Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DIETARY FATS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources
PubMed1987

Inhibition of chemically induced mammary and colon tumor promotion by caloric restriction in rats fed increased dietary fat.

Tumor promotion associated with increased dietary fat may be inhibited by reduction in total caloric intake. This hypothesis was tested in rats given either 7,12-dimethylbenz(a)anthracene to induce mammary tumors or 1,2-dimethylhydrazine to induce colon tumors. One week after dosage with either carcinogen, the rats were fed semipurified diets that provided 4% fat with ad libitum calories or 13.1% fat with a reduction of calories by 40% from ad libitum intake. Rats treated with 7,12-dimethylbenz(a)anthracene and subjected to caloric restriction weighed 40% less than those fed ad libitum; rats treated with 1,2-dimethylhydrazine were heavier at the onset of caloric restriction and lost weight and weighed approximately 40% less than animals fed ad libitum. At 20 weeks after 7,12-dimethylbenz(a)anthracene administration, rats fed ad libitum had 80% tumor incidence while in those fed restricted calories, 20% had tumors (P less than 0.001). All other measures of mammary tumor growth were significantly reduced in rats given restricted calories. Six months after 1,2-dimethylhydrazine administration, colon tumor incidence was 100% in rats fed ad libitum and 53% in those fed the calorie-restricted diet (P less than 0.001). This reduction of colonic carcinogenesis was seen despite a significant increase in mucosal labeling index following [3H]thymidine autoradiography. This paradoxical finding may be due to the increased fat content of the calorie-restricted diet. These data demonstrate that the tumor-promoting effects of dietary fat can be more than offset by a reduction in total caloric intake and that the promoting effect of fat may be due, at least in part, to its greater caloric density.

Animals↗
PubMed1998

Is dietary fat a major determinant of body fat?

The percentage of energy from dietary fat is widely believed to be an important determinant of body fat, and several mechanisms have been proposed to account for such a relation. Comparisons of both diets and the prevalence of obesity between affluent and poor countries have been used to support a causal association, but these contrasts are seriously confounded by differences in physical activity and food availability. Within areas of similar economic development, regional intake of fat and prevalence of obesity have not been positively correlated. Randomized trials are the preferable method to evaluate the effect of dietary fat on adiposity, and are feasible because the number of subjects needed is not large. In short-term trials, a modest reduction in body weight is typically seen in individuals randomly assigned to diets with a lower percentage of energy from fat. However, compensatory mechanisms appear to operate because in trials lasting > or = 1 y, fat consumption within the range of 18-40% of energy appears to have little if any effect on body fatness. Moreover, within the United States, a substantial decline in the percentage of energy from fat consumed during the past two decades has corresponded with a massive increase in obesity. Diets high in fat do not appear to be the primary cause of the high prevalence of excess body fat in our society, and reductions in fat will not be a solution.

Adipose Tissue↗
PubMed2002

Influence of dietary fat on beta-carotene absorption and bioconversion into vitamin A.

Dietary fat facilitates the utilization of carotenoids and, based on serum beta-carotene or retinol responses following ingestion of meals containing carotene and fat sources, it has been reported that the amount of fat required in a meal may be minimal (approximately 3-5 g). However, the dietary fat requirement for optimal carotene utilization in humans cannot be fully ascertained without longer-term dose-response studies that measure the changes in vitamin A body stores in response to varying levels of dietary fat. In humans, vitamin A body stores can be determined by use of stable isotope-dilution methods. Animal studies have shown that although the level of dietary fat has no effect on serum vitamin A concentrations of animals fed beta-carotene, higher liver vitamin A concentrations were found in those that ingested higher fat levels. Other factors that might influence the relationship of fat intake and beta-carotene utilization include the type of fat ingested, physicochemical properties of the carotenoid source, amount of carotene ingested, whether fat and beta-carotene sources are provided in the same meal, the presence of helminthic infections, age, and vitamin A status.

Adolescent↗
PubMed1994

Failure to increase lipid oxidation in response to increasing dietary fat content in formerly obese women.

The effect of an increase in dietary fat content on fat and carbohydrate balances and energy expenditure (EE) was studied in nine formerly obese women with genetic predisposition to obesity (postobese) and a closely matched control group. Isocaloric low- (20% fat energy) and high-fat diets (50%) were consumed for 3 days preceding and during a 24-h respiratory chamber stay, whereas a medium-fat diet (30%) was consumed only on the day of measurement. After adjustment for 24-h energy intake to equal 24-h EE, 24-h fat balance was increased when the dietary fat content increased (P < 0.0002). No differences in macronutrient balances were found on the low-fat and medium-fat diets, but on the high-fat diet the postobese women failed to increase ratio of fat to carbohydrate oxidation appropriately (0.59 g/g, 95% confidence interval 0.47-0.67 vs. controls 1.02 g/g, 0.88-1.12; P = 0.002). This caused a positive adjusted fat balance (+11.0 g/day, 2.3-19.6 vs. controls -8.9 g/day, -17.5 to -0.2; P < 0.001) and a negative carbohydrate balance (-41.8 g/day, -69.5 to -14.0 vs. controls +23.2 g/day, -4.6 to +50.9; P < 0.001). Decreasing the dietary fat content increased 24-h EE in the postobese women (P = 0.02), whereas it was unaffected in the control group. Independent of energy balance, an increase in dietary fat content to 50% fat energy results in preferential fat storage, impaired suppression of carbohydrate oxidation, and reduction of 24-h EE in postobese women.

Adult↗
PubMed1991

Characterization of high-density lipoprotein binding to guinea pig hepatic membranes: effects of dietary fat quality and cholesterol feeding.

The effects of dietary fat quality and cholesterol intake on expression of guinea pig hepatic membrane high-density lipoprotein (HDL) binding sites were studied. Animals were fed semisynthetic diets containing 7.5% (wt/wt) of either corn oil (CO), olive oil (OL), or lard. The cholesterol diet was prepared by incorporating 0.25% recrystallized cholesterol into standard guinea pig chow. Plasma cholesterol levels of guinea pigs on the CO diet were significantly lower (P less than .02) than animals on the OL or lard diets. HDL cholesterol levels did not differ between the polyunsaturated, monounsaturated, and saturated dietary fat groups. Guinea pigs on the high cholesterol diet had increased total and HDL cholesterol levels compared with animals on the chow diet (P less than .01). Initial studies demonstrated that HDL binding to hepatic membranes was temperature-dependent. A threefold increase in binding was observed when assays were performed at 37 degrees C, as compared with 4 degrees C, for all membrane preparations. Dietary fat quality and dietary cholesterol intake significantly altered HDL binding to hepatic membranes with increased HDL binding to membranes of animals fed polyunsaturated fat and the high cholesterol diet. At 37 degrees C, HDL binding to hepatic membranes of CO-fed animals was 26% and 46% higher than for membranes of OL- and lard-fed guinea pigs, respectively. A high cholesterol intake increased HDL binding by 24% at both 4 degrees C and 37 degrees C. Scatchard analysis demonstrated that while membrane affinity for HDL (Kd) was not affected by diet, changes did occur in the total number of HDL binding sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Dietary fat interacts with QTLs controlling induction of Pgc-1 alpha and Ucp1 during conversion of white to brown fat.

To identify novel regulatory factors controlling induction of the brown adipocyte-specific mitochondrial uncoupling protein (Ucp1) mRNA in the retroperitoneal white fat depot, we previously mapped quantitative trait loci (QTLs) that control this trait to chromosomes 2, 3, 8, and 19. Since the peroxisome proliferator activator receptor-gamma coactivator-1alpha (PGC-1alpha) regulates Ucp1 and other genes of energy metabolism, we have evaluated whether the QTLs controlling Ucp1 mRNA levels also modulate Pgc-1alpha mRNA levels by analysis of backcross progeny from the A/J and C57BL/6J strains of mice. The results indicate that a locus on chromosome 3 orchestrates expression of Pgc-1alpha and Ucp1 in retroperitoneal fat of mice fed a low-fat diet; however, the effect of this locus on Pgc-1alpha is lost, and a significant correlation between Ucp1 and Pgc-1alpha is severely reduced in mice fed a high-fat diet. An additional QTL located on chromosome 5 has also been identified for the selective regulation of Ucp1 mRNA levels. Similar to the effects of a high-fat diet on the chromosome 3 QTL, linkage of the chromosome 5 QTL is also lost in mice on a high-fat diet. Thus dietary fat has a profound influence on PGC-1alpha-regulated pathways controlling energy metabolism in white fat. The allelic variation observed in the regulation of Ucp1 and Pgc-1alpha expression in brown adipocytes of white fat but not interscapular brown fat suggests that fundamentally different regulatory mechanisms exist to control the thermogenic capacities of these tissues.

Adipocytes↗
PubMed1992

Short-term effects of dietary-fat ingestion on energy expenditure and nutrient balance.

Joule for joule, dietary fat may promote obesity more than protein or carbohydrate. In this study we determined whether the addition of 50 g dietary fat to a standard breakfast would increase energy expenditure or fat oxidation during the immediate 6-h postprandial period or over the ensuing 18 h. We also determined whether subjects with a high level of aerobic physical fitness would show a greater increase in fat oxidation after the ingestion of the extra fat than would less fit subjects. Adding fat did not increase fat oxidation or energy expenditure either during the immediate 6-h postprandial period or over the following 18 h. This was true regardless of the subject's fitness level. Acutely, dietary fat ingested in excess of its usual rate of oxidation appears to be stored in the body. Being physically fit does not appear to provide an advantage in avoiding short-term storage of excess dietary fat.

Adult↗
PubMed1992

Adjuvant dietary fat intake reduction in postmenopausal breast cancer patient management. The Women's Intervention Nutrition Study (WINS).

Management of localized breast cancer now commonly involves a breast-sparing approach combined with systemic adjuvant therapy resulting in improved cosmetic results and patient survival. Reducing dietary fat intake represents a conceptually new approach to further improve outcome of patients with resected breast cancer. The rationale supporting evaluation of dietary fat reduction in the management of patients with localized breast cancer is based on: (1) epidemiologic observations (along with biochemical and hormonal correlates) of major differences in stage-by-stage survival of patients with localized breast cancer comparing outcome in countries with low fat (Japan) versus high fat (U.S.A.) dietary intakes; (2) relationships between dietary fat intake and factors prognostic of clinical outcome in patients with established breast cancer; (3) effects of weight gain (especially that associated with adjuvant chemotherapy) on breast cancer clinical outcome; (4) in vivo animal studies demonstrating adverse influence of increased dietary fat intake (especially linoleic acid) on growth and metastatic spread of mammary cancer; (5) direct adverse effects of increased linoleic acid on human breast cancer growth in vitro; (6) plausible mechanisms which could mediate the effects of dietary fat intake reduction on breast cancer growth and metastatic spread; (7) demonstration of adherence to dietary fat reduction regimens in ongoing clinical feasibility studies including those involving postmenopausal patients with resected breast cancer; and (8) favorable sample size requirements for definitive assessment of dietary fat intake reduction influence on breast cancer growth and metastases (using as endpoints relapse-free survival and overall survival) in postmenopausal breast cancer patients with localized disease.

Animals↗
PubMed1983

The influence of dietary fat on the toxicity of orally ingested lead in rats.

The influence of dietary fat on the toxicity of orally ingested lead was investigated. Groups of ten male weanling Wistar rats were maintained on diets providing 11.5, 20, 40 or 60% of energy from fat for 8 wk. All diets were supplemented with a low level of lead--1.25 mg Pb (as lead acetate) per 1000 kJ energy in the diet. Groups receiving 11.5 and 20% of energy as fat had similar lead levels for each tissue studied. Raising the fat level to 40 or 60% of energy resulted in significant increases in tissue-lead concentrations with each increment in dietary fat. The groups receiving 60% of energy as fat had more than twice the level of lead in the femur, kidney, liver and brain than the control rats maintained on the diet containing 11.5% energy as fat, even though the amount of lead ingested was the same for all groups. delta-Aminolaevulinic acid dehydratase activity was not affected when dietary fat was increased from 11.5 to 20%. There was a significant reduction in activity when fat was increased to 40 or 60% of energy. Free erythrocyte protoporphyrin was not affected by the level of dietary fat. This work demonstrates that increasing the level of dietary fat significantly increases lead toxicity and indicates the need for further research on the interaction between dietary factors and lead toxicity.

Administration, Oral↗
PubMed2006

Low-fat dietary pattern and risk of invasive breast cancer: the Women's Health Initiative Randomized Controlled Dietary Modification Trial.

CONTEXT: The hypothesis that a low-fat dietary pattern can reduce breast cancer risk has existed for decades but has never been tested in a controlled intervention trial. OBJECTIVE: To assess the effects of undertaking a low-fat dietary pattern on breast cancer incidence. DESIGN AND SETTING: A randomized, controlled, primary prevention trial conducted at 40 US clinical centers from 1993 to 2005. PARTICIPANTS: A total of 48,835 postmenopausal women, aged 50 to 79 years, without prior breast cancer, including 18.6% of minority race/ethnicity, were enrolled. INTERVENTIONS: Women were randomly assigned to the dietary modification intervention group (40% [n = 19,541]) or the comparison group (60% [n = 29,294]). The intervention was designed to promote dietary change with the goals of reducing intake of total fat to 20% of energy and increasing consumption of vegetables and fruit to at least 5 servings daily and grains to at least 6 servings daily. Comparison group participants were not asked to make dietary changes. MAIN OUTCOME MEASURE: Invasive breast cancer incidence. RESULTS: Dietary fat intake was significantly lower in the dietary modification intervention group compared with the comparison group. The difference between groups in change from baseline for percentage of energy from fat varied from 10.7% at year 1 to 8.1% at year 6. Vegetable and fruit consumption was higher in the intervention group by at least 1 serving per day and a smaller, more transient difference was found for grain consumption. The number of women who developed invasive breast cancer (annualized incidence rate) over the 8.1-year average follow-up period was 655 (0.42%) in the intervention group and 1072 (0.45%) in the comparison group (hazard ratio, 0.91; 95% confidence interval, 0.83-1.01 for the comparison between the 2 groups). Secondary analyses suggest a lower hazard ratio among adherent women, provide greater evidence of risk reduction among women having a high-fat diet at baseline, and suggest a dietary effect that varies by hormone receptor characteristics of the tumor. CONCLUSIONS: Among postmenopausal women, a low-fat dietary pattern did not result in a statistically significant reduction in invasive breast cancer risk over an 8.1-year average follow-up period. However, the nonsignificant trends observed suggesting reduced risk associated with a low-fat dietary pattern indicate that longer, planned, nonintervention follow-up may yield a more definitive comparison. CLINICAL TRIALS REGISTRATION: ClinicalTrials.gov Identifier: NCT00000611.

Aged↗
PubMed2001

Melanocortin-4 receptor is required for acute homeostatic responses to increased dietary fat.

In response to moderately increased dietary fat content, melanocortin-4 receptor-null mutant (MC4R-/-) mice exhibit hyperphagia and accelerated weight gain compared to wild-type mice. An increased feed efficiency (weight gain/kcal consumed) argues that mechanisms in addition to hyperphagia are instrumental in causing weight gain. We report two specific defects in coordinating energy expenditure with food intake in MC4R-/- mice. Wild-type mice respond to an increase in the fat content of the diet by rapidly increasing diet-induced thermogenesis and by increasing physical activity, neither of which are observed in MC4R-/- mice. Leptin-deficient and MC3R-/- mice regulate metabolic rate similarly to wild-type mice in this protocol. Melanocortinergic pathways involving MC4-R-regulated neurons, which rapidly respond to signals not requiring changes in leptin, thus seem to be important in regulating metabolic and behavioral responses to dietary fat.

Adipose Tissue, Brown↗
PubMed1987

Dietary fat and nitrogen composition of milk from lactating cows.

Effects of dietary fat on milk composition, particularly milk N, were evaluated in lactating dairy cows at two stages of lactation. Complete mixed diets containing 0, 3.5, or 7% of the diet DM as animal fat were fed to 12 cows in a 3 X 3 Latin square. Cows were divided into two status categories based on stage of lactation resulting in two squares of early and two of late lactation cows. Percentages of fat, solids, lactose, and protein were decreased and ash increased in the milk of cows fed the 7% fat diet. Percent of casein N was elevated while nonprotein N was depressed by fat fed in diet. Percentage of solids and protein was higher and lactose lower for cows in late lactation than for those in early lactation. Dietary fat reduced the proportion of short-chain fatty acids in milk fat and increased C18:0 and C18:1 fatty acids. Digestibility of DM, energy, and fiber was not significantly affected by dietary fat, but estimates decreased with increased dietary fat. Cows in late lactation had a higher digestibility of dietary fractions than early lactation cows even though intakes of DM were similar.

Animals↗
PubMed1988

Compliance in a randomized clinical trial of dietary fat reduction in patients with breast dysplasia.

Dietary compliance was studied in 57 women participating for 1 y in a randomized clinical trial of dietary fat reduction. Nutrient analysis of food records, collected at 0, 6, and 12 mo, was compared with changes observed in lipid profiles and with chemical analysis of duplicate diets. Both food records and duplicate meals showed a significant decrease in fat intake (from 36 to 23% of total calories, p less than 0.0001) and a significant increase in carbohydrate (from 43 to 56% of total calories, p less than 0.0001) in the intervention group. The calculated nutrient intake from food records tended to overestimate the intake of protein, fat, and carbohydrate compared with the chemically analyzed method. The mean level of plasma cholesterol in the intervention group was significantly reduced (7.3%, p less than 0.01) in the first 6 mo after a reduction in dietary fat but the levels observed did not differ significantly between the groups at any time.

Adult↗
PubMed2004

Dietary fat and obesity: a review of animal, clinical and epidemiological studies.

The First Law of Thermodynamics provides a framework for understanding the imbalance between energy intake and expenditure that produces obesity, but it does not help understand the role of genetics, the regulation of food intake, the distribution of body fat, the mechanisms by which diets work or the mechanism by which portion control has gotten out of control. In animals, increasing dietary fat increases body fat, and it is unlikely that humans escape this important biological rule. In epidemiological studies, increasing dietary fat is associated with increased prevalence of obesity probably by increasing the intake of energy dense foods. In the National Weight Loss Registry, three things were associated with weight loss: continued monitoring of food intake, lowering dietary fat intake, and increased exercise. The relation of dietary fat is most evident when physical activity is low. The speed of adaptation to dietary fat is increased by exercise. When dietary fat is reduced, weight is lost, but weight loss eventually plateaus. The rate of weight loss during the initial phase is about 1.6 g/day for each 1% decrease in fat intake. When dietary fat is replaced with olestra to reduce fat intake from 33% to 25% in obese men, weight loss continues for about 9 months reaching a maximum of nearly 6% of body weight and a loss of 18% of initial body fat. In the control group with a 25% reduced-fat diet, weight loss stopped after 3 months and was regained over the next 6 months, indicating the difficulty of adhering to a conventional low-fat diet. Thus, dietary fat is an important contributor to obesity in some people.

Animal Experimentation↗
PubMed1992

Relationship between dietary fat and experimental mammary tumorigenesis: a review and critique.

That dietary fat can significantly affect mammary tumorigenesis in mice and rats has been clearly established. The purpose of this communication is to review and critique this interesting and potentially important relationship. This review focuses on the relationship between the amount and type of dietary fat and the role of calories in rodent mammary tumor development and metastasis. Additionally, the influence of dietary fat on development of human breast carcinoma transplants in immunodeficient mice is examined. The numerous studies cited in this review provide a compelling biological foundation for a potentially important relationship between dietary fat and/or calorie consumption and breast carcinoma development in human populations.

Animals↗
PubMed2002

Effect of dietary fat content in meals on pharmacokinetics of quazepam.

Dietary fat content in meals has been reported to increase the absorption of several drugs proportionately. However, there is no information about the effects of dietary fat in meals on the sedative hypnotic agent quazepam, although limited data suggest that food intake alters quazepam absorption. Therefore, the authors measured and compared pharmacokinetic parameters of quazepam taken in a fasted state and taken 30 minutes after consuming meals containing different amounts of dietary fat. A three-arm randomized crossover study was conducted. Nine healthy male volunteers took a single oral 20-mg dose of quazepam under the following conditions: (1) after fasting overnight for at least 12 hours, (2) 30 minutes after consuming a low-fat meal (two slices of bread and 200 ml of apple juice), or (3) 30 minutes after consuming high-fat meal (two slices of bread with 30 gm of butter and 200 ml of apple juice). Plasma concentrations of quazepam and its metabolite, 2-oxoquazepam, were monitored up to 48 hours after the dosing. In comparison with corresponding plasma values for quazepam taken in a fasting state, the peak concentrations (Cmax) of quazepam taken 30 minutes after consuming a low-fat meal and high-fat meal were 243% (90% confidence interval [CI] = 161%-325%) and 272% (90% CI = 190%-355%), respectively. Area under the plasma concentration-time curve from 0 to 8 hours (AUC(0-8)) and 0 to 48 hours (AUC(0-48)) of quazepam was increased with the low-fat meal by 2-fold (90% CI = 1.5- to 2.7-fold) and 1.4-fold (90% CI = 1.0- to 1.7-fold), respectively, and with the high-fat meal by 2.2-fold (90% CI = 1.3- to 3-fold) and 1.5-fold (90% CI = 0.7- to 2.4-fold), respectively. The pharmacokinetic change in 2-oxoquazepam to the parent compound was similar. Quazepam was well tolerated, with no significant difference in the Stanford Sleepiness Scale between fasted and fed conditions. These findings show that food intake has an evident effect on quazepam absorption, but further studies are needed to clarify a determinant factor of this alteration (2.5-fold for Cmax and 2.1-fold for AUC(0-8), on average). It might not be necessary to do dose adjustment with meal content because quazepam is well tolerated.

Adult↗