids were present in nearly equal amounts.This paper also presents the following hypothesis for the lipid-lowering effect of unsaturated dietary fat: since unsaturated fatty acids occupy a greater area than saturated acids, they alter the spatial configuration of the lipids into which they are incorporated; as a result, fewer lipid molecules can be accommodated by the apoprotein of the low-density lipoproteins (LDL), and thus the lipid content of the lipoprotein is lowered. The experimental findings of this study, while not proving this hypothesis, are consistent with it.

Adult↗
PubMed1995

Regulation of guinea pig very low density lipoprotein secretion rates by dietary fat saturation.

We investigated the effects of dietary fat saturation on very low density lipoprotein (VLDL) production in guinea pigs fed semipurified diets containing 15% (w/w) fat, either corn oil (CO, 58% linoleic acid), lard (LA, 42% oleic and 24% palmitic acids) or palm kernel oil (PK, 52% lauric and 18% myristic acids) for 4 weeks. Animals were given an intravenous injection of Triton WR 1339 to block VLDL catabolism and rates of VLDL triacylglycerol (TAG) and apolipoprotein (apo) B secretion were measured over time. Plasma TAG concentrations increased linearly for 8 h (r = 0.99) and VLDL-TAG secretion rates were significantly higher (P < 0.01) in guinea pigs fed LA (72.7 +/- 14.7 mg/kg-h, n = 12) compared to animals fed PK (55.4 +/- 13.4 mg/kg-h, n = 12) or CO (48.6 +/- 17.5 mg/kg-h, n = 15). VLDL apoB secretion rates were highest in PK-fed animals (3.1 +/- 1.8 mg/kg-h) compared to guinea pigs fed LA (1.5 +/- 0.8 mg/kg-h) or CO (1.1 +/- 0.6 mg/kg-h) diets (P < 0.005). Concurrent with analysis of VLDL secretion, turnover of 125I-labeled LDL was measured. Low density lipoprotein (LDL) fractional catabolic rates were not altered by Triton treatment and LDL apoB specific radioactivity (cpm/microgram) did not change over time indicating that: a) the Triton blockage of VLDL catabolism was complete, and b) there was no direct secretion of LDL by the liver. These data demonstrate that intake of lard increases the rate of VLDL-triacylglycerol secretion and that nascent VLDL particles from the lard and corn oil diet groups have the same relative triacylglycerol content, whereas palm kernel oil intake increases secretion of VLDL particles which have a reduced triacylglycerol content. These results demonstrate that dietary fat chain length and saturation have specific effects on VLDL secretion rates affecting both particle number and composition.

Animals↗