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PubMed2000

Decreasing dietary fat saturation lowers HDL-cholesterol and increases hepatic HDL binding in hamsters.

In order to study the mechanism by which increasing unsaturation of dietary fat lowers HDL-cholesterol levels, we studied various measures of HDL metabolism in hamsters fed with fats with different degrees of saturation. Hamsters were fed on a cholesterol-enriched (1 g/kg) semipurified diet containing 200 g/kg of maize oil, olive oil, or palm oil for 9 weeks. Increasing saturation of dietary fat resulted in increasing concentrations of total plasma cholesterol (4.29 (SD 0.51), 5.30 (SD 0.67) and 5.58 (SD 0.76) mmol/l respectively, n 12) and HDL-cholesterol (3.31 (SD 0.50), 3.91 (SD 0.12) and 3.97 (SD 0.43) mmol/l) and these concentrations were significantly higher (P < 0.05) in the palm-oil and olive-oil-fed hamsters compared with the maize-oil group. Total plasma triacylglycerol levels also increased with increasing fat saturation (1.01 (SD 0.59), 1.56 (SD 0.65) and 2.75 (SD 1.03) mmol/l) and were significantly higher (P < 0.05) in the palm-oil group compared with the olive-oil and maize-oil-fed hamsters. The three diets did not have differential effects on plasma activity levels of lecithin: cholesterol acyltransferase (LCAT) and cholesteryl ester transfer protein (CETP). Levels of phospholipid transfer protein (PLTP) tended to be higher with increasing fat saturation but this effect was not significant. The capacity of liver membranes to bind human HDL3 was significantly higher (P < 0.05) in the hamsters fed with maize oil (810 (SD 100) ng HDL3 protein/mg membrane protein, n 4) compared with those fed on palm oil (655 (SD 56) ng/mg), whereas the olive-oil group had intermediate values (674 (SD 26) ng/mg). The affinity of HDL3 for the binding sites was not affected by the type of dietary fat. Hepatic lipase (EC 3.1.1.3) activity, measured in liver homogenates, increased with increasing fat saturation. We conclude that dietary maize oil, when compared with either olive oil or palm-oil, may lower HDL-cholesterol concentrations by enhancing HDL binding to liver membranes.

Animals↗

PubMed1999

The effect of dietary fat on malondialdehyde concentrations in Fischer 344 rats.

The effects of dietary fat and age on the level of malondialdehyde (MDA), a product of lipid peroxidation, were investigated in cerebellum, kidney, and liver tissues of female Fischer 344 rats. Groups of rats were fed diets containing various levels of corn oil (3, 5, 10, 15, or 20%), starting at 57 days of age, for a duration of 2, 10, or 20 weeks. High fat diets are thought to promote tumor formation, diabetes, and cardiovascular diseases via induction of oxidation stress, and this can begin early in the lifespan. However, it was observed that rats chronically consuming 3 and 5% corn oil diets yielded significantly higher levels of MDA, as analyzed by high-performance liquid chromatography, compared with those fed higher fat diets. After 20 weeks of feeding, the concentration of MDA in each of the three organs studied showed no significant differences among rats consuming diets containing 10, 15, or 20% corn oil. The levels of MDA were highest in the cerebellum, followed by kidney, and lowest in liver. Over the 20-week feeding period, a decrease in MDA level in both cerebellum and liver was observed.

Aging↗

PubMed1997

Dietary fats and lung cancer risk among women: the Missouri Women's Health Study (United States)

In a population-based case-control study of women in Missouri (United States), most of whom were smokers, we obtained information on adult diet to evaluate the effects of dietary fats in relation to lung cancer risk. All newly diagnosed, primary lung cancer cases among women 35 to 84 years of age reported to the Missouri Cancer Registry from 1 January 1993 to 31 January 1994 were invited to participate, as were population-based controls. The analysis focused on interviews obtained from 624 controls and 587 cases. In-person interviews were obtained from 99.0 percent of controls and 60.6 percent of cases. Age and energy-adjusted relative risks suggested a direct relation between risk of lung cancer and intake of dietary fats (e.g., total fat, saturated fat) and frequency of meat consumption. After adjusting for confounders, dietary fats were no longer associated with risk, but the adverse effect of frequent consumption of meat persisted. Risk was elevated about 90 percent (95 percent confidence interval = 1.2-3.0) among women in the highest quintile of red meat intake compared with those in the lowest quintile. Risk estimates associated with red meat consumption, however, were dependent on interview status; the effect was restricted to cases whose dietary information was provided by proxy. In summary, after adjusting for potential confounders and removing data obtained from proxy respondents, dietary fats and consumption of red meat were not associated with lung cancer risk among women in Missouri.

Adult↗

PubMed1978

Dietary fat and cholesterol metabolism in adult rats undergoing rapid tissue repletion.

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.

Animals↗

PubMed1986

Methodological issues in epidemiologic studies of dietary fat and cancer.

Every scientific discipline has unique methodological constraints. Each scientific discipline also has differing degrees of power to resolve different questions. The methods of epidemiology are not exempt from these generalizations. In this brief review, several categories of methodological problems in epidemiological studies of dietary fat and cancer have been cited. Other problems could have been discussed and, several more examples illustrating the occurrence of the problems in research could have been presented. These problems notwithstanding, epidemiologic study of the association of dietary fat to cancer is an essential investigative tool in moving toward a better understanding of the public health impact of dietary fat. There are no known biological universals, and, as persuasive as data from animal models may be, extrapolation from the laboratory environment to human experience always is tentative. Laboratory methods require human validation before application to populations at risk of disease. Given the mutual dependency of epidemiologic studies and laboratory approaches, it is useful that the evidence from both realms be integrated and evaluated together as they are in this volume. Finally, given the limitations of any single epidemiologic method applied to the topic, future progress in understanding the role of dietary fat in cancer cause and prevention must rely on the application of multiple methodologies. By this means, it may be possible to compare and contrast the findings from different approaches to yield insights which would not otherwise be achievable.

Dietary Fats↗

PubMed2001

Defective dietary fat processing in transgenic mice lacking aquaporin-1 water channels.

Immunocytochemistry showed expression of aquaporin-1 (AQP1) water channels at sites involved in dietary fat processing, including intrahepatic cholangiocytes, gallbladder, pancreatic microvascular endothelium, and intestinal lacteals. To determine whether AQP1 has a role in dietary fat digestion and/or absorption, mice were placed on a diet that contained 50% fat. Whereas wild-type mice (3-3.5 wk of age, 10-12 g) gained 49 +/- 5% (SE, n = 50) body weight in 8 days, and heterozygous mice gained 46 +/- 4%, AQP1 null mice gained only 4 +/- 3%; weights became similar after return to a 6% fat diet after 6 days. The null mice on a high-fat diet acquired an oily appearance, developed steatorrhea with increased stool triglyceride content, and manifested serum hypotriglyceridemia. Supplementation of the high-fat diet with pancreatic enzymes partially corrected the decreased weight gain in null mice. Absorption of [(14)C]oleic acid from small intestine was not affected by AQP1 deletion, as determined by blood radioactivity after duodenal infusion. Lipase activity in feces and small intestine was remarkably greater in AQP1 null than wild-type mice on low- and high-fat diets. Fluid collections done in older mice (that are less sensitive to a high-fat diet) by ductal cannulation showed threefold increased pancreatic fluid flow in response to secretin/cholecystokinin, but volumes, pH, and amylase activities were affected little by AQP1 deletion, nor were bile flow rates and bile salt concentrations. Together, these results establish a dietary fat misprocessing defect in AQP1 null mice.

Age Factors↗

PubMed2001

Health benefits of dietary fat reduction by a novel fat replacer: Mimix.

The primary goals of this study were to identify any health benefits of the replacement of dietary fat with a novel fat replacer, Mimix, and to assure that the consumption of this fat replacer did not convey any deleterious health effects. Male, weanling, Fischer 344 rats were fed one of six diets containing between 5 and 20% w/w as fat for 8 weeks. These diets included two high fat diets (safflower oil or lard), a low fat diet and three diets where 15% of the fat in the high fat diets was replaced with various amounts of Mimix. When animals were fed a diet rich in saturated fat they consumed significantly more energy than other diet groups. When 15% saturated fat (lard) was replaced with safflower oil animals adjusted their food intake so that no difference in energy intake was observed between the high safflower diet and the low fat and Mimix diets. When the various Mimix fat replacements were compared to animals fed a high fat lard diet there was incomplete compensation of energy intake. Animals fed the high fat lard diet also had higher glucose and total serum cholesterol than their low fat and fat replacement counterparts. Feeding a high fat safflower oil diet to rats resulted in a significantly lower total serum cholesterol and serum triglyceride than all other diets. Replacement of dietary fat with Mimix demonstrated no deleterious effects on the heart, liver and intestinal tract that were all of normal weight, morphology and colour compared to other diet groups. Body composition analysis demonstrated that animals fed high fat diets had higher body fat mass at the expense of lean body mass. This was most obvious for animals fed high fat lard diets who had heavier epididymal fat pads. These data demonstrate that the replacement of dietary fat with the novel fat replacer Mimix can convey a number of health benefits in the absence of any deleterious effects.

Analysis of Variance↗

PubMed2004

Dietary fat and prostate cancer.

PURPOSE: Data from histopathological and migratory studies suggest that 1 or more late stage environmental promoters are involved in the development of clinical carcinoma of the prostate. Laboratory investigations and variously designed epidemiological studies in man have suggested that dietary fat may be one of these candidate tumor promoters but other studies have questioned this association. The biologically plausible associations that have been hypothesized include total energy consumption, altered androgen metabolism, oxidative stress, specific fatty acid consumption and pesticide intake. We provide a critical appraisal of the existing evidence for an association between dietary fat consumption and prostate cancer, and review the biologically plausible relationships. MATERIALS AND METHODS: All 33 published case-control and cohort studies that examined the relationship between prostate cancer and dietary fat or specific fatty food types were critically appraised. Eight studies suggested a statistically significant association, and many studies noted significant associations for specific types of fatty foods (eg milk or meat) and prostate cancer. RESULTS: In light of the inherent biases in the methodology of studying dietary fat intake and carcinoma of the prostate, we conclude that the evidence is consistent. CONCLUSIONS: Corroborative studies in humans are required to better define this relationship. Prospective studies of dietary intervention should be encouraged.

Androgens↗

PubMed2001

A role for dietary fat in leptin receptor, OB-Rb, function.

Leptin is a hormone believed to control appetite and regulate body weight via receptors in the hypothalamus. Much is known about the structure of the functional, or long, form of the leptin receptor, OB-Rb. However, the mechanism by which the receptor regulates leptin's biological action is unknown. Both the type and amount of dietary fat have been shown to affect factors involved in OB-Rb binding and signaling, as well as the morphology of hypothalamic cell membranes. Thus, the following review article examines possible mechanisms by which dietary fat may affect OB-Rb functioning at the hypothalamic level. Dietary fat can alter the fatty acid make-up of membranes, such as the polyunsaturated:saturated fat ratio, changing membrane fluidity and possibly leading to an enhancement or impairment of the structure and/or function of any membrane-associated receptor complexes. Dietary fat also interferes in biochemical pathways involving leptin, OB-Rb, and other neurons containing neuropeptides under OB-Rb's control, such as neuropeptide Y (NPY), proopiomelanocortin (POMC), and cocaine- and amphetamine-regulated transcript (CART). Increased monounsaturated fat increases cyclic adenosine monophosphate (cAMP) levels, possibly reducing mitogen-activated protein kinase (MAPK) activation and interrupting leptin signaling through Janus kinase/signal tranducers and activators of transcription (JAK/STAT) pathways. Dietary induced alterations in hypothalamic cell membranes, SNS activity, or other factors involved in OB-Rb function form a possible basis for the control of leptin's effects on body composition and appetite. Improving the biological activity of leptin by diet modification may exist as a practical strategy for the treatment of obesity and related disorders.

Animals↗

PubMed1999

Dietary fat type alters glucose metabolism in isolated rat hepatocytes.

Dietary fat type can influence the regulation of carbohydrate metabolism in multiple tissue types. The influence of feeding high-fat (40% of kilocalories) diets containing either menhaden oil (MO) or coconut oil (CO) on hepatic glycogenolytic and gluconeogenic capacities was studied in isolated rat hepatocytes. Estimates of both glycogenolytic and gluconeogenic capacities were performed on hepatocytes isolated from fed and fasted animals, respectively. In MO-fed animals, both basal and hormone-stimulated rates of glucose production were significantly greater than those in CO-fed animals. However, both groups displayed a similar maximal increase in glucose production above basal for glucagon and epinephrine (2.3- and 1.9-fold, respectively). Basal rates of adenosine 3',5'-cyclic phosphate (cAMP) production were not different between groups whereas glucagon-stimulated cAMP production was increased twofold in the MO-fed group. In both MO and CO groups, the addition of 10 nM insulin reduced glucose production in fed animals to similar absolute rates. In animals fasted for 24 hours, gluconeogenic capacity was estimated using 10 mM pyruvate, lactate, or glycerol. Glucose production from all substrates was significantly greater in CO-fed animals. In addition to increased gluconeogenic rates, maximal phosphoenolpyruvate carboxykinase (PEPCK) activity was increased in the CO-fed group. Insulin reduced glucose production in both dietary groups, but the absolute rate of glucose production was 28% greater in the CO-fed group relative to the MO-fed group. In summary, dietary fat type can markedly influence the regulation of hepatic glucose metabolism in multiple metabolic pathways. MO feeding promoted glycogenolysis and sensitivity to insulin whereas CO feeding favored gluconeogenesis and reduced insulin sensitivity.

Journal Article↗

PubMed1985

The role of high levels of dietary fat in 7,12-dimethylbenzanthracene-induced mouse mammary tumorigenesis: lack of an effect on lipid peroxidation.

The effects of dietary fat on 7,12-dimethylbenzanthracene (DMBA)-induced mammary tumorigenesis were examined in BALB/c female mice. In the first experiment, BALB/c mice were treated with a total dose of 1, 3, or 6 mg DMBA to induce mammary tumors. One week after the last dose of DMBA, the mice were placed on a 5% (LF) or 20% (HF) corn oil semi-purified diet. The 20% corn oil diet resulted in a significantly decreased mean tumor latency period in each of the three groups of mice (p less than 0.05). However, the mammary tumor incidences at 11 months after DMBA treatment were the following: 6 mg DMBA (LF-14/32, HF-17/32); 3 mg DMBA (LF-13/50, HF-14/50); 1 mg (LF-2/50, HF-6/50). In the second experiment, prolonged hormonal stimulation by pituitary isografts, but not a HF diet, enhanced the incidence of mammary tumors in BALB/c mice given a threshold dose of DMBA (0.5 mg). In a further attempt to examine the mechanism of the enhancing effects of dietary fat, lipid peroxidation was measured in the microsomal-mitochondrial fractions of the mammary glands by two assays; measurements of conjugated dienes and TBA reactants (malonyldialdehyde). The high fat diet had no effect on the levels of conjugated dienes in mammary cell membrane preparations and decreased the levels of TBA reactants (malonyldialdehyde). The results indicated that a high fat diet did not lead to enhanced levels of lipid peroxidation in preparations of microsomal mitochondrial membranes from mouse mammary glands. The implications of these results are discussed with respect to the role of dietary fat as a promoter of mouse mammary tumorigenesis.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1994

The impact of ractopamine, energy intake, and dietary fat on finisher pig growth performance and carcass merit.

An experiment was conducted to determine the effect of ractopamine, energy intake, dietary fat level, and sex on performance and carcass composition in finishing pigs. Three hundred six barrows and gilts were used in a factorial arrangement of treatments replicated over three seasons. Treatments consisted of two ractopamine levels (0 vs 44.7 mg/d), two sexes (barrows and gilts), two levels of fat addition (0 vs 5% added fat), and four energy intake levels (8.3, 8.9, 9.5, and 10.1 Mcal of ME/d for barrows and 7.7, 8.3, 8.9, and 9.5 Mcal of ME/d for gilts). Diets were formulated to maintain an equal lysine (28.5 g/d) intake at each feeding level through cornstarch dilution of the basal (7.7 Mcal of ME/d) diets. Pigs were fed daily based on a standard feed intake curve and prior weekly body weights. At slaughter (104 kg), carcass measurements and TOBEC HA-1 scanner measurements were recorded. Dietary fat addition improved live weight and lean efficiency (grams of carcass lean gain/kilogram of feed, P < .05). Dietary fat addition did not affect growth rate or carcass composition. Increasing energy intake resulted in a linear increase in average daily gain for both barrows and gilts (P < .01). Dietary ractopamine influenced the response of lean tissue accretion, lean tissue accretion efficiency, and fat tissue accretion to energy intake. Pigs with no added ractopamine demonstrated increased lean tissue accretion and improved efficiency and decreased fat tissue accretion with increasing energy intake (up to 9.5 Mcal of ME intake for barrows and 8.9 Mcal of ME intake for gilts). In contrast, pigs with added ractopamine did not respond to increasing energy intake and demonstrated increased fat tissue accretion with increasing energy intake. The response to ractopamine for growth was greatest from d 6 to 22 on test or during the test gain period of 7 to 18 kg. After d 22, the response of ractopamine declined linearly. These results indicate that ractopamine increases growth rapidly at the onset of feeding until a plateau is reached, after which there is a linear decline in growth response.

Adipose Tissue↗

PubMed1997

Dietary fat affects lipids and anti-cardiolipin antibody levels in autoimmune-prone NZB/W F1 mice.

Studies in autoimmune-prone NZB/W F1 mice have demonstrated that the amount of dietary fat can affect autoantibody production and the disease course of autoimmune diseases. Anti-cardiolipin antibodies have been found to play a major role in thrombus formation and the increase of abortion rate in both human lupus patients and murine lupus. The present study investigated further the effect of dietary fat on lipid and anti-cardiolipin antibody production in autoimmune-prone mice. Two groups of NZB/W F1 mice were fed on diets containing 200 g dietary fat/kg and 50 g dietary fat/kg respectively, the fat being composed of equal amounts of lard and soyabean oil. Serum levels of lipids, immunoglobulin (Ig) anti-single stranded DNA and anti-cardiolipin antibodies were followed regularly every month and mice were killed for in vitro experiments after 5 months on the experimental diets. The results showed that serum triacylglycerol concentration was lower in mice fed on the high-fat diet than in those fed on 50 g fat/kg. There was no significant difference in hepatic lipid contents; however, the fatty acid contents were different between these two groups. Hepatic linoleic acid (18:2n-6) and arachidonic acid (20:4n-6) concentrations were higher in mice fed on the high-fat diet. There were no significant differences in serum IgM concentrations or IgM anti-cardiolipin antibody levels between these two groups. However, IgG anti-cardiolipin antibody levels were higher in mice fed on the high-fat diet at the age of 3-4 months. Total serum IgG concentration was noted to be higher, but in contrast, serum IgA was lower, in the high-dietary-fat group. These findings suggest that high dietary fat may affect lipid metabolism and autoantibody levels in autoimmune diseases.

Animals↗

PubMed1992

Effect of the amount of dietary fat on the development of mammary tumors in BALB/c-MTV mice.

The relationship between dietary fat consumption and the incidence of breast cancer, if any, needs to be quantified so that dietary guidelines can be issued for the prevention of breast cancer. Frequently, only two widely different dietary fat levels, often differing in essential fatty acid content, have been compared in animal models. Moreover, the latent period in common animal models for breast cancer is very short and does not reflect the relatively long latent periods in human breast cancer. We describe a study with BALB/c-MTV mice, a strain with a high average tumor incidence and a latent period of over 60 weeks on average. The mice were fed diets with fat levels ranging from 10% to 40% of energy, in which fat was isocalorically substituted for carbohydrates. The level of linoleic acid in these diets was kept constant at 6.5% of energy. Both the mean tumor incidence and latent periods of the groups fed diets with 10-16% of energy as fat were not significantly different from each other. There were also no differences between these parameters in the groups fed 22-40% of energy as fat. However, the mean incidence and latent period of the groups fed 22% or more of energy as fat was significantly higher than that of the groups fed less fat. We conclude that above about 22% of energy, fat does not influence the incidence and latent period of mammary tumors in BALB/c-MTV mice.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1985

Effects of dietary fat on postprandial substrate oxidation and on carbohydrate and fat balances.

To study the effect of dietary fat on postprandial substrate utilization and nutrient balance, respiratory exchange was determined in seven young men for 1 h before and 9 h after the ingestion of one of three different breakfasts: i.e., bread, jam, and dried meat (482 kcal: 27% protein, 62% carbohydrate, and 11% fat); bread, jam, and dried meat plus 50 g of margarine containing long-chain triglycerides (LCT); or bread, jam, and dried meat plus 40 g medium-chain triglycerides (MCT) and 10 g LCT margarine (858 kcal: 15% protein, 35% carbohydrate, and 50% fat). Plasma glucose concentrations peaked 45 min after the start of the meals. When compared with the low fat meal, the LCT margarine supplement had no effect at any time on circulating glucose and insulin concentrations, nor on the respiratory quotient. When MCTs were consumed, plasma glucose and insulin concentrations remained lower and plasma FFA concentrations higher during the first 2 h. 9 h after the breakfasts, the amounts of substrates oxidized were similar in each case, i.e., approximately 320, 355, and 125 kcal for carbohydrate, fat, and protein, respectively. This resulted in comparable carbohydrate (mean +/- SD = -22 +/- 32, -22 +/- 37, and -24 +/- 22 kcal) and protein balances (-7 +/- 9, +7 +/- 7, and -8 +/- 11 kcal) after the low fat, LCT- and MCT-supplemented test meals, respectively. However, after the low fat meal, the lipid balance was negative (-287 +/- 60 kcal), which differed significantly (P less than 0.001) from the fat balances after the LCT- and MCT-supplemented meals, i.e., +60 +/- 33 and +57 +/- 25 kcal, respectively. The results demonstrate that the rates of fat and of carbohydrate oxidation are not influenced by the fat content of a meal.

Blood Glucose↗

PubMed1988

Effects of type and amount of dietary fat on rabbit and rat lymphocyte proliferation in vitro.

To investigate whether dietary linoleic acid inhibits lymphocyte proliferation, rabbits were fed diets containing 35% of the digestible energy (35 en%) as sunflower seed oil (25 en% linoleic acid) or palm oil (3.5 en% linoleic acid). No differences in the mitogen-induced proliferation of peripheral blood lymphocytes (PBL) or splenocytes or in the effect of sera on PBL proliferation were observed. To investigate whether the amount of dietary fat affects lymphocyte proliferation, rats were fed diets containing 10 or 35 en% as fat. No difference in the mitogen-induced proliferation of splenocytes was obtained. However, serum from fed rats but not from fasted rats of the 35 en% fat group inhibited splenocyte proliferation, in comparison with serum from rats of the 10 en% fat group. Removing chylomicrons from the sera did not affect proliferation. The very low density lipoprotein + chylomicron fraction of the plasma inhibited proliferation. The inhibition was stronger for the 35 en% fat group than for the 10 en% fat group and was increased by fasting. No systematic differences in the effects on proliferation were obtained with the low or high density lipoprotein fractions of both groups. Diets containing a high amount of linoleic acid do not inhibit lymphocyte proliferation. The amount of dietary fat might affect lymphocyte proliferation through one or more factors in the plasma.

Animals↗

PubMed1984

Effects of saturated and unsaturated dietary fat on aflatoxin B1 metabolism.

Male Fisher 344 rats were fed diets containing either 20% corn oil, 20% coconut oil or 18% coconut oil plus 2% corn oil for 3 wk. A single dose of [3H]aflatoxin B1 [(3H]AFB1) was administered ip and the biliary excretion of aflatoxin metabolites and the binding of 3H to nucleic acids were studied. In other experiments the in vitro metabolism of AFB1 by liver postmitochondrial supernatants prepared from rats fed the different sources of dietary fat was determined. The major nonextractable aqueous metabolite of AFB1 was the aflatoxin B1-glutathione conjugate (AFB1-GSH). Variation in the source of dietary fat did not affect production of the conjugate, nor was in vivo binding of AFB1 to nucleic acids affected. Aflatoxin P1 ( AFP1 )--mostly conjugated--and aflatoxin M1 (AFM1) were also identified in the bile, and the quantities of these metabolites produced were unaffected by the dietary treatments. The metabolites recovered in the in vitro study included aflatoxins Q1, P1 and M1. The corn oil diet produced a higher microsomal cytochrome P-450 level than the coconut oil diet. Associated with the higher level of cytochrome P-450 was increased in vitro conversion of AFB1 to AFQ1 and AFM1, but not to AFP1 . The in vitro production of aqueous metabolites and the covalent binding of metabolites to protein was unaffected by the dietary treatments. The results of the in vivo and in vitro studies suggest that the formation of the putative carcinogenic metabolite, AFB1-epoxide, which undergoes detoxification through glutathione conjugation, is not affected by the type of dietary fat. These observations further suggest that dietary fat, in particular unsaturated fat, affects AFB1 carcinogenesis through a mechanism other than by alteration of the metabolic activation of AFB1.

Aflatoxin B1↗

PubMedDate not supplied

Assessing dietary fat intake in chronic disease rehabilitation programs.

PURPOSE: Previous work has established that the Heart Fit Rx Diet Habits Survey (HFD), formerly the Food Frequency Assessment Tool, compares favorably (r = 0.78; P <.01) with the Oregon Health Sciences University Diet Habit Survey. The purpose of this study was to assess the validity and reliability of the HFD in estimating fat intake as a percentage of calories. METHODS: The validity study assessed 137 patients undergoing cardiac rehabilitation (age, 60.7 +/- 11.3 years) who completed the HFD (29 questions, 11 of which were dietary fat related [fat subscore]) and a 3-day food record. A regression equation was obtained using HFD subscores to estimate fat intake as a percentage of calories. The regression equation was tested using 50 patients not included in the original cohort. Reliability was assessed using a third group of 31 patients in a 4-week test-retest analysis. RESULTS: The correlation coefficient between the 3-day record and the HFD fat subscore was 0.65 (P <.01). The correlation coefficient for women (r = 0.77) was slightly higher than for men (r = 0.62). The regression equation derived from the HFD fat subscore was as follows: percentage of dietary fat = 50.65 - 0.736 (HFD fat subscore). The correlation coefficient for actual and predicted values was 0.58 (P <.01). Differences between estimated fat intake, as determined by the 3-day record and the HFD, ranged from 0% to 25% and were within 5% for 26 of the 50 subjects (52%), and within 10% for 41 of the 50 subjects (82%). The mean difference between the two measures was 1.5% (P =.17). Test-retest reliability was high for both the HFD total score (r = 0.95) and the HFD fat subscore (r = 0.85; P <.01). CONCLUSIONS: The HFD is an inexpensive, valid, and reliable clinical instrument for assessing dietary fat. It can be a viable alternative to other time-consuming methods, including computerized analysis.

Aged↗