[Influence of the type of fat incorporated into the milk substitute on lipid metabolism in marketable lambs].
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The report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults published in 1988 evoked great interest from the medical profession, the public, and food manufacturers. The merits of different dietary interventions to lower plasma cholesterol are debated in advertising, popular publications, and research publications. The present paper is a review of the contributions of saturated and trans fatty acids (FA) to the US diet, their metabolism, and effects upon plasma cholesterol. Saturated (SFA) and trans FA are metabolized to yield energy. They are not dietary essentials; SFA can be biosynthesized, and trans FA are not naturally occurring in plants, with only very small amounts in animals. Trans FA are produced in hydrogenation of liquid vegetable oils and are estimated to contribute 3-7% of the fat consumed. Most of the SFA in the US diet (35% of total fat consumed) is obtained from meat, poultry, fish, and dairy products (approximately 60%). The fats and oils consumed directly or as components of food products, mostly baked goods, contribute approximately 20% of the SFA. More than 30 years of research led the NCEP to conclude that SFA was the most potent dietary component in increasing plasma cholesterol, and that no more than 10% of the energy (en%) of the diet should be SFA. Trans FA are metabolized similarly to SFA, but no recommendation has been made about their consumption. Reduction of consumption of SFA should be practiced in a prudent manner, by reducing consumption of foods high in SFA, and not by eliminating classes of foods. Some changes in formulations of foods or preparation practices (type of frying fat) can be made. These modifications may decrease the palatability of the food, thereby presenting a challenge to the food industry. Substitution of fats hydrogenated to contain trans FA for fats high in SFA may not be beneficial to health. Labeling of foods would improve the ability of the consumer to make appropriate choices.
Hydrolyzable carbohydrate intake in horse diets may become excessive when rapidly growing pastures are supplemented with grain-based concentrates. The substitution of fat and fiber for hydrolyzable carbohydrate in concentrates has been explored in exercising horses but not in young, growing horses. Our objective was to compare bone development in foals that were fed pasture and concentrates rich in sugar and starch (corn, molasses) or fat and fiber (corn oil, beet pulp, soybean hulls, oat straw). Forty foals were examined, 20 each in 1994 and 1995. In each year, 10 mares and their foals were fed a corn and molasses supplement (SS) and 10 others were fed a corn oil and fiber supplement (FF). The concentrates were formulated to be isocaloric and isonitrogenous, and mineral content was balanced to complement the pastures and meet or exceed NRC requirements. Dorsopalmar radiographs were taken of the left third metacarpal monthly from birth to weaning and then every other month until 1 yr of age. Bone density was estimated using imaging software and an aluminum stepwedge. Radiographic examination indicated differences in medial, lateral, and central bone mineral content of the metacarpal III. Bone mineral content increased with age, and a plateau was observed during winter. Bone mineral content was lower in weanlings and yearlings fed the FF supplement than in those fed SS. Subjective clinical leg evaluations indicated differences in physitis, joint effusion, and angular and flexural limb deformities in response to age, and possibly to season. Regression analysis indicated positive relationships between bone mineral content and body weight, age, and body measurements. Nutrient and chemical interactions, such as the binding of calcium by fat and fiber, may alter the availability of elements necessary for bone development.
The Drosophila fat facets gene encodes a deubiquitinating enzyme required during eye development to limit the number of photoreceptors in each facet to eight. Ubiquitin is a small polypeptide that targets proteins for degradation by the proteasome. Deubiquitinating enzymes cleave ubiquitin-protein bonds. In order to investigate the role of FAT FACETS in the ubiquitin pathway, genetic interactions between fat facets and the Drosophila UbcD1 gene were assessed. In addition, three yeast deubiquitinating enzyme genes were tested for their ability to substitute for fat facets in the developing Drosophila eye and for their effects on eye morphology. The results of these experiments support the hypothesis that FAT FACETS activity antagonizes that of the proteolytic machinery. The implications of these results for the specificity of FAF and yeast UBPs are discussed as well.
The main objectives of this study were to explore the role of diet-induced thermogenesis in the regulation of voluntary feed intake and to determine the glucose oxidation of broiler chicken strains, known to differ in glucose-insulin balance. From 2 to 7 wk of age, male broiler chickens of a fat and a lean line were reared on 1 of 2 isoenergetic diets with constant gross energy and carbohydrate levels but with substitutions between fat and protein. The low protein (LP/HF) diet contained 126 g of protein/kg and 106 g of fat/kg, whereas the low fat (LF/HP) diet contained 242 g of protein/kg and 43 g of fat/kg. There was no significant effect of the genetic background of the broilers on the glucose oxidation rate (as measured by stable isotope breath test) or protein oxidation (as measured by plasma uric acid levels). Considering the difference in carcass composition (fat content) of both lines, this leads to the hypothesis that the lines differ predominantly in fat metabolism. Although there was no line effect on plasma triglyceride and free fatty acid concentrations, it was hypothesized that there might be differences in fat oxidation or de novo lipogenesis, or both, between the genotypes. Diet-induced thermogenesis per metabolic body weight (kg of BW0.75) per 24 h, expressed per gram of feed intake, was not significantly influenced by genetic background or by diet composition. Therefore, a model linking feed intake to diet-induced thermogenesis, as postulated for adult mammals, could not be corroborated for growing broiler chickens.
Experimental rats were given rations with 100% substitution of fats for phospholipid concentrate, during 1 and 3 months. It was found that such rations produced hypolipidemic and hypocholesterolemic effects, that were most pronounced at the end of the experiment. A control ration with sunflower oil containing high levels of unsaturated fatty acids induced accumulation of lipid peroxides in the hepatic tissue and blood plasma of the animals fed with the ration during 3 months. The ration containing the phospholipid concentrate did not produce such an effect. The data obtained have evidenced a positive influence of the phospholipid concentrate on the lipid metabolism parameters studied.
OBJECTIVE: A low-fat diet is hypothesized to be associated with significant weight loss. However, most previous studies have been limited to low-fat, low-calorie restrictive diets. This study evaluated the effect of isocaloric diets given "ad libitum" but different in relative amounts of fat and carbohydrate on body size, energy metabolism, body composition, insulin-like growth factor-1, and leptin serum levels in growing Wistar rats. METHODS: Weanling male rats were fed with one of three diets that contained a ratio of carbohydrate to fat of 1:1, 2:1, or 3:1. Food intake, body weight, body length, oxygen consumption, and body composition were measured at ages 21 to 50 d. Serum levels of insulin-like growth factor-1 and leptin were also determined. RESULTS: Energy intake was similar across groups. The ratio of body weight to body length remained adequate throughout the experimental period. However, groups that received 3:1 and 2:1 showed increased weight and progressive decreases in energy expenditure, body fat composition, and serum level of leptin, but the ratio of insulin-like growth factor-1 to body length was not affected. CONCLUSIONS: Dietary substitution of fat with carbohydrates contributes to weight gain by decreasing energy expenditure and possibly by decreasing leptin secretion.
Good reasons exist to reduce intake of animal and partially hydrogenated fat. Existing data, however, provide little support for the hypothesis that reduction in dietary fat composition, even to 20% of energy during adulthood, will lead to a substantial reduction in breast cancer in Western cultures. Some evidence suggests that substituting monounsaturated fat for other sources of energy may even reduce risk of breast cancer; this deserves further examination. Also, the avoidance of weight gain during adulthood has many benefits, which are likely to include an important reduction in risk of postmenopausal breast cancer.
The aim of this study was to determine whether substituting enzymatically interesterified butter for native butter in the usual diet affects lipid and lipoprotein levels in man. Parameters studied were serum total cholesterol, LDL-cholesterol, HDL-cholesterol, free cholesterol, phospholipids, triglycerides, apoA1 and apoB and the fatty acid composition of serum triglycerides, free fatty acids, phospholipids and cholesterol esters. Subjects were healthy volunteers and a controlled design was used. The only mathematically significant difference found when interesterified butter was substituted for butter was an about 7% lower fraction of oleic acid in the serum cholesterol esters (p = 0.005). In contrast to an earlier study where chemically interesterified butter fat was substituted for native butter, no indications are found in this study that replacing native butter by enzymatically interesterified butter, in amounts normally consumed, may have any beneficial effect on health.
It has been stated that energy adjustment can control for recall bias in case-control studies. Simulation of recall bias and cases and controls in a nutritional survey of German adults was conducted to examine its impact on five dietary effects, (adding a macronutrient, substituting one macronutrient for another, adding a macronutrient while keeping the other energy sources constant, and changing the macronutrient to energy ratio through addition or substitution) using various energy adjustment models. If energy adjustment were an effective means of correcting measurement error, the energy adjusted dietary effects, after a subtraction of energy and fat intake, should equal those in the original data set. Simulation of differential under-reporting of fat and energy intake by cases but not controls showed this to dramatically impact all five considered dietary effects, even after energy adjustment. The influence of the assumed recall bias on the different effects depends on the error type structure, inflating an odds ration of 1.8 to as much as 12.3 or reducing it to 0.45 when 100 kcal of fat was substituted for 100 kcal of other macronutrients. Although energy adjustment may serve many functions, it cannot correct for differential error. Depending upon the nature of the hypothesized effect and the error type, energy adjustment may also distort risk ratios in the presence of non-differential bias. The concern that cases and controls report their energy intakes with different degrees of error remains a critical consideration that must be addressed through improved measurements, and not energy adjustment under any of the currently used models.
To determine the influence of free fatty acid (FFA) content on the subsequent nutritive value of fats, the following were studied: tallow (FFA content of 138.4 g/kg) and tallow acid oil (FFA = 952.1 g/kg) in Experiment 1; palm oil (FFA = 57.5 g/kg) and palm acid oil (FFA = 917.5 g/kg) in Experiment 2; and soybean oil (FFA = 14.4 g/kg) and soybean acid oil (FFA = 683.4 g/kg) in Experiment 3. The two fats within each experiment were blended in proportions to give three mixtures of intermediary FFA content. Thus, each experiment investigated five fats by substituting them into a basal diet at the expense of the energy-yielding ingredients at rates of 40, 80, and 120 g/kg. Experimental diets were evaluated for apparent fat availability (AFA) of broiler chicks 1.5 and 7.5 wk of age. Corresponding values for fats were obtained through extrapolation of the linear response, or interpolation of the quadratic response, of AFA of diets. The AME was calculated as the product of fat AFA and gross energy. The degree of saturation had a pronounced effect upon the AME of fats; values decreased in the following order: soybean oil, tallow, and palm oil. Overall AME of fats linearly decreased with increasing FFA content, and the decrease was more pronounced with the younger birds. This rate of reduction appeared to be influenced by degree of saturation of the fat, but only with younger birds. Thus, AME of fats declined from 30.9 to 20.4, 27.7 to 14.8, and 38.5 to 33.1 MJ/kg (1 MJ = .239 Mcal) for young birds in Experiments 1, 2, and 3, respectively. Corresponding data for older birds were from 32.9 to 28.3, 32.3 to 27.5, and 38.5 to 35.1 MJ/kg. Effects of rate of inclusion of fats were minor and, generally, were confined to fats of a higher degree of saturation with greater contents of FFA evaluated with younger birds.
Nutrition plays a very important role in regulating blood pressure. If we reverted to our evolutionary diet the problem of high blood pressure would disappear. However, this is unlikely and we, therefore, need to identify the most important factors in our diet that predispose to high blood pressure and, therefore, to vascular disease. Studies clearly demonstrate the very important role of our current intake of salt in our diet as being the major factor in regulating blood pressure in populations. Other dietary factors have also been identified as playing an important role, particularly potassium intake and fruit and vegetable consumption. A more healthy diet, that is a diet with much less salt and increased potassium through an increase in fruit and vegetable consumption, a reduction in fat intake with substitution of saturated by monounsaturated fat, a reduction in meat and dairy products with an increase in fish consumption will have large effects on blood pressure but, at the same time, will decrease other cardiovascular risk factors, particularly cholesterol and glucose intolerance. This healthier diet will reduce cardiovascular disease and is similar to the diet now being advocated for the prevention of some forms of cancer. Diet is by far the most important environmental factor determining our longevity and for those who wish to live longer, a change in diet as early in life as possible will have substantial effects.
This report describes the development and evaluation of a behavioral measure of dietary patterns related to selecting low-fat diets. An 18-item questionnaire, based on an anthropological theory of dietary change, was developed to assess four relevant dimensions of dietary behavior: (a) excluding high-fat ingredients and preparation techniques, (b) modifying high-fat foods, (c) substituting specially manufactured low-fat foods for their higher-fat counterparts, and (d) replacing high-fat foods with low-fat alternatives. In this study, 99 women completed the diet behavior questionnaire twice and, to characterize precisely their dietary fat intake, also completed two 4-day food records and a food frequency questionnaire. Participants were aged 45 to 59 years and were selected to have a wide range of fat intakes (19.4% to 49.4% of calories from fat). Confirmatory factor analysis identified five scales that corresponded to those hypothesized, except for exclusion, which split into avoiding meat and avoiding fat as a seasoning. The scales had high test-retest and internal consistency reliabilities, and correlations with percent of calories from fat ranged from 0.34 to 0.57 (p less than .01). The correlation of the sum of the five scales (18 items) with percent of calories from fat was 0.68 (p less than .001) and, in multiple regression models, the multiple R2 using all factors to predict percent of calories from fat was 0.47. Overall, these findings supported the validity of the theoretical model of dietary patterns related to selecting diets low in fat. We conclude that a standardized, behavioral approach to measuring fat-related dietary behavior may be useful for designing and evaluating nutrition intervention programs.
The biochemistry, etiology, and evaluation of hyperlipidemia and its management, including dietary and drug therapies, are discussed. Strong evidence supports the role of increased cholesterol concentrations as an independent risk factor for coronary artery disease (CAD); however, evidence that elevated triglyceride concentrations are also an independent risk factor remains questionable. The cornerstone of the laboratory diagnosis of hyperlipidemia involves repeated measurement of serum or plasma cholesterol and triglyceride concentrations. The goals of therapy should be to reduce cholesterol or triglyceride concentrations or both to below the 75th percentile, modify co-existing risk factors, individualize the treatment, and minimize any adverse effects. Specific interventions must be determined on the basis of patient age, gender, etiology of hyperlipidemia, presence of other risk factors, and degree of lipid abnormality. The majority of patients may be managed with dietary therapy alone. The three-phase diet developed by the American Heart Association emphasizes a gradual reduction in cholesterol and fats with the substitution of polyunsaturated for saturated fats. Patients at risk for CAD with sustained elevations in plasma cholesterol concentrations above the 95th percentile or a triglyceride concentration above 500 mg/dL after an adequate dietary trial should be considered for drug therapy. The effects of cholestyramine and colestipol hydrochloride, niacin, dextrothyroxine, clofibrate, neomycin sulfate, probucol, gemfibrozil, and mevinolin and compactin on lipids and lipoproteins are reviewed. Hyperlipidemia should be managed systematically using information about the association between increased lipid concentrations and CAD, patient risk factors, and limitations of both diet and drug therapy.
No matter how healthy a food or recipe might be, if it does not taste good, people will not eat it. The professional and personal challenge is to find ways to cook favorite foods in a low-fat and delicious style to maintain health while enjoying foods without guilt. A number of strategies can be employed to reach that goal, including ingredient choices, low-fat product substitutes, cookware, cooking techniques, seasonings, basic cooking and recipe modifications, and the creation of new recipes.
Development of alcohol-related liver and other diseases appears to be modified by host and environmental factors that include diet and nutritional status, exposure to other drugs and toxins, and infection. The relative importance of alcohol toxicity and malnutrition in the induction of fatty liver and cirrhosis, the subject of this report, has been debated. Male rhesus (M mulatta) monkeys were fed purified liquid diets, adequate or marginally deficient in lipotropes (choline, methionine, and folate), containing ethanol to supply 40-50% of calories for 1.5-4.5 years. Controls, fed the diets with sucrose and fat isocalorically substituted for ethanol, grew well and were clinically normal. Ethanol-fed monkeys in both diet groups failed to gain weight and were slightly anemic, with mild derangements of serum electrolytes and small amounts of fat in their livers. None had fibrosis or cirrhosis until the severity of the lipotrope-deficiency was increased; then two of four deficient animals developed cirrhosis and one developed fibrosis. (The severe deficiency induced weight loss and fatty liver, but not fibrosis, in one of two controls.) We conclude that alcohol does not induce hepatic fibrosis or cirrhosis in rhesus monkeys fed a nutritionally complete diet, a result supported by studies in rats and another monkey, M radiata. Alcohol does induce cirrhosis when fed in combination with a lipotrope-deficient diet that is not, by itself, cirrhogenic.
Neonatal intrahepatic cholestasis is a heterogeneous disease of undetermined cause. There is an unreported subset of idiopathic neonatal intrahepatic cholestasis with an unusual histological combination of hepatic siderosis and macrovesicular steatosis. The patients were a 34-day-old female and a 39-day-old male with normal birth weights. Their mothers had received oral iron supplement 4-6 weeks before delivery. The patients had obstructive jaundice noticed at the well-baby clinic at 1 month of life. They had high levels of serum galactose and tyrosine, hyperferritinemia. Urinary organic acid and bile acid analyses were negative, and galactose-1-phosphate uridyltransferase activity in red cells was normal. Liver biopsies showed diffuse iron deposits and macrovesicular fat. By substituting formula milk with lactose-free milk, the patients responded, and had normal biochemical tests within 5 months of life. Follow-up biopsies, at the age of 12 months, showed mild residual fibrosis without iron or fat deposits. They are both well at 3 and 6 years of age, respectively, without biochemical liver dysfunction and neurologic impairment. Prenatal iron-overload might contribute to the pathogenesis of the disease, but further studies are needed to confirm the assumption.
We discuss a newborn with congenital intestinal lymphangiectasia. Primary intestinal lymphangiectasia is a rare disease which represents a congenital disorder of mesenteric lymphatics and is associated with typical clinical signs. The diagnosis can be made on the basis of the typical histological findings in the endoscopic biopsies, the laboratory findings and the radiographic findings. Treatment is palliative by introduction of medium chain triglycerides and by restricting the dietary fat intake. Substitution therapy may be necessary. The longer-term prognosis appears to be good.