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Background: The use of dietary supplements, especially those for weight control, is increasing. Advertising claims for some of these supplements may give consumers unrealistic expectations. For example, it is claimed that the supplement chitosan can block the absorption of up to 120 g of dietary fat per day., Objective: To test the effect of a chitosan supplement used as directed, on the absorption of dietary fat., Design: Seven healthy male volunteers with average age 28, range 23-30, average body mass index (BMI) 26, range 23-31, maintained a high fat intake (>120 g/day) for 12 days. On days 6-9, chitosan was taken as directed by the manufacturer prior to meals and snacks and totaled 15 capsules or 5.25 g of chitosan daily. A charcoal marker was consumed on days 2, 6 and 10 to mark the baseline and supplement periods. All feces were collected on days 2-12, and were divided based on the appearance of charcoal in the feces. Fecal fat content corresponding to the four baseline and four chitosan-supplemented days was measured., Results: Average dietary fat intake did not differ between baseline (135+/-5 g), and chitosan (135+/-3 g) periods. Fecal fat excretion did not differ between the two periods (6.9+/-1.0 g/day baseline; 6.8+/-0.4 g/day chitosan). The fecal fat content as a percentage of fat consumed did not differ (5.1+/-0.7% baseline, 5.0+/-0.3% chitosan). Fecal mass did not differ (176+/-26 g/day baseline, 182+/-14 g/day chitosan)., Conclusion: Consumption of this chitosan supplement did not increase fecal fat content and therefore did not block fat absorption.

Leptin, the product of the human homologue of the ob gene, which is defective in the obese (ob/ob) mouse, may be a humoral regulator of human adiposity. Plasma leptin concentrations were measured by RIA in 19 normal weight [body mass index (BMI) = 24.5 +/- 0.6 kg/m2] and 19 overweight to obese (BMI = 34.7 +/- 1.2 kg/m2) nondiabetic postmenopausal women on sequential controlled weight-maintaining diets containing 31%, 23%, and 14% of energy as fat, each for 4-6 weeks. Thereafter, the subjects ate a very low fat diet (< 15%) ad libitum; plasma leptin and insulin concentrations, BMI, percent body fat (%BF), and resting energy expenditure were determined after 6 and 8 months. Absolute and adiposity-corrected plasma leptin levels were higher in overweight/obese women (37.7 +/- 3.5 ng/mL; 1.01 +/- 0.07 ng.mL-1.%BF-1) than in normal weight women (16.9 +/- 2.2 ng/mL; 0.57 +/- 0.06 ng.mL-1.%BF-1, both P < 0.005 vs. obese), but were not different between the 31%, 23%, and 14% fat diets when body weight was stable. Plasma leptin was highly correlated with BMI (r = 0.81, P < 0.0001), %BF (r = 0.80, P < 0.0001), and fasting plasma insulin (r = 0.61, P < 0.0001). After 8 months on the ad libitum low fat diet, the women had lost an average of 6.9 +/- 1.0% of body mass (-2.0 +/- 0.3 kg/m2, P < 0.0001). In 15 subjects who lost more than 7% of body mass (-12.3 +/- 1.0%), plasma leptin concentrations decreased (-9.6 +/- 1.9 ng/mL, P < 0.0005), and the decrease of plasma leptin per change of adiposity (delta leptin/delta %BF) was greater in overweight/obese women (3.6 +/- 0.5) than in normal weight women (0.9 +/- 0.4, P < 0.01 vs. obese). In 18 other subjects who lost less than 7% of body mass (-2.7 +/- 0.6%), plasma leptin was unchanged (+1.4 +/- 1.4 ng/mL). Overall, the change of plasma leptin was significantly correlated with change of BMI (r = 0.43, P < 0.02), the change of %BF (r = 0.49, P < 0.005), the change of resting energy expenditure (r = 0.40, P < 0.02), and with the change of plasma insulin independently of changes of body adiposity (r = 0.45, P < 0.01). We conclude that plasma leptin concentrations are: 1) not affected by dietary fat content per se; 2) highly correlated with BMI, %BF, and plasma insulin in both overweight/obese and normal weight women; 3) decreased in parallel with plasma insulin after sustained weight loss; and 4) decreased more in overweight/obese than in normal weight women.

This study investigates the relationship between exercise and dietary macronutrient selection. Female Sprague-Dawley rats (5 months old) were placed on a macronutrient self-selection diet for 15 wk. Three food cups, each containing a separate vitamin and mineral supplemented macronutrient, i.e., fat, carbohydrate, or protein, were placed in the cage. Animals were either sedentary (Sed) or treadmill exercised (Ex) at 20 m.min-1, 60 min.d-1, for 6 d.wk-1. Cumulative daily energy and macronutrient intake were determined during this period. Energy intake was not different between Sed and Ex, 211.4 vs 213.5 kjoules.d-1, respectively. However, macronutrient intake differed with less fat eaten for Ex than Sed (81.5 kjoules and 38% for Ex; 114.0 kjoules and 47% for Sed). Carbohydrate and protein intake did not differ significantly between groups. Fifteen weeks of exercise training decreased dietary fat selection, but daily energy intake was not affected.

To determine if diet-induced obesity is associated with depressed serotonergic activity (as is genetic obesity), we examined hypothalamic biogenic amines in 11-wk-old genetically lean (Fa/Fa) male Zucker rats raised in small (3 pups/dam) or control (8-9 pups/dam) litters. Five-week-old rats were adrenalectomized or sham-operated and, 1 wk later, fed either 11% of energy as fat (low fat) or 68% of energy as fat (high fat) diets for 5 wk. Tissue punches from the ventromedial nucleus (VMN), the paraventricular nucleus and the preoptic area were assayed via HPLC. Rats fed high vs. low fat had a greater percentage of body fat and brown fat mitochondrial GDP binding, whereas serotonergic turnover was lower. Small litter vs. control litter animals had lower VMN and preoptic concentrations of 3,4-dihydroxyphenylacetic acid, a major metabolite of dopamine. Although adrenalectomy resulted in smaller, leaner rats, it did not differentially affect the rats that became fatter. Because VMN and preoptic dopaminergic activities were depressed in small litter vs. control litter rats but the percentage of body fat was unchanged, this decreased dopamine metabolism is probably not causal to the obesity development. However, the same cannot be said for the attenuated serotonergic activity, although such activity may not be directly related to the degree of obesity.

Lean and obese Zucker fatty rats were adrenalectomized or sham operated at 10 wk of age. At 15 wk one-half of each group was placed on a high-fat diet. At 32 wk of age the experiment was ended. Several conclusions can be drawn about the effects of adrenalectomy, high-fat diets, and their interaction in the Zucker fatty rat. First, adrenalectomy slowed the weight gain in both obese fatty rats and in the lean animals, although the effect was greater in the fatty rats. Second, weight gain was accelerated in intact lean and fatty rats eating a high-fat diet. Third, adrenalectomy attenuated the weight gain associated with a high-fat diet and reduced the body content of fat and protein in the lean animals and fatty rats fed the low-fat diet. Fifth, adrenalectomy significantly affected the retroperitoneal and subcutaneous fat depots but not the epididymal fat depot. Sixth, adrenalectomy decreased fat cell number in retroperitoneal and subcutaneous fat depots, but this was much less evident in the epididymal fat depot. Seventh, lipoprotein lipase activity expressed per milligram protein increased after adrenalectomy in the fatty rat but was reduced on the same basis in lean animals regardless of diet. Finally, the increase in retroperitoneal lipoprotein lipase activity expressed per fat cell observed in lean animals fed the high-fat diet was not observed in the fatty rat. These studies show that a high-fat diet and adrenalectomy interact in the development of obesity in both lean and fatty Zucker rats.

The association among changes in glucose status, glutamate decarboxylase (GAD) activity, and food intake was evaluated in several hypothalamic areas of streptozotocin-diabetic rats fed a low- (12% of calories as fat) or high-fat diet (59% of calories as fat). Control rats consumed approximately 90 kcal/24 h of either diet, whereas diabetic rats consumed approximately 150 kcal/24 h of the low-fat diet and approximately 100 kcal/24 h of the high-fat diet. At the end of the study, diabetic rats fed the high-fat diet weighed more and had higher retroperitoneal fat depot weights (P less than 0.05) than diabetic rats fed the low-fat diet. In diabetic rats, GAD activity was 15-20% higher in the ventromedial nucleus (P less than 0.01) but similar to controls in the lateral hypothalamus, paraventricular nucleus, and area postrema. Diet did not affect GAD activity in the brain areas studied. The increase in ventromedial nucleus GAD activity was not associated with the level of food intake and was the likely result of altered glucose homeostasis in diabetic rats.

Weight cycling (weight loss and regain) increases fat intake in rats allowed to self-select a diet from protein, carbohydrate, and fat sources. This study reports the effects of exercise on macronutrient self-selection. Female Sprague-Dawley rats (5 mo old) self-selected their diet. After 3 wk, rats were assigned to one of the following three groups: ad libitum fed sedentary (Con), sedentary food restricted to 40% Con intake (R-Sed), or treadmill exercised (20 m/min, 1 h/day, 6 day/wk) food restricted to 40% Con intake (R-Ex). Food restriction was for 3 wk followed by 5 wk of refeeding. This was repeated for a second cycle. During restriction, body weight decreased by 30% in R-Sed and by 33% in R-Ex than in R-Sed, fat regain was greater in R-Sed. By week 3 of refeeding, total caloric consumption did not differ. However, fat selection increased in R-Sed (56% kcal) vs. R-Ex (30%) and Con (35%). Fat selection in R-Sed increased further during cycle 2 (73% kcal). Resting oxygen consumption decreased during food restriction in R-Sed and R-Ex. After refeeding, resting metabolic rate in R-Ex was significantly greater than in R-Sed. In conclusion, weight cycling increases dietary fat selection and adiposity. Exercise mitigates this effect.

The effects of high fat feeding on brown fat thermogenesis in rodents are controversial. In this study, we examined the effects of 8 d of high fat feeding on brown fat mitochondrial GDP binding (an in vitro index of thermogenic activity) in lean (Fa/?) and obese (fa/fa) Zucker rats. Six-week-old female rats were fed a defined low fat control diet (9.5% of energy from fat) only during the dark cycle (1200-2400 h), and food intake was measured daily at 1200, 1600, 2300, and 2400 h for 7 d (the control period). For the next 8 d, half of the lean and obese rats were fed a high fat diet (65% of energy from fat), and the others remained on the low fat control diet. Each rat was fed the amount of energy equivalent to its average energy intake during the 7-d control period. Rats were killed at 0800-1000 h. In the lean rats, high fat feeding increased GDP binding. This increased binding in the lean rats appeared to reflect levels of dietary fat and carbohydrate and was independent of caloric intake. The blunted GDP binding of the obese rats failed to respond to dietary changes.

The effect of a high fat diet in stimulating adipocyte proliferation, as measured by the incorporation of [3H]-thymidine into fat cell DNA, was studied in 22-month-old female Sprague-Dawley rats. Rats were fed a low fat (n = 10) or a high fat diet (n = 9) for a total of six days. On days 4 and 5 of dietary manipulation, rats were injected with 80 microCi/100 g body weight of [3H]-thymidine. Rats were continued on their respective diets for one more day, starved for 72 h and then refed a stock diet for three weeks in order to increase turnover of stroma cells, thus diluting the specific activity of stromal DNA with minimal effect on specific activity of fat cell DNA. The diet groups did not differ significantly with respect to body masses, food intake, parametrial (PARA) and retroperitoneal (RP) depot masses, cell number or cell size. The specific activity of DNA in both PARA and RP depots was greater in the adipocyte than in the stromavascular fraction. Specific activity of fat cells was significantly greater from rats fed the high fat than the low fat diet in both PARA and RP depots. Radioautography of adipose tissue confirmed that there was a greater percentage of adipocyte nuclei labeled in the rats fed the high fat diet. Also, there were few labeled nuclei found in stroma cells. In conclusion, older female rats increased adipocyte proliferation when fed a high fat diet.

Five-week-old male obese and lean Zucker rats were made comparably diabetic by intracardiac injections of alloxan (65-72 mg/kg body wt). Lean rats were then given daily injections of protamine zinc insulin at 3 doses: 0.25, 1.25, and 4.0 U.100 g body wt-1.day-1 for 3 wk. Obese rats received identical amounts as corresponding lean controls independent of body weights. The drop of blood glucose concentration after injections of regular insulin and the percentage fall in radioactive plasma insulin after injections of 125I-insulin were comparable in lean and obese rats. Weight gain, fat gain, and protein gain over 21 days increased with increasing amounts of insulin administered. However, at the same dose of insulin, although weight gain was comparable, fat gain was higher and protein gain was lower in obese rats when compared to lean controls. These results suggest that the enhanced lipid deposition of the obese Zucker rat is not totally dependent on insulin levels, but is exaggerated by hyperinsulinemia.

Dietary fat intake, with special emphasis on dairy products, was estimated from questionnaires for 42 underweight, 80 normal weight, and 64 overweight adult women. Frequency of consumption of fresh and processed meats, frozen dairy desserts, pastries, and snacks such as potato chips was greater for the overweight than for the underweight subjects. However, preferences between verbally-described high- and low-fat versions of 14 food pairs did not differ by body size. Overweight subjects reported that they consumed more non-fat milk and less whole milk than did the other groups. Discrimination, perceived intensity, paired preference, and hedonic rating of fat in milk and in chocolate milk did not differ significantly according to body size, fat intake, or type of milk consumed. Ad libitum mixing of non-fat milk and "half and half" (12% fat) to individual levels of liking also showed no significant variation with body size. However, subjects with higher dietary fat intakes mixed to higher fat-preference levels in milk than did the low- and medium-fat intake subjects. Those reporting consumption of regular milk (3.5% fat) mixed to higher fat levels than did those who consumed low-fat (2% fat) or non-fat milk. The ad libitum procedure gave better reproducibility and appeared to be a more realistic measure of liking than the hedonic rating or paired-preference tests.

Five-week-old male, Osborne-Mendel rats were fed a control (CON) or high fat diet (HF) (18 and 68% calories as fat, respectively). At 15 weeks of age HF rats weighed more and had a greater percent body fat than CON rats. Half the rats in each diet group were then exercised for 6 weeks on a treadmill. During exercise, food intake was unaffected in both diet groups, while body weight gain was reduced only in HF rats compared to sedentary rats. Exercise lowered fat gain and decreased lipoprotein lipase (LPL) activity in all rats, reduced in vivo lipogenesis in CON rats, and attenuated the development of obesity in HF rats. Following exercise, rats were kept inactive (i.e., detrained) for 2 weeks. Detraining increased food intake, weight gain, fat deposition and LPL activity in comparison to sedentary rats. In CON detrained rats lipogenesis returned to sedentary levels; in all detrained rats retroperitoneal fat cell number increased over that found in exercised rats. Thus, HF feeding induced obesity while exercise attenuated its development. Exercise-induced effects were not long lasting as they were reversed within 2 weeks of exercise termination as evidenced by a rapid increase in food intake, weight gain and lipogenesis.

The purpose of this study was to describe the effects of high fat (HF) and low fat (LF) diets in male and female Fischer 344 (F344) rats ages 5, 23 and 27 mo. Rats were fed the diet for 3 mo, and then resting metabolic rate, body composition and adipose tissue cellularity were evaluated. Although body mass was greater in rats fed the HF diet, this difference was due to a rapid increase in mass within the first 2 wk. There was no difference in the rate of body mass gain after this period. Resting mass-independent metabolic rate did not significantly differ due to age, diet or gender. In general, percentage fat mass was greater in rats fed the HF diet and in female than in male rats in both diet groups. However, lean body mass (%) was not altered due to diet or age. Cell number of the retroperitoneal depot increased with age and diet between 5 and 23 mo of age in both male and female rats. There was no effect of age, diet or gender on retroperitoneal cell size or gonadal cell number and size. These data suggest that age, gender and diet do not significantly alter the ability of F344 rats to regulate body composition or fat cell proliferation.

To investigate the influence of fatty acid geometric isomers on the growth and experimental metastasis of mammary tumors, mice were fed diets containing fat high in either cis or trans fatty acids. The cis fat was prepared to have a fatty acid composition similar to that of the trans fat; both were provided at 5 or 20% (by weight) of the diet. Line 168 mammary tumor cells were transplanted: 1) subcutaneously into female BALB/c mice to observe the effects of dietary fat on latency and local tumor growth, and 2) intravenously to observe influences on experimental metastasis. No differences in the latency or rate of primary tumor growth were observed among the groups fed the diets containing cis or trans fatty acids. In addition, there were no differences in fatty acid composition except the levels of trans-C18:1 in the primary tumor cells among the groups fed the experimental diets. Livers and spleens from animals fed both the 5 and 20% cis diet contained significantly more viable radiolabeled tumor cells than those fed the trans diets. Although body weight and composition were not significantly different among the groups, livers from animals fed the diets containing trans fatty acids were significantly heavier than those fed diets containing only cis fatty acids. Thus, trans fatty acids behaved similarly to cis fatty acids with respect to promotion of transplantable mammary tumor growth but trans fatty acids were less effective than cis fatty acids in promoting the blood-borne implantation and distant survival of the tumor cells.

Effects of a diet high in fat on body weight, adiposity, and energy expenditure were investigated. Male rats were fed 8% (control) or 50% fat (by weight) for 6 mo. The high-fat group increased body weight (+26%), adipocyte size (+61%), and adipocyte number (+48%). However, food intake and resting oxygen consumption, although higher in absolute amount, were normal in that both were commensurate with the greater body mass the rats maintained. When body weight and adipocyte size were reduced by caloric restriction, the high-fat group displayed the same adaptive adjustments in resting oxygen consumption as controls. We conclude that rats fed high-fat diets for prolonged periods 1) have energy intakes and expenditures appropriate for the greater tissue mass and adipocyte number they maintain, and 2) show adaptive reductions in energy expenditure when food is restricted, which provide further evidence that the regulated level of body weight can be altered by such diets.

Adult female lean and obese Zucker rats were allowed to compose their own diets by giving them access to three macronutrient sources. After a baseline period, the fat source was serially diluted. In all, eight concentrations of fat were used. Dilution of the fat source promoted significant increases in the intake of fat by both lean and obese rats. The increased intake of fat was not simply compensatory in nature, but rather represented significant increases in fat consumption. These results suggest that the reported increased appetite for fat of the obese rat is not a unique trait of that genotype. Further, results from this experiment demonstrate that caloric and protein regulation mechanisms may not be controlling the intake of obese and lean rats as precisely as once believed.

Postprandial oxygen uptake of whole animals and rate of blood flow into the scapular and cervical brown adipose tissue (BAT) of Osborne-Mendel male rats (200 g) were compared for those receiving a high carbohydrate meal or an equicaloric high fat meal. Blood flow was determined by the use of radiolabeled microspheres injected into the left ventricle of anesthetized animals, 2-3 hours after the test meal. In vivo oxygen uptake was elevated by about 10% (P less than 0.05) and blood flow by more than 100% (P less than 0.05) in the group receiving the high carbohydrate meal compared to the high fat meal. The rate of blood flow into tissues other than brown fat was not significantly altered by the composition of the test meal. These tissues included heart, gastrocnemius and soleus muscles, GI tract and white adipose tissue. Our data suggest that a high carbohydrate meal is more thermogenic than a high fat meal, and that the difference in the magnitude of the thermic effect produced by the two meals is paralleled by a corresponding difference in brown fat thermogenesis.