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Biomedical subjects

A Raben

Publications and source records attributed to A Raben.

At least 73 records · Page 4Linked to original sources
PubMed1995

[Objective assessment of the habitual dietary fat content in patients with obesity].

A diet rich in fat may be an important precipitating factor of obesity, but studies on this relation have been hampered by the lack of an objective method to assess habitual dietary fat content. We measured 24-h fat oxidation in a respiration chamber in 38 overwight or obese and 35 nonobese women, and used it as an estimate of habitual dietary fat energy (%). After adjustment for confounders, obese women had higher oxidative fat energy than nonobese women [40.2% (37.8-42.6) vs. 36.0% (33.6-38.5), p < 0.02]. Adjusted oxidative fat energy (%) increased with increasing size of fat mass, and this relation suggest that a 10-kg change in fat mass may be caused by a change in dietary fat energy of > or = 1.6%. This objective assessment supports the contention that obese subjects consume a diet with a higher fat content than nonobese individuals, and the high-fat diet may have causal importance for the development and maintenance of obesity.

Adult↗
PubMed1995

The reproducibility of subjective appetite scores.

Although subjective appetite scores are widely used, studies on the reproducibility of this method are scarce. In the present study nine healthy, normal weight, young men recorded their subjective appetite sensations before and during 5 h after two different test meals A and B. The subjects tested each meal twice and in randomized order. Visual analogue scale (VAS) scores, 10 cm in length, were used to assess hunger, satiety, fullness, prospective food consumption and palatability of the meals. Plasma glucose and lactate concentrations were determined concomitantly. The repeatability was investigated for fasting values, delta-mean 5 h and mean 5 h values, delta-peak/nadir and peak/nadir values. Although the profiles of the postprandial responses were similar, the coefficients of repeatability (CR = 2SD) on the mean differences were large, ranging from 2.86 to 5.24 cm for fasting scores, 1.36 to 1.88 cm for mean scores, 2.98 to 5.42 cm for delta-mean scores, and 3.16 to 6.44 cm for peak and delta-peak scores. For palatability ratings the CR values varied more, ranging from 2.38 (taste) to 8.70 cm (aftertaste). Part of the difference in satiety ratings could be explained by the differences in palatability ratings. However, the low reproducibility may also be caused by a conditioned satiation or hunger due to the subjects' prior experience of the meals and therefore not just be a reflection of random noise. It is likely, however, that the variation in appetite ratings is due both to methodological day-to-day variation and to biological day-to-day variation in subjective appetite sensations.

Adult↗
PubMed1995

The effect of raw potato starch on energy expenditure and substrate oxidation.

Because resistant starch (RS) is not absorbed as glucose in the small intestine of healthy humans, postprandial thermogenesis should be lower after the intake of RS as compared with digestible starch. To evaluate this hypothesis, we measured 5-h postprandial thermogenesis and substrate oxidation by indirect calorimetry after ingestion of 50 g pregelatinized (0% RS) and 50 g raw potato starch (54% type II RS) in 15 healthy, normal-weight young males. The subjects consumed each starch (mixed in diluted fruit syrup) twice on separate days and in random order. RS intake was followed by lower thermogenesis (46.5 +/- 13.1 compared with 115.4 +/- 10.4 kJ/5 h; P = 0.008), lower glucose oxidation (P < 0.0005), and greater fat oxidation (P = 0.013) than was pregelatinized starch consumption. Our results suggest that RS has no thermogenic effect and that its presence does not influence the size of the thermic response to digestible starch.

Adult↗
PubMed1995

Spontaneous weight loss during 11 weeks' ad libitum intake of a low fat/high fiber diet in young, normal weight subjects.

OBJECTIVE: During the first 11 weeks of 8 months' ad libitum intake of a low fat/high fiber diet (25.5 energy-% fat, 58.5 energy-% carbohydrate, 3.9 g dietary fiber/MJ) primarily aimed at investigating the effect on blood lipids, spontaneous, unintended body weight changes occurred. The objective of the present paper was to elaborate the analyses on changes in body weight and composition during the 11 weeks' intervention period. MEASUREMENTS: Dietary intake, body weight and composition. SUBJECTS: Subjects in the intervention (I) (n = 24) and control group (C) (n = 24) were normal weight, young, healthy students. RESULTS: In the intervention group an overall decrease in body weight (-1.3 +/- 0.4 kg) (mean +/- s.e.m.) (P < 0.01) and fat mass (-1.6 +/- 0.2 kg, P < 0.001) occurred. Fat free mass remained unchanged (0.1 +/- 0.3 kg, n.s.). Subjects with the initially lowest level of body fat (n = 10) gained fat-free mass (0.6 +/- 0.2 kg) (n.s.) and lost fat mass (-0.9 +/- 0.2) (P < 0.01). In the intervention group initial body weight and fat mass correlated significantly to change in body weight (r = -0.59, P = 0.003 and r = -0.53, P = 0.008) and fat mass (r = -0.52, P = 0.01, and r = -0.50, P = 0.01). No changes were observed in the control group. CONCLUSION: The ad libitum intake of a low fat/high fiber diet lead to a spontaneous loss of body weight and fat mass in young, normal weight subjects.

Adult↗
PubMed1994

Plasma adrenaline concentration is lower in post-obese than in never-obese women in the basal state, in response to sham-feeding and after food intake.

1. Plasma pancreatic polypeptide, plasma catecholamine, blood glucose, plasma insulin and plasma peptide YY concentrations were studied to assess differences between eight formerly obese and eight never-obese control women during 25 min of sham-feeding (with the sight and smell of an English breakfast) and for 5 h after they had ingested the meal (3514 kJ, 50% fat, 35% carbohydrate). The post-obese women had maintained their normal body weight for at least 3 months before the study. 2. The plasma noradrenaline concentration was not different between the groups either during fasting (post-obese women 0.08 +/- 0.01 ng/ml versus control women 0.10 +/- 0.01 ng/ml) or in the significant postprandial increase (P < 0.001). The plasma adrenaline concentration increased significantly during sham-feeding in the control group from 0.024 +/- 0.004 ng/ml to 0.033 +/- 0.004 ng/ml (P = 0.02) in contrast with the post-obese women, who had significantly lower plasma concentrations of adrenaline in the fasting state (post-obese 0.016 +/- 0.003 ng/ml versus control women 0.024 +/- 0.004 ng/ml, P = 0.003), during sham-feeding (post-obese women 0.018 +/- 0.002 ng/ml versus control women 0.033 +/- 0.004 ng/ml, P = 0.003) and in the postprandial increase (P = 0.003). The maximal postprandial response concentrations recorded 5 h after the meal were 0.025 +/- 0.003 ng/ml in post-obese women and 0.035 +/- 0.004 ng/ml in control subjects (P = 0.04). There were no significant differences in plasma pancreatic polypeptide, plasma peptide YY, plasma insulin, or blood glucose concentrations between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Insulin sensitivity in post-obese women.

1. Both increased and decreased sensitivity to insulin has been proposed to precede the development of obesity. Therefore, insulin sensitivity was measured during a 2 h hyperinsulinaemia (100 m-units min-1 m-2) euglycaemic (4.5 mmol/l) glucose clamp combined with indirect calorimetry in nine weight-stable post-obese women and in nine matched control women preceded by 12 h fasting after 48 h on a standardized diet. 2. Both glucose disposal rate (post-obese women, 9.5 +/- 2.2 mg min-1 kg-1, control women, 11.2 +/- 1.4 mg min-1 kg-1, not significant) and glucose oxidation (3.6 +/- 0.5 mg min-1 kg-1 versus 4.0 +/- 0.7 mg min-1 kg-1, not significant) were similar in the two groups during the last 30 min of the clamp. Lipid oxidation also decreased similarly during the clamp in the post-obese women (from 30.4 +/- 12 to 2.0 +/- 7 J min-1 kg-1) and in the control women (from 33.6 +/- 11 to 5.4 +/- 8 J min-1 kg-1, not significant). Basal plasma concentrations of free fatty acids were similar, but at the end of the clamp free fatty acids were lower in the post-obese women than in the control women (139 +/- 19 and 276 +/- 48 mumol/l, P = 0.02). 3. We conclude that the insulin sensitivity of glucose metabolism is unaltered in the post-obese state. The study, however, points to an increased antilipolytic insulin action in post-obese subjects, which may favour fat storage and lower lipid oxidation rate postprandially.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Obesity as an adaptation to a high-fat diet: evidence from a cross-sectional study.

Expansion of the fat stores has been proposed as a prerequisite for increasing fat oxidation in response to a high-fat diet in individuals with a predisposition to obesity. In a cross-sectional design we measured 24-h substrate oxidations on a standardized diet in 38 overweight or obese and 35 nonobese women. Fat oxidation (g/d) was mainly a function of total energy requirements (r = 0.71, P < 0.0001). To account for this we used for further analysis oxidative fat energy (%), a counterpart to dietary fat energy (%). After differences in fat energy of consumed food (%), age, and 24-h energy balance were adjusted for, obese women had higher oxidative fat energy than did nonobese women [40.2% (37.8-42.6) vs 36.0% (33.6-38.5), P < 0.02]. Adjusted oxidative fat energy (%) increased with increasing size of fat mass (r = 0.31, P < 0.01). This relation suggests that a 10-kg change in fat mass may be caused by a change in dietary fat energy of > or = 1.6% (0.4-2.7%). The study supports the concept that in susceptible individuals the expansion of fat stores is a prerequisite to increase the oxidative fat energy to an amount commensurate with a high percentage of dietary fat energy.

Adipose Tissue↗
PubMed1994

Decreased postprandial thermogenesis and fat oxidation but increased fullness after a high-fiber meal compared with a low-fiber meal.

The effect of a high-fiber (4.7 g/MJ) and an isoenergetic low-fiber (1.7 g/MJ) meal on 6-h postprandial thermogenesis, substrate metabolism, hormones, and satiety was investigated in 10 healthy, normal-weight male subjects. Diet-induced thermogenesis (DIT) was significantly reduced after the high-fiber meal (416.4 +/- 28.6 kJ/6 h) compared with the low-fiber meal (498.5 +/- 23.1 kJ/6 h; ANOVA: P < 0.0001), as was postprandial fat oxidation (P < 0.0001). The difference in DIT was correlated with the different palatability of the test meal (r = 0.89, P < 0.01). No differences were observed in plasma concentrations of glucose, insulin, norepinephrine, epinephrine, or gastrointestinal hormones, but C-peptide increased less (P < 0.05) and nonesterified fatty acids decreased more (P < 0.05) after the high-fiber meal. Finally, fullness was increased and desire to eat decreased after the high-fiber meal (P < 0.0001). In conclusion, a high-fiber meal decreased DIT and fat oxidation but increased fullness compared with a low-fiber meal.

Adult↗
PubMed1994

Resistant starch: the effect on postprandial glycemia, hormonal response, and satiety.

The effect of resistant starch (RS) on postprandial plasma concentrations of glucose, lipids, and hormones, and on subjective satiety and palatability ratings was investigated in 10 healthy, normal-weight, young males. The test meals consisted of 50 g pregelatinized starch (0% RS) (S) or 50 g raw potato starch (54% RS) (R) together with 500 g artificially sweetened syrup. After the R meal postprandial plasma concentrations of glucose, lactate, insulin, gastric inhibitory polypeptide (GIP), glucagon-like peptide-1, and epinephrine were significantly lower compared with after the S meal. Moreover, subjective scores for satiety and fullness were significantly lower after the R meal than after the S meal. Differences in GIP, texture, and palatability may have been involved in these findings. In conclusion, the replacement of digestible starch with RS resulted in significant reductions in postprandial glycemia and insulinemia, and in the subjective sensations of satiety.

Adult↗
PubMed1994

Differences in glycaemia, hormonal response and energy expenditure after a meal rich in mono- and disaccharides compared to a meal rich in polysaccharides in physically fit and sedentary subjects.

Postprandial glycaemia, hormonal response and energy expenditure (EE) were measured after two isocaloric carbohydrate-rich meals (69 energy-percent [E%] carbohydrate, 16 E% fat) rich in either mono- and disaccharides (47 E%, half of which sucrose) (MD) or polysaccharides (64 E%; P). Both meals were based on natural food items and were tested in a cross-over design in a group of sedentary (S) and trained (T) healthy, young subjects. Compared with the P meal blood glucose concentrations were significantly decreased and plasma insulin concentration significantly increased after the MD meal. A group difference was observed after the P meal with increased glucose and decreased insulin concentrations for T compared with S. Plasma norepinephrine concentrations were significantly increased after the MD meal compared with the P meal, but for S only. For both groups a significantly increased EE was observed 3 and 5 h after the MD meal compared with the P meal. However, no significant differences between the meals were observed in plasma insulin or catecholamine concentrations 3 and 5 h postprandially, when EE was measured. In conclusion, significant differences were observed in postprandial glucose and hormone responses as well as energy expenditure after two meals based on either mono- and disaccharide-rich or polysaccharide-rich food items. Physical fitness level influenced the glucose and hormonal responses but not the relative increases in postprandial energy expenditure.

Adult↗
PubMed1994

Evidence for an abnormal postprandial response to a high-fat meal in women predisposed to obesity.

The present study was undertaken to investigate fat metabolism after a high-fat meal [50 energy percent (E%) fat] in formerly obese subjects with a familial history of obesity. Twelve normal-weight postobese women (PO) and 12 closely matched controls were given the test meal after a 2-day carbohydrate-rich weight-maintenance diet (58 E% carbohydrate). Whereas the thermic effect of the meals was similar in the two groups, postprandial fat oxidation was 2.5 times more suppressed in PO compared with controls (P < 0.05). A similarly enhanced suppression of arterialized plasma concentrations of nonesterified fatty acids was seen postprandially in PO (P < 0.05), possibly due to a more marked suppression of epinephrine and a reduced glucagon response in PO than in controls. Moreover, the postprandial plasma triglyceride response was attenuated and only amounted to 43% of that in controls (P < 0.05). This may be explained by a more pronounced increase in gastric inhibitory polypeptide in PO, giving rise to a higher adipose tissue lipoprotein lipase activity. No other differences were found in plasma substrates and hormones or in subjective appetite scores. In conclusion, a metabolic and hormonal pattern favoring lipid storage was observed in postobese subjects after a high-fat meal.

Adult↗
PubMed1992

Obesity: an inherited metabolic deficiency in the control of macronutrient balance?

It has generally been assumed that the body is 'energy blind' and calories from all three macronutrients contribute with the same value to energy balance. There is, however, accumulating evidence to suggest that during ad-libitum conditions energy balance is achieved by a separate regulation of carbohydrate, fat and protein balances. Regulation of carbohydrate balance has the highest priority in the hierarchy, which is appropriate because the limited glycogen stores are only capable of covering the carbohydrate oxidation for a few days. Due to the higher satiating power of carbohydrate and protein compared with fat, a reduction in the dietary fat/carbohydrate ratio produces a negative fat balance in normal subjects consuming the diet ad libitum, while an increase in dietary fat/carbohydrate ratio results in a positive fat balance and weight gain. Subjects with a genetically determined predisposition to obesity become obese when they are exposed to a particular range of environmental conditions. The available knowledge suggests that the genetic propensity to weight gain is caused by a susceptibility to dietary fat due to an impaired capacity to increase their lipid/carbohydrate oxidation when fed a high-fat/low-carbohydrate diet. This in turn promotes lipid storage, depletion of carbohydrate stores and increases appetite. By enlarging the fat stores, the accompanying insulin resistance and higher levels of circulating non-esterified fatty acids increase lipid oxidation until it is commensurate with the dietary fat intake. The development of obesity may therefore be viewed as a regulatory mechanism by which the impaired lipid oxidation rate is raised to match a high fat intake. However, by decreasing the dietary ratio of fat to carbohydrate, macronutrient balance may be achieved with a high energy expenditure and a normal body composition. The results support current dietary recommendations, but with less emphasis on carbohydrate source, and they are also applicable for the prevention and treatment of obesity.

Dietary Fats↗
PubMed1992

Serum sex hormones and endurance performance after a lacto-ovo vegetarian and a mixed diet.

Serum sex hormones and endurance performance after a lacto-ovo vegetarian and a mixed diet. Med. Sci. Sports Exerc., Vol. 24, No. 11, pp. 1290-1297, 1992. The effect of a lacto-ovo vegetarian (V) and a mixed, meat-rich (M) diet on the level of serum sex hormones, gonadotropins, and endurance performance of eight male endurance athletes was investigated in a 2 x 6 wk cross-over study. The energy contribution from carbohydrate, fat, and protein was 58%, 27%, and 15% on the V diet and 58%, 28%, and 14 E% on the M diet. For total fasting serum testosterone (T) there was a significant interaction between diet and time (P < 0.01). Thus, the V diet resulted in a lower total T level (13.7, 9.8-32.4 nmol.l-1) (median and range) compared with the M diet (17.4, 11.8-33.5 nmol.l-1). During exercise after 6 wk on the diets total T was also significantly lower on the V than on the M diet (P < 0.05). Serum free testosterone, however, did not differ significantly during the 6 wk dietary intervention periods and neither did serum concentrations of sex hormone binding globulin, dihydrotestosterone, dehydroepiandrosterone sulphate, 4-androstenedione, estrone, estradiol, estrone sulphate, or gonadotropins. Endurance performance time was higher for six and lower for two after the mixed diet compared with the vegetarian diet. This was not significant, however. In conclusion, 6 wk on a lacto-ovo vegetarian diet caused a minor decrease in total testosterone and no significant changes in physical performance in male endurance athletes compared with 6 wk on a mixed, meatrich diet.

Diet↗
PubMed1991

Immune parameters in male atheletes after a lacto-ovo vegetarian diet and a mixed Western diet.

The influence of a lacto-ovo vegetarian diet versus a meat-rich Western diet on in vitro measures of immune function was studied in eight male endurance athletes. Subjects consumed two different diets for 2 x 6 wk, separated by 4 wk on an ad libitum diet, in a cross-over design. Both diets consisted of 57 energy % (E%) carbohydrates, 14 E% protein and 29 E% fat. One diet was a mixed meat-rich diet (M) prepared with 69% animal protein sources, whereas the other diet (V) was a lacto-ovo vegetarian diet prepared with 82% vegetable protein sources. Blood for determination of leukocyte subpopulations and in vitro function was collected at the end of each diet period 36 h after the last training bout. Fiber content and P/S ratio of fatty acids were twice as high on the V diet as on the M diet. Training volume was similar on the two diets, and maximal aerobic capacity did not change during diet periods. The number of CD3+ (pan T-cells), CD8+ (mainly T suppressor cells), CD4+ (mainly T helper cells), CD16+ (natural killer cells), and CD14+ (monocytes) was similar after the two different diets. Similarly, proliferations of mononuclear cells after stimulation with interleukin-2 (IL-2), phytohemagglutinin, and purified derivative of tuberculin (PPD), as well as activity of natural killer cells in the unstimulated state and after stimulation with IL-2, indomethacin, and interferon-alpha (IFN-alpha), were identical after the two diet periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Novel membrane-interactive ether lipid analogs that inhibit infectious HIV-1 production and induce defective virus formation.

A new class of membrane-active ether lipid (EL) analogs of platelet-activating factor were studied for in vitro anti-HIV-1 activity. Human T-cell (CEM-ss) monolayers or suspension cultures were used to determine effects of structural modifications of Type A phosphorus-containing and Type B nonphosphorus EL analogs on (a) the inhibitory concentration50 (IC50) for HIV-1 syncytial plaque formation and cell growth, and, (b) virus budding at the cell plasma membrane. Results indicate that representative Type A and Type B EL inhibit HIV-1 but not herpes simplex virus type 2 plaque formation when added before or up to 2 days after viral infection. Anti-HIV-1 activity does not involve direct inactivation of virus infectivity. Type A EL (IC50 range = 0.2-1.4 microM) with alkyoxy, alkylthio, or alkyamido substitution at glycerol position 1 and ethoxy or methoxy substitution at position 2, and Type B compounds (IC50 range = 0.33-0.63 microM) with an inverse choline or nitrogen heterocyclic substitution at position 3 have selective activity against HIV-1-infected T-cells. EL treatment of HIV-1-infected cells is associated with subsequent release of reverse transcriptase activity, but infectious virus production is inhibited with time after infection. Electron microscopic examination of HIV-1-infected and EL-treated cells revealed absence of detectable budding virus at the plasma membrane but presence of intracytoplasmic vacuolar virus particles. In summary, these data suggest that EL analogs are a novel class of agents that induce defective intracytoplasmic vacuolar HIV-1 formation in T-cells. Being membrane interactive, EL are ideally suited for combination chemotherapy with DNA-interactive anti-HIV nucleoside analogs.

Cell Membrane↗