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The physiology of fat absorption and its relevance to chylous fistula following neck dissection is discussed. Three patients with postoperative chylous fistulae were successfully managed conservatively using medium chain triglycerides as a substitute for normal dietary fat.
This short demonstration accomplishes several goals. People see where fat comes from and learn amounts needed to be removed. They practice substituting complex carbohydrate foods for fat. Most important, they learn that changing is not an "all-or-nothing" proposition. They can reduce dietary fat and still eat many of their favorite foods. This demonstration is a useful tool for nutrition educators who want to promote dietary change.
BACKGROUND: As part of a study on the effects of a fat-supplemented phenylalanine (phe)-free protein substitute on the fatty acid status of children with phenylketonuria (PKU), the adequacy of the diets of children aged 1-10 years for fat and essential fatty acids (EFA) was assessed. METHODS: Subjects randomized in a 1 : 1 ratio to a phe-free protein substitute supplemented with EFA (test-treatment group) or a phe-free, fat-free protein substitute (control group) for 20 weeks. 3-day semi-weighed records of food intakes collected at the end of the study period. RESULTS: Total fat and alpha-linolenic acid (alpha-LA) intakes were found to be poor in the control group (n = 19). Those in the test-treatment group (n = 24) had higher fat and EFA intakes (P < 0.05), bringing intakes closer to population norms. The youngest children (<5 years of age) in the control group appeared to be especially vulnerable to poor fat intakes because of the restricted diversity of their diets and, regardless of age, alpha-LA intakes by this group were poor compared with the non-PKU population. CONCLUSIONS: The quantity and quality of fat in the diets of children with PKU, in particular young children, should be given careful consideration in trying to optimize the ratio of linoleic acid: alpha-LA in their diets and in satisfying the requirements of this group for fat and alpha-LA.
This study has evaluated whether uremic patients on chronic haemodialysis with subnormal plasma levels of free carnitine show any alterations in whole body fat oxidation before and after one week with carnitine supplementation (60 mg/kg/day). Carnitine plasma levels changed from subnormal to supranormal levels of both free and total carnitine concentrations. This increase was not associated with any alteration in either oxygen uptake, carbon dioxide production, respiratory quotient or blood substrate levels such as glucose, glycerol, free fatty acids and lactate. The fractional oxidation of an intravenously infused fat emulsion (Intralipid) was 17% before and 19% after carnitine supplementation. No side effects were observed in spite of the rather high dose of carnitine administration. This study failed to demonstrate any impact on net whole body fat oxidation in carnitine substituted uremic patients with initially subnormal levels of free plasma carnitine.
Fecal bile acid and neutral sterol excretion rates were determined in five healthy young men when serum cholesterol changes were induced by isocaloric substitution of an unsaturated (safflower oil) for a saturated fat (butter). The isotope balance method was used after the intravenous injection of cholesterol-4-(14)C. A feces extraction method is presented which permits essentially complete separation of fecal neutral sterols and bile acids. There was a significant increase in the total excretion of the fecal end products of cholesterol metabolism from 966 +/- 42 mg/day on saturated fat to 1147 +/- 45 mg/day on unsaturated fat, and the increase was equally distributed between the neutral sterol and bile acid fractions. With the substitution of dietary fats, regardless of the sequence of their feeding, there was a 28% reduction in serum cholesterol concentration during ingestion of the unsaturated fat. There were reciprocal changes in serum cholesterol levels and fecal steroid excretion with the substitution of one type of fat for the other. The changes in plasma cholesterol content were more than adequately balanced by the reciprocal changes in fecal cholesterol end product excretion. The findings in this study agree with several previous reports in supporting the hypothesis that the hypocholesteremic action of dietary unsaturated fatty acids is associated with an increase in the fecal loss of bile acids and neutral sterols.
PURPOSE: To compare the usefulness of short inversion recovery (STIR) and T1-weighted, contrast-enhanced, fat-suppressed (T1W-CEFS) sequences for the evaluation of bone tumors. MATERIALS AND METHODS: Eighteen patients with 19 bone tumors who underwent both STIR and T1W-CEFS imaging were evaluated. The tumors were categorized in pairs as follows: bone marrow and soft-tissue components, benign and malignant tumors, and tumors with and without mineralization. The signal difference-to-noise ratio (SDNR), signal-to-noise ratio (SNR), and tumor volume were calculated in each group. An additional qualitative analysis was performed by means of the ratings of imaging contrast. RESULTS: The mean SDNRs of all bone marrow components and bone marrow components without mineralization were significantly higher on fast STIR images than on T1W-CEFS images (P < 0.05). There was no significant difference in the mean SDNR and SNR of the other group (surrounding soft tissue components, bone marrow components with mineralization, benign and malignant lesions) between fast STIR images and T1W-CEFS images. The mean volume of the tumors was significantly higher with STIR than with the T1W-CEFS sequence (P < 0.05). CONCLUSION: The STIR sequence should be used instead of T1W-CEFS imaging for the evaluation of bone tumors.
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Rates of breast cancer vary approximately fivefold among countries and are strongly correlated with national per capita availability of dietary fat. However, this relation may be substantially confounded by many other factors associated with affluent lifestyles, such as reduced parity and physical activity. In large prospective epidemiologic studies, little evidence has been seen to support any major positive association between dietary fat and risk of breast cancer over the range of 15-45% or more of energy from fat. The observation that women in counties in China consuming approximately 25% of energy from fat have much lower rates of breast cancer than U.S. women with similar fat intakes provides additional evidence that factors other than dietary fat account for the large international differences. Some epidemiologic evidence suggests that monounsaturated fat and olive oil in particular may reduce risk of breast cancer when substituted for other types of fat. In contrast to findings for dietary total fat, most types of epidemiologic studies provide indirect support for a protective effect of energy restriction and reduced growth rates against breast cancer, which is consistently observed in animal studies of mammary carcinogenesis.
It has been variously hypothesized that the insulin resistance induced in rodents by a high-fat diet is due to increased visceral fat accumulation, to an increase in muscle triglyceride (TG) content, or to an effect of diet composition. In this study we used a number of interventions: fish oil, leptin, caloric restriction, and shorter duration of fat feeding, to try to disassociate an increase in visceral fat from muscle insulin resistance. Substituting fish oil (18% of calories) for corn oil in the high-fat diet partially protected against both the increase in visceral fat and muscle insulin resistance without affecting muscle TG content. Injections of leptin during the last 4 days of a 4-wk period on the high-fat diet partially reversed the increase in visceral fat and the muscle insulin resistance, while completely normalizing muscle TG. Restricting intake of the high-fat diet to 75% of ad libitum completely prevented the increase in visceral fat and muscle insulin resistance. Maximally insulin-stimulated glucose transport was negatively correlated with visceral fat mass (P < 0.001) in both the soleus and epitrochlearis muscles and with muscle TG concentration in the soleus (P < 0.05) but not in the epitrochlearis. Thus we were unable to dissociate the increase in visceral fat from muscle insulin resistance using a variety of approaches. These results support the hypothesis that an increase in visceral fat is associated with development of muscle insulin resistance.
Orchidectomy of rats resulted in increased concentration and whole organ amount of DNA both in the epididymal fat pad and liver. Liver hexokinase (HK) and phosphofructokinase (PFK) activities were raised after orchidectomy, but were normalized by testosterone substitution. Several glycolytic enzymes, and fumarase and aspartate aminotransferase were increased by orchidectomy in epididymal fat. Most of the enzyme changes tended to normalize after testosterone administration. Activities of NADPH generating enzymes were increased after orchidectomy both in liver and epididymal fat. When related to DNA, several enzyme activities in both tissues fell following castration. However, liver HK, PFK and NADPH generating enzymes, as well as epididymal fat HK and isocitrate dehydrogenase were elevated after castration also when related to DNA. The results suggest that the influence of testosterone on cell proliferation is organ-specific. The observed enzyme alterations after orchidectomy might partly explain fat accumulation and hyperlipoproteinemia encountered in castrates.
INTRODUCTION: In healthy men, body weight and total fat content increase with advancing age, while serum testosterone levels decrease. In order to elucidate whether a causal relationship between these phenomena exists, we investigated the influence of testosterone or human chorionic gonadotrophin substitution on body mass index (BMI), total fat mass and serum leptin in testosterone-treated and untreated hypogonadal patients in comparison with ageing eugonadal men. METHODS: In a cross-sectional study, the inter-relationships of body weight, total fat mass, serum sex hormones and leptin were analysed in untreated hypogonadal men (n=24; age 19-65 years), treated hypogonadal men (n=61; age 20-67 years) and healthy eugonadal men (n=60; age 24-78 years). Total fat mass was assessed by bioimpedance measurement. Univariate and multiple linear regression analysis was used to detect possible differences. RESULTS: In eugonadal men, serum testosterone levels decreased with advancing age (correlation coefficients: r=-0.71; P<0.0001), while BMI (r=0.39; P=0.002), total fat content (r=0.51; P<0.0001) and leptin (r=0.48; P<0.0001) increased significantly. In untreated hypogonadal patients, an increase in BMI (r=0.50; P=0.013) and total fat mass (r=0.41; P=0.044) was also observed with advancing age. However, in substituted hypogonadal patients, no age-dependent change in BMI (r=0.067; P=0.606), body fat content (r=-0.083; P=0.522), serum testosterone (r=-0,071; P=0.59) or serum leptin (r=-0.23; P=0.176) was found. CONCLUSION: Since testosterone-substituted older hypogonadal men show BMI and fat mass similar to those of younger eugonadal men and since non-treated hypogonadal men are similar to normal ageing men, testosterone appears to be an important factor contributing to these changes. Thus ageing men should benefit from testosterone substitution as far as body composition is concerned.
OBJECTIVE: We have previously shown in an acute inpatient setting that dietary substitution of 77.5% of fat kcal as medium chain triglycerides (MCT) increased insulin-mediated glucose metabolism in patients with non-insulin-dependent diabetes mellitus (NIDDM), and that this effect appeared to be mediated by increases in insulin-mediated glucose disposal. The purpose of this study was to test the application of dietary substitution of medium chain triglycerides as an adjunctive tool in ambulatory therapy of NIDDM. METHODS: Five subjects with NIDDM underwent a baseline 6 hour insulin/glucose euglycemic clamp study, with simultaneous 3H-glucose infusion for calculation of glucose disposal rate and hepatic glucose output. Subjects were then randomized to begin one of two 30-day experimental diets, with long chain (LCT) or medium chain triglycerides (MCT), and subsequent crossover to the other diet. A 6 hour euglycemic clamp was repeated after each diet phase. RESULTS: Diet records and urinary organic acid excretion indicated a high level of dietary compliance by the study participants. Postprandial blood glucose excursions were less after one month on the diet with MCT than after the LCT diet (p = 0.004). However, fasting serum glucose, serum fructosamine (a measure of glycemia), fasting insulin, hepatic glucose output, and insulin-mediated glucose metabolism were not improved by the dietary substitution of MCT. CONCLUSION: These data indicate that supplementation of a tolerable amount of MCT in a conventional diabetic exchange diet has little impact on glycemic control in subjects with NIDDM in an ambulatory setting.
In the past, many have avoided nuts because of their high fat content. The Dietary Approaches to Stop Hypertension (DASH) diet, however, recommends regular consumption of this food along with seeds and dried beans (4-5 servings per week) as part of a diet to control hypertension. Nuts are nutrient-dense and most of their fat is unsaturated. They are also perhaps the best natural source of vitamin E and are relatively concentrated repositories of dietary fiber, magnesium, potassium, and arginine, the dietary precursor of nitric oxide. Human feeding studies have demonstrated reductions of 8-12% in low-density lipoprotein (LDL) cholesterol when almonds and walnuts are substituted for more traditional fats. Other studies show that macadamias and hazelnuts appear at least as beneficial as fats in commonly recommended diets. Whether consuming modest quantities of nuts daily may promote weight gain is not known with certainty, but preliminary data suggest that this is unlikely. Four of the best and largest cohort studies in nutritional epidemiology have now reported that eating nuts frequently is associated with a decreased risk of coronary heart disease of the order of 30-50%. The findings are very consistent in subgroup analyses and unlikely to be due to confounding. Possible mechanisms include reduction in LDL cholesterol, the antioxidant actions of vitamin E, and the effects on the endothelium and platelet function of higher levels of nitric oxide. Although nuts may account for a relatively small percentage of dietary calories, the potential interacting effects of these factors on disease risk may be considerable.
The mammary tumor-promoting effect of a high-fat diet containing 20% evening primrose oil (PO) was compared to that of a 20% corn oil (CO) diet. Mammary tumors were induced in female Sprague-Dawley rats using 10 mg (Study 1) and 5 mg (Study 2) 7,12-dimethylbenz(a)anthracene (DMBA). The 10 mg dose of DMBA gave a total mammary tumor incidence of 47% in rats fed the PO diet and 80% for those fed the CO diet. When only adenocarcinomas were counted, the malignant mammary tumor incidences were 41% in rats fed the PO diet and 73% in rats fed the CO diet. In a second study using 5 mg DMBA to induce mammary tumors, total tumor incidences were 50% for PO-fed rats and 63% for those receiving a CO diet. Again, when only adenocarcinomas were counted, tumor incidences were 27% for PO- and 63% for CO-dieted rats. Analysis of plasma fatty acid profiles indicated that animals fed a 20% PO diet showed significant increases in 18:3 and 20:4 fatty acids and significant decreases in 16:0 and 18:1 compared to animals fed a 20% CO diet. These results indicate that the mammary tumor promoting effect of a diet containing 20% fat can be diminished by substituting PO for CO. Moreover, the promoting effect on mammary cancer by a high-fat diet could be depressed by feeding a source of gamma-linolenic acid (GLA).
The protein metabolism of rats bearing bilateral lesions in the ventromedial area of hypothalamus (VMH) was studied in nitrogen balance experiments employing high protein and high fat diets. The catabolic effect of VMH destruction was to a great extent counterbalanced by increased protein intake. This indicates that increased amino acid catabolism, rather than impaired mechanisms for protein synthesis, is responsible for the poor nitrogen retention of VMH-lesioned rat fed normal amounts of protein. A trend of increasing nitrogen excretion with increasing dietary fat was found when the caloric intake of VMH-lesioned animals was elevated by substitution of dietary carbohydrates with fat. Persistent liponeogenesis in spite of the high fat intake, is suggested as a possible explanation for this observation.
Inhibition of fatty acid synthase (FAS) induces a rapid decline in fat stores in mice, suggesting a role for this enzyme in energy homeostasis. The human FAS gene (FAS) maps to chromosome 17q25, a region previously shown to have suggestive linkage to adiposity in a genome-wide linkage scan for genetic determinants of obesity in Pima Indians. To investigate the potential role of FAS in the pathophysiology of human obesity, the FAS gene was sequenced and 13 single nucleotide polymorphisms (SNPs) were identified. Five representative SNPs were genotyped in 216 full-blooded, nondiabetic Pima Indians for association analyses. A Val1483Ile polymorphism (GTC to ATC; allele frequency of A = 0.10) was associated with percentage of body fat and 24-h substrate oxidation rates measured in a respiratory chamber. Compared with homozygotes for the Val variant, subjects with Ile/x had a lower mean percentage of body fat (30 +/- 1 vs. 33 +/- 1%, P = 0.002; adjusted for age, sex, and family membership) and a lower mean carbohydrate oxidation rate (983 +/- 41 vs. 1,094 +/- 19 kcal/day, P = 0.03), which resulted in a lower mean 24-h respiratory quotient (0.845 +/- 0.01 vs. 0.850 +/- 0.01 kcal/day, P = 0.04; both adjusted for age, sex, family membership, percentage of body fat, and energy balance). Our findings indicate that the Val1483Ile substitution in FAS is protective against obesity in Pima Indians, an effect possibly explained by the role of this gene in the regulation of substrate oxidation.
A new experimental approach was used to determine whether a eucaloric, low fat, high carbohydrate diet increases fatty acid synthesis. Normally volunteers consumed low fat liquid formula diets (10% of calories as fat and 75% as glucose polymers, n = 7) or high fat diets (40% of calories as fat and 45% as glucose polymers, n = 3) for 25 d. The fatty acid composition of each diet was matched to the composition of each subject's adipose tissue and compared with the composition of VLDL triglyceride. By day 10, VLDL triglyceride was markedly enriched in palmitate and deficient in linoleate in all subjects on the low fat diet. Newly synthesized fatty acids accounted for 44 +/- 10% of the VLDL triglyceride. Mass isotopomer distribution analysis of palmitate labeled with intravenously infused 13C-acetate confirmed that increased palmitate synthesis was the likely cause for the accumulation of triglyceride palmitate and "dilution" of linoleate. In contrast, there was minimal fatty acid synthesis on the high diet. Thus, the dietary substitution of carbohydrate for fat stimulated fatty acid synthesis and the plasma accumulation of palmitate-enriched, linoleate-deficient triglyceride. Such changes could have adverse effects on the cardiovascular system.