Physiology of fat replacement and fat reduction: effects of dietary fat and fat substitutes on energy regulation.
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Ubiquinol and the papaverine derivative caroverine prevent the expression of tumour- promoting factors in adenoma and carcinoma colon cancer cells induced by dietary fat.
High consumption of dietary fat promotes colon carcinogenesis. While this effect is well known the underlying mechanism is not understood. Fatty acid hydroperoxides (LOOH) arise from unsaturated fatty acids in the presence of oxygen and elevated temperature during food processing. An approach was made starting from the assumption that LOOH are present in dietary fats as a result of boiling. LOOH undergoes homolytic cleavage in the presence of iron. We studied their effects on gene expression in colorectal tumour cells using linoleic acid hydroperoxide (LOOH) as model compound. Addition to the medium of LT97 adenoma and SW480 carcinoma cells enhanced the production of hydrogen peroxide. Both cell lines were observed to increase VEGF and COX-II expression based on mRNA. Expression of VEGF was inhibited by caroverine and ubiquinon.
Adenoma↗
Enhancement of experimental pancreatic cancer in Syrian golden hamsters by dietary fat.
The effects of dietary fat on the induction and development of pancreatic ductular adenocarcinoma were studied in randombred Syrian golden hamsters. Diets containing low-fat (LF) or high-fat (HF) levels of corn oil [4.5 or 18.0 g/385 kilocalorie (kcal)], contributing 10 or 41% of the calories, respectively, were fed either before or after a single injection of N-nitrosobis(2-oxopropyl)amine (BOP) (10 mg/kg body wt). Control hamsters were fed corn oil at a medium-fat (MD) level (9 g/385 kcal) for life. The incidence of ductular adenocarcinomas increased in both males and females (LF diet, 16%; HF diet, 34%) when the HF diet was fed after BOP treatment. The average number of carcinomas per carcinoma-bearing animal also increased (LF diet, 1.3; HF diet, 3.0), but the carcinoma incidence was not influenced by these diets being fed before carcinogen treatment. The incidence of ductular adenomas was high with all treatments and was not influenced by diet. However, the number of adenomas was increased in animals fed HF diets. In addition, the incidence of acinar cell nodules was elevated in animals fed the MF and HF diets after BOP administration. These results showed that dietary fat modified the development of experimental ductular adenocarcinoma of the pancreas.
Adenoma↗
In vitro studies on the effect of different dietary fats and different proportions of dietary protein on the synthesis of lipids by rat arterial tissue.
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Acetates↗
Recent insights into dietary fats and cardiovascular disease.
1. Fat deposition in the arterial intima is fundamental to the atheroma process. Circulating lipoproteins are thought to be the source of much of the deposited fat. The interplay of dietary fat has not been fully clarified. 2. Observational studies have furnished evidence of relationships between the different dietary fats and clinical cardiovascular events. In these, total fat and in particular, saturated fat appear culprit. Mono-unsaturated (MUFA) and poly-unsaturated (PUFA) fats have less consistent relationships with cardiovascular disease, though all classes of fatty acid are found in atheroma. 3. Comparing the effects on lipoproteins of saturates, mono-unsaturates and polyunsaturates, they all increase high density lipoproteins (HDL) and reduce triglycerides when substituted isocalorically for carbohydrate. Saturates increase low density lipoproteins (LDL), while PUFA > MUFA reduce LDL. 4. Upon oxidative modification, lipoproteins are more liable to arterial deposition and, in vitro at least, LDL oxidizability is enhanced by enrichment with PUFA. 5. Trans-MUFA have some unique properties in that they somewhat resemble saturates and seem to predispose to coronary disease, quite possibly because of their adverse effects on LDL, HDL and Lp(a) levels. 6. omega-3 fatty acids seem unique among the dietary fats in that they inhibit thrombosis and platelet aggregation, and can lower blood pressure. 7. The net effect of these various potential influences of fatty acids on atherogenesis in vivo is unclear. It may well be that all fats, with the exception of the omega-3 class, are detrimental with response to atherogenesis. Modification of the diet, with particular attention to fat, has been demonstrated to reduce clinical coronary events in several studies.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Adaptive response of rat pancreatic lipase to dietary fat: effects of amount and type of fat.
Pancreatic lipase adapts to changes in dietary fat by parallel changes in synthesis. The adaptation to changes in type of dietary fat (saturation or chain length) is unclear. The effects of changes in amount and type of dietary fat were examined in weanling rats fed for 1 wk diets low in fat (LF) with 10% kcal as corn oil, moderate in fat (MF) with 40% kcal as fat (corn oil, lard, safflower oil, butter, olive oil or coconut oil), or high in fat (HF) with 67% kcal as fat (as for MF). Growth was comparable among rats fed these diets. Pancreatic lipase activity increased in all HF diets (180%) compared to the LF diet. In MF diets, only the highly unsaturated safflower oil increased pancreatic lipase (162%) compared to the LF diet. Food consumption varied, but was not related to the response of pancreatic lipase. When weanling rats were fed diets with 11, 40, 47, 54, 67 and 75% kcal as corn oil, pancreatic lipase activity was not stimulated at or below 47% kcal fat, but was maximally stimulated (twofold) by 54 or 67% fat. These findings suggest that pancreatic lipase activity adapts primarily to the amount of dietary fat and responds to the type of fat only below the threshold level of dietary fat (47% kcal).
Amylases↗
Is dietary fat intake related to liking or household availability of high- and low-fat foods?
OBJECTIVE: Despite the increasing availability of low- and reduced-fat foods, Americans continue to consume more fat than recommended, which may be a contributing factor to the obesity epidemic. This investigation examined relationships between liking and household availability of high- and low-fat foods and their association with dietary fat intake. RESEARCH METHODS AND PROCEDURES: A food frequency questionnaire assessed percent calories from fat consumed over the past year in 85 men and 80 women. Participants reported their degree of liking 22 "high-fat foods" (>45% calories from fat) and 22 "low-fat foods" (<18% calories from fat), and the number and percentage (number of high- or low-fat foods/total number of foods x 100) of these high- and low-fat foods in their homes. RESULTS: Hierarchical regression analyses examined the ability of liking and household availability of low- and high-fat foods to predict percent dietary fat intake. After controlling for age, sex, and BMI, liking ratings for high- and low-fat foods and the interaction of liking for low-fat foods by the percentage of low-fat foods in the household were significant predictors of percent dietary fat consumed. Greater liking of high-fat foods and lower liking of low-fat foods, both alone and combined with a lower percentage of low-fat foods in the home, were predictive of higher dietary fat intake. DISCUSSION: Interventions designed to reduce dietary fat intake should target both decreasing liking for high-fat foods and increasing liking for low-fat foods, along with increasing the proportion of low-fat foods in the household.
Adult↗
Lipogenesis and body fat in chicks: effects of calorie-protein ratio and dietary fat.
Two experiments were conducted with battery-reared, broiler chicks from day-old through 19 or 20 days of age. In each experiment, body weight, feed consumption, liver weight, liver fat, body fat, in vivo lipogenesis, and the hepatic activities of the lipogenic enzymes, acetyl-Coenzyme A carboxylase (ACC) and fatty acid synthetase (FAS), were measured. In Experiment 1, four diets having calorie-protein (C/P) ratios expressed as kilocalories of metabolizable energy per kilogram of diet per percent crude protein of 120, 139, 158, or 177 were used. Growth was decreased with ratios above 139. The C/P ratio had no significant effect on feed conversion, liver weight, liver fat, or FAS activity. In vivo lipogenesis and ACC activity were increased by C/P ratios above 120. Body fat increased with increasing C/P ratios, but only the C/P 177 diet produced significantly fatter chicks. In Experiment 2, four diets containing total fat 2.0, 4.1, 6.3, or 8.6% at a constant C/P ratio of 139 were used. All fat levels above 2.0% improved growth and feed conversion. Fat levels had no effect on liver weight, liver fat, or body fat. In vivo lipogenesis and ACC and FAS activities decreased with increasing dietary fat. The data indicate that C/P ratio affects body fat by increasing lipogenic activity as the ratio is increased. Although dietary fat depressed lipogenesis, the depression appears to be offset by increased availability of fatty acids from the diet for deposition in adipose tissue. Hence, added dietary fat does not change body fat content.(ABSTRACT TRUNCATED AT 250 WORDS)
Adipose Tissue↗
In vitro hepatic thyroid hormone deiodination in iron-deficient rats: effect of dietary fat.
The effects of different dietary fats on thyroid indices were studied in weanling iron-deficient rats. Rats were fed one of five different diets (safflower oil with a casein protein source, safflower oil with defatted beef as the protein source, prime rib, beef tallow with casein and stearate with casein). Both dietary fat and iron status (adequate, CN; deficient, ID; or iron-deficient replete, ID-replete) had significant effects on body weight and hemoglobin concentrations. The tallow-fed animals weighed the least relative to animals fed the other fats; ID rats were smaller than CN rats. The tallow- and stearate-fed animals had the highest hemoglobin concentrations. Type of dietary fat affected plasma thyroxine (T4), but not plasma triiodothyronine (T3) or rate of deiodination of reverse T3 (rT3). Iron deficiency decreased plasma concentrations of T3 and T4 and increased in vitro hepatic rT3 deiodination, suggesting that the ID animals tend to metabolize thyroid hormones via deactivating pathways. The alterations in thyroid hormone metabolism associated with iron deficiency are reversible with iron repletion.
Animals↗
Stimulatory effects of high-fat diets on colon cell proliferation depend on the type of dietary fat and site of the colon.
To compare the effects of various types of dietary fat on colon cell proliferation used as an intermediate biomarker for colon carcinogenesis, groups of 10 male Sprague-Dawley rats were fed one of four high-fat diets (45% of total calories from corn oil, butter, beef tallow, and fish oil) for three weeks. As a control, a low-fat diet (15% of total calories from corn oil) was fed to a separate group. Cell proliferation was measured by in vivo incorporation of bromodeoxyuridine into DNA in the proximal and distal colon. Total lipids in feces were measured by a gravimetric method. There were significant differences in colon cell proliferation among the diet groups, where the high corn oil diet stimulated cell proliferation in proximal and distal colon compared with the high fish oil diet (p < 0.05). The protective effect of the high fish oil diet on cell proliferation was similar to that of the low corn oil diet. The effects of high beef tallow and butter diets on colon cell proliferation were highly dependent on sites of the colon, because the hyperproliferative effects by these diets were found only in the distal colon (p < 0.05). Fecal total lipids and fecal lipid concentrations were significantly affected by the dietary fat sources, in that the groups fed the saturated fats, such as butter and beef tallow, excreted more lipids into feces than did the groups fed the unsaturated fats, such as corn oil and fish oil. Fecal lipids were significantly correlated to colon cell proliferation in the way that distal colon cell proliferation increases as fecal lipids increase. Therefore, these data suggest that high levels of dietary fats may not always promote colon carcinogenesis, and the effects may be dependent on the types of dietary fat and sites of the colon.
Animals↗
Relative effects of weight loss and dietary fat modification on serum lipid levels in the dietary treatment of obesity.
The independent effects of weight loss and dietary fat modification on serum lipids were investigated in two groups of healthy moderately obese men and women. In one group (sequential group, n = 19), a weight-stable low-fat, low-saturated-fat diet (Low-Sat) was given for 7 weeks (= dietary modification), followed by a 4.2 MJ/day deficit Low-Sat diet for 13 weeks (i.e., weight loss alone). Another group (simultaneous group, n = 22) received a 4.2 MJ/day deficit Low-Sat diet for 13 weeks (i.e., weight loss+dietary fat modification). Each group was subject to an initial weight-stable high-fat, high-saturated fat diet for 3 weeks and a final weight stable Low-Sat diet for 3 weeks. Both groups lost similar amounts of body weight, about 13 kg, and had similar overall changes in total cholesterol, low density lipoprotein (LDL), cholesterol, high density lipoprotein (HDL) cholesterol, the HDL/LDL ratio, and triglycerides. Analysis of the separate effects of the Low-Sat diet without energy restriction and of weight loss in the sequential group showed that weight loss per se was responsible for about 50% of the total reduction in total cholesterol, and for about 60% and 70% of the fall in LDL cholesterol and triglycerides, respectively. Fat modification without weight loss reduced HDL cholesterol by 11.1% and the HDL/LDL ratio by 7.7%, while weight loss per se led to increases in HDL cholesterol of 12.5% and in the HDL/LDL ratio of 24.0%. We conclude that the effects of reduction in fat and saturated fat intake and weight loss are additive.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Effects of partial replacement of dietary fat by olestra on dietary cholesterol absorption in man.
Olestra, a nonabsorbable fat substitute comprising long-chain fatty acid esters of sucrose, had been previously shown to reduce cholesterol absorption in humans when ingested at a level of 50 g/d. To determine whether or not a lower level of dietary olestra would also reduce cholesterol absorption, we studied the effect of 7 g of olestra twice a day in 20 normocholesterolemic male inpatients in a double-blind, crossover trial. Two 6-day diet treatment and stool collection periods were separated by a 14-day washout period. Half of the subjects received butter, and half, a butter-olestra blend during each treatment period according to a crossover design. All subjects ingested trace amounts of 3H-cholesterol and 14C-beta-sitosterol with the butter or the butter-olestra blend. Cholesterol absorption was determined from the 3H/14C ratios in the diet and in saponified and extracted stools according to previously validated methodology. Cholesterol absorption during the butter regimen was significantly greater than that during the olestra regimen (56.1% +/- 1.6% v 46.7% +/- 1.1%, P less than .01).
Adult↗
Dietary fat and mammary carcinogenesis.
Evidence that dietary fat has an influence on carcinogenesis comes from both epidemiological data and experiments with animals. The experimental studies have indicated that dietary fat acts primarily as a promoter of carcinogenesis and that the effect depends on the type as well as the amount of fat in the diet. Vegetable oils containing polyunsaturated fatty acids of the linoleic acid family (n-6) have been shown to enhance mammary tumorigenesis, but a fish oil containing polyunsaturated fatty acids of the linolenic acid family (n-3) had an inhibitory effect at higher levels of intake. These and other findings suggest that the effect may be related to prostaglandins or other biologically active products of polyunsaturated fatty acids. Epidemiological data show a positive correlation between dietary fat and mortality from cancer at various sites, and this is supported by results of animal experiments in the case of colon cancer and pancreatic cancer as well as breast cancer. In the epidemiological data, cancer mortality shows strong positive correlations with total dietary fat and with animal fat, but not with fat derived from plants. Fats and oils used as spreads, cooking fats, and salad oils are the main source of fat in the American diet. Other major sources are meats and dairy products. Fat intake could probably be reduced substantially without serious deleterious effects, and this might help to decrease the risk of developing certain types of cancer.
9,10-Dimethyl-1,2-benzanthracene↗
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.
Animals↗
Role of dietary fat type in the development of adiposity from dietary obesity-susceptible Sprague-Dawley rats.
The present study was designed to define how dietary fat type regulates body adiposity in dietary obesity-susceptible (DOS) Sprague-Dawley (SD) rats. Eighty-three SD rats received a purified diet containing 50 g maize oil (MO)/kg for 3 weeks and then thirty-nine of the rats, designated as the DOS rats, were allotted to diets containing 160 g MO (DOS-MO), beef tallow (DOS-BT) or fish oil (DOS-FO)/kg for 9 weeks. As a result of the experiment, the DOS-FO rats had significantly (P<0.05) reduced weight gain and abdominal and epididymal fat-pad mass than the DOS-MO and DOS-BT rats. Serum leptin level was also significantly (P<0.05) lower in the DOS-FO rats; however, hypothalamic leptin receptor (a and b) mRNA and neuropeptide Y expressions were not altered by dietary fat sources. A lower acetyl-CoA carboxylase mRNA expression in the liver was observed in the DOS-FO group, whereas hepatic peroxisome proliferator-activated receptor-gamma mRNA and protein expressions were markedly elevated in the DOS-FO group compared with those in the other groups. We did not observe differences in acetyl-CoA carboxylase and peroxisome proliferator-activated receptor-gamma expressions in epididymal fat of the DOS rats consuming MO, BT or FO. It is concluded from our present observations that dietary fat type, especially that rich in FO, plays a potential role in down-regulation of adiposity by altering hepatic lipogenic genes, rather than feeding behaviour, in the DOS-SD rats.
Acetyl-CoA Carboxylase↗
Lactational responses of dairy cows fed unsaturated dietary fat and receiving bovine somatotropin.
Feeding unsaturated dietary fat to lactating dairy cows receiving bST may effectively alter the fatty acid composition of milk fat. This was tested using 16 Holstein cows assigned to one of four treatments during midlactation. Treatments were control, control diet with 15.5 mg of bST/d per cow, dietary fat from sunflower seeds and bST, or dietary fat from safflower seeds and bST. Diets were formulated to contain 19% CP and contained 25% corn silage, 25% alfalfa hay, and 50% concentrate mix on a DM basis. Milk yield was not significantly higher when bST was administered and increased with added fat diets (29.5, 32.7, 40.0, and 34.1 kg/d for the control, control with bST, sunflower seed with bST, and safflower seed with bST treatments, respectively). Percentage of milk fat was similar for all treatments. Concentrations of long-chain and unsaturated fatty acids in milk were increased slightly by bST and substantially with added fat. Milk protein percentages were not influenced by bST but were reduced by approximately .2 unit with added fat. Added unsaturated dietary fat coupled with bST increased milk yield and produced a greater concentration of unsaturated fatty acids in milk.
Animal Feed↗
Effects of saturated and polyunsaturated dietary fat on the concentrations of HDL subpopulations in African green monkeys.
The effect of the type of dietary fat on the concentrations and compositions of high density lipoprotein (HDL) subpopulations was studied in groups of African green monkeys consuming 40% of calories as fat supplied as saturated fat (P/S = 0.3) or polyunsaturated fat (P/S = 2.2) in the presence of either 0.8 mg or 0.03 mg cholesterol/kcal. Plasma HDL cholesterol concentrations were lower in polyunsaturated fat-fed animals. The distribution of mass among HDL subfractions was assessed by analytic ultracentrifugation (AnUC), density gradient ultracentrifugation (DGUC), and polyacrylamide gradient gel electrophoresis (GGE). This made it possible to characterize and quantitate the HDL subpopulations HDL2b, HDL2a, HDL3a, HDL3b, and HDL3c (arranged in order of decreasing particle size and decreasing cholesterol content). Polyunsaturated fat-fed animals had lower concentrations of the large, cholesterol-rich HDL2b subpopulation, as well as higher concentrations of intermediate size HDL (HDL2a and HDL3a on the high cholesterol diet; HDL3a and HDL3b on the low cholesterol diet). Consistent with the observed fat-related redistribution of HDL mass, the saturated fat-fed monkeys had higher apo A-I/apo A-II ratios. The larger HDL often contained detectable apo E; however, the concentration of apo E in HDL was low in both saturated and polyunsaturated fat-fed animals. Thus, compared to saturated fat, dietary polyunsaturated fat induced the formation of smaller size HDL subpopulations and, therefore, an overall lower cholesterol content per particle for plasma HDL.
Animals↗
Increased dietary fat promotes islet amyloid formation and beta-cell secretory dysfunction in a transgenic mouse model of islet amyloid.
Transgenic mice expressing the amyloidogenic human islet amyloid polypeptide (hIAPP) in their islet beta-cells are a model of islet amyloid formation as it occurs in type 2 diabetes. Our hIAPP transgenic mice developed islet amyloid when fed a breeder chow but not regular chow. Because the breeder chow contained increased amounts of fat, we hypothesized that increased dietary fat enhances islet amyloid formation. To test this hypothesis, we fed male hIAPP transgenic and nontransgenic control mice diets containing 15% (low fat), 30% (medium fat), or 45% (high fat) of calories derived from fat for 12 months, and we measured islet amyloid, islet endocrine cell composition, and beta-cell function. Increased dietary fat in hIAPP transgenic mice was associated with a dose-dependent increase in both the prevalence (percentage of islets containing amyloid deposits; 34 +/- 8, 45 +/- 8, and 58 +/- 10%, P < 0.05) and severity (percentage of islet area occupied by amyloid; 0.8 +/- 0.5, 1.0 +/- 0.5, and 4.6 +/- 2.5%, P = 0.05) of islet amyloid. In addition, in these hIAPP transgenic mice, there was a dose-dependent decrease in the proportion of islet area comprising beta-cells, with no significant change in islet size. In contrast, nontransgenic mice adapted to diet-induced obesity by increasing their islet size more than twofold. Increased dietary fat was associated with impaired insulin secretion in hIAPP transgenic (P = 0.05) but not nontransgenic mice. In summary, dietary fat enhances both the prevalence and severity of islet amyloid and leads to beta-cell loss and impaired insulin secretion. Because both morphologic and functional defects are present in hIAPP transgenic mice, this would suggest that the effect of dietary fat to enhance islet amyloid formation might play a role in the pathogenesis of the islet lesion of type 2 diabetes in humans.
Amyloid↗