Semisolid meal enriched in oat bran decreases plasma glucose and insulin levels, but does not change gastrointestinal peptide responses or short-term appetite in healthy subjects.

BACKGROUND AND AIMS: Dietary fibre (DF) may play an important role in weight control. The amount, type and way of processing of DF modify food structure and subsequent postprandial appetitive, metabolic and hormonal effects, but current understanding about the magnitude of effects that specific types and amounts of DF exert are still poorly understood. METHODS AND RESULTS: We investigated the effects of wheat and oat brans alone and as combination in semisolid food matrix on postprandial appetite profile and gastrointestinal (GI) hormonal responses. Twenty healthy, normal-weight subjects (5 male/15 female, aged 23.3 ± 0.85y) participated in the study. Isoenergetic and isovolumic (1250 kJ, 300 g) puddings with different insoluble and soluble DF content were tested in a randomised order: pudding with 1) no added fibre, 2) 10 g wheat bran DF, 3) 10 g oat bran DF and 4) combination including 5 g wheat bran DF + 5 g oat bran DF. Blood samples were drawn before and 15, 30, 45, 60, 90, 120 and 180 min after the test meals to determine plasma glucose, ghrelin, peptide YY (PYY) and serum insulin concentrations. Subjective profiles of appetite were assessed using visual analogue scales (VAS). Plasma glucose (P = 0.001) and serum insulin (P < 0.001) responses were the lowest after the pudding with the greatest amount of ß-glucan. In contrast, postprandial ghrelin or PYY responses or appetite sensations did not differ among the meals. CONCLUSION: Oat ß-glucan decreased postprandial plasma glucose and serum insulin responses, yet had no significant effects on GI peptide responses or appetite ratings.

Effect of protein, fat, carbohydrate and fibre on gastrointestinal peptide release in humans.

Short-term regulation of food intake controls what, when and how much we eat within a single day or a meal. This regulation results from an integrated response to neural and humoral signals that originate from the brain, gastrointestinal (GI) tract and adipose tissue. In the GI tract, multiple sites including the stomach, duodenum, distal small intestine, colon, and pancreas are involved in this process. Ingested food evokes satiety by mechanical stimulation and by release of peptides in the GI tract. The intestine in particular plays a key role in satiety through various peptides secreted in response to food. Many of the intestinal peptides inhibit also gastric emptying thus enhancing gastric mechanoreceptor stimulation. In this review, the current knowledge about the effects of different macronutrients and fibre on the release of GI satiety-related peptides in humans is discussed.

Regional cerebral blood flow during exposure to food in obese binge eating women.

Cerebral responses elicited by the sight of food were evaluated in eight obese binge eating, 11 obese and 12 normal-weight non-binge eating women. Regional cerebral blood flow (rCBF) was mapped while the subjects were looking at a picture of a landscape (control) or at a portion of food (food exposure), and was measured by [99mTc]ethyl-cysteine-dimer and single photon emission computed tomography. Exposure to food was associated with different changes in the cerebral blood flow (normalized to mean cerebellar counts) of the right and left hemispheres in the obese binge eating than in the obese or normal-weight non-binge eating women. As compared with the non-binge eating groups, the obese binge eating women had, due to food exposure, a greater increase in the cerebral blood flow in the left than right hemisphere, especially in the frontal and pre-frontal regions. In addition, strong linear correlations were observed in this group between the rCBF of the left frontal and pre-frontal regions and the increase in the feeling of hunger during the exposure to food. Left hemisphere and its frontal and pre-frontal regions could thus play a role in binge eating behavior in humans.

The effect of orlistat on the fatty acid composition of serum lipid fractions in obese subjects.

OBJECTIVE: To determine whether there are any changes in the fatty acid composition of serum triglycerides, cholesterol esters, and phospholipids induced by administration of orlistat three times a day compared with placebo as combined with a low-fat hypocaloric diet. METHODS: After 4 weeks of placebo administration, 75 obese subjects were randomized to receive either one capsule (120 mg) of orlistat or placebo three times a day with meals for 1 year in conjunction with a nutritionally balanced hypocaloric diet. Food records were kept to estimate the nutrient intake. The fatty acid composition of serum lipids were analyzed with gas chromatograph. The molar percentage proportions of fatty acids in serum lipid fractions were calculated. RESULTS: Compared with placebo, there was a significant decrease in the proportion of linoleic acid in triglycerides, cholesterol esters, and phospholipids in the orlistat group, even after the effect of the decrease in the linoleic acid dietary intake (percent of energy), weight change, and gender were taken into account. However, the use of orlistat explained only 9% to 13% of the decrease in the proportion of linoleic acid in serum cholesterol esters, triglycerides, and phospholipids. CONCLUSION: The long-term treatment with orlistat may result in a small decline in the proportion of diet-derived fatty acids in serum lipid fractions when used in conjunction with low-fat diet.

Serum leptin and regional cerebral blood flow during exposure to food in obese and normal-weight women.

Leptin is an adipocyte-derived product of the ob gene thought to be involved in the regulation of eating. Receptors for leptin have been found in multiple regions in the brain. In particular, hypothalamic receptors seem to be of fundamental importance for the biological effects of leptin. However, the association of leptin with cerebral function in humans has not been studied. Therefore, in order to assess the possible functional relationships between leptin and cerebral activity in humans, simultaneous serum leptin and regional cerebral blood flow (rCBF) measurements were made in 10 obese [BMI 33.5 (29.3-39.1) kg/m2] and 12 normal-weight [BMI 22.2 (20.3-24.6) kg/m2] women during exposure to food. The rCBF measurements were performed by 99mTc-ethyl-cysteine-dimer single photon emission computed tomography. A strong inverse association was observed between the leptin and rCBF of hypothalamus during the exposure to food in the obese (r = -0.73, p = 0.02, n = 10), but not in the normal-weight subjects (r = 0.22, p = 0.48, n = 12). This suggests that the association of leptin with cerebral activity could be different in obese and normal-weight women; depressed activity of hypothalamic neurones in response to the high peripheral leptin concentration could be postulated to occur in obese women during exposure to food.

Serum leptin, food intake and preferences for sugar and fat in obese women.

OBJECTIVE: To examine the association of leptin with food intake and preferences for sugar and fat in obese humans. METHOD: Food intake and preferences for sugar and fat were measured in 35 obese women by a four-day food record and three hedonic tests, respectively. RESULTS: High fasting serum leptin concentration adjusted for body fat mass and dietary underreporting was associated with low dietary energy and fat intakes. In addition, trends towards lower preference for chocolate as well as for the taste of high-fat, low-sugar mixture were observed in those with higher leptin concentration. CONCLUSION: High serum leptin concentration could be associated in obese women with lower dietary energy and fat intakes, and possibly with the lower preference for fat. These findings need to be verified in further human studies.

Regional cerebral blood flow during food exposure in obese and normal-weight women.

The cerebral responses elicited by the sight of food and food-related cues are poorly known in humans. Therefore, regional cerebral blood flow (rCBF) was measured during food exposure in 11 obese and 12 normal-weight women. The rCBF was mapped while the subject was looking at a picture of a landscape (control) or at a portion of food (food exposure), and was measured by 99mTc-ethyl-cysteine-dimer single photon emission computed tomography. In the obese women, the rCBF was higher in the right parietal and temporal cortices during the food exposure than in the control condition. In addition, in the obese women the activation of the right parietal cortex was associated with an enhanced feeling of hunger when looking at food. No such changes or associations were seen in the normal-weight women. In conclusion, exposure to food is associated with increases in the rCBF of right parietal and temporal cortices in obese women, but not in normal-weight women.

Serum leptin in obesity is related to gender and body fat topography but does not predict successful weight loss.

OBJECTIVE: Leptin is the product of the ob gene shown to regulate body fat and appetite in mice. It is produced by human adipose tissue also, but its physiological functions in man are poorly known. STUDY DESIGN AND METHODS: We studied serum leptin concentrations in ten obese men and 35 obese women (age and body mass index 42 +/- 7 years and 35.1 +/- 3.6 kg/m2 respectively) before (baseline) and at 17 and 57 weeks during weight loss of 10.9% of the initial weight. RESULTS: Serum leptin concentrations at baseline were 55% higher in women than in men (after adjustment for age and body fat mass, P = 0.002) and remained so during the follow-up. At baseline, serum leptin correlated with fat mass (r = 0.60, P < 0.001) estimated by bioelectrical impedance, and the changes in leptin concentrations from baseline to week 17 correlated with the changes in fat mass (r = 0.73, P < 0.001), but baseline leptin levels were not predictive of the successful weight loss. Leptin concentrations correlated with hip circumference (r = 0.49, P < 0.001 at baseline adjusted for age and sex), but the correlation with waist circumference became evident only during the weight loss (at week 57, r = 0.63, P < 0.001). CONCLUSIONS: Serum leptin concentrations are higher in obese women than in obese men before and during weight loss, but the topography of fat tissue influences serum leptin concentrations. Serum leptin concentrations do not predict the response to weight reduction.

Subjective and physiological cephalic phase responses to food in obese binge-eating women.

OBJECTIVE: The subjective and physiological cephalic phase reactivity to food was investigated in obese binge-eating women. METHOD: Eleven obese binge-eating women and 10 obese nonbinge-eating women participated in a cephalic phase response test consisting of baseline, anticipation, food exposure, and free eating periods. Serum insulin, free fatty acids, and plasma glucose concentrations as well as salivation, feeling of hunger, and desire to eat were repeatedly measured during the test. RESULTS: During the food exposure, the binge eaters reported more desire to eat than did the nonbinge eaters. No differences were found between the groups in the physiological cephalic phase responses except for the lower salivation in the binge eaters during the food exposure. The amount of food eaten after the food exposure was similar in both groups. DISCUSSION: Binge-eating women are characterized by stronger subjective but not stronger physiological cephalic phase reactivity to food.

Serum leptin in relation to resting energy expenditure and fuel metabolism in obese subjects.

OBJECTIVE: Leptin is the product of ob gene shown to regulate body fat in mice. It is produced by human adipose tissue as well, but its physiological functions in man are not known. We explored if there is a relationship in obese humans with serum leptin and energy and fuel metabolism. DESIGN: Cross-sectional study including 45 obese (10 men, 35 women; age and body mass index: 42 +/- 7 y and 35.1 +/- 3.6 kg/m2, respectively). MEASUREMENTS: Food intake by a four-day-food record, blood samples for serum leptin concentrations and resting energy expenditure by indirect calorimetry. RESULTS: Leptin concentrations showed an inverse association (adjusted for fat mass, age and sex) with resting energy expenditure, respiratory quotient and carbohydrate oxidation rate (r = -0.324, P < 0.05; r = -0.420, P < 0.01; r = 0.478, P = < 0.01, respectively), and interestingly, also with dietary fat intake (unadjusted r = -0.30, P < 0.05). Especially, leptin concentrations were elevated in those with low resting energy expenditure and respiratory quotient (below the median). CONCLUSION: Serum leptin concentrations in obese subjects showed an inverse association with resting energy expenditure, respiratory quotient and carbohydrate oxidation rate. The physiological significance of these associations is unclear at the moment but could indicate that obese subjects show resistance to the actions of leptin also outside the brain in terms of regulating metabolic rate and fuel metabolism.

Determinants of the cephalic-phase insulin response in obese nondiabetic subjects.

Large interindividual variation is characteristic of the cephalic-phase insulin response (CPIR). Our aim was to examine the largely unknown determinants of CPIR in obese nondiabetic subjects before and after weight reduction. After a 12-hour overnight fast, 20 healthy, obese (body mass index, 31.1 to 41.4 kg/m2) subjects were individually exposed to food without being allowed to eat it. Levels of insulin, glucose, C-peptide, free fatty acids, and salivation, together with assessments of feeling of hunger and desire to eat, were measured during the experiment. Subjects were divided into three groups according to CPIR before the weight reduction: positive (PR), intermediate (IR), and negative (NR) responders. CPIR measurements before and after weight reduction correlated significantly with each other (r = .61, P < . 01,n=18). At the beginning of the study, NR had higher fasting plasma glucose and insulin values, as well as higher postload plasma glucose values, as compared with PR and IR. These differences disappeared after weight reduction. In an intravenous glucose tolerance test (IVGTT) performed 9 to 12 months afterward, first-phase insulin secretion was significantly lower in NR. Thus, the negative CPIR during visual and olfactory exposure to food-related stimuli may be related to the attenuated first-phase insulin secretion and mildly impaired glucose metabolism, possibly related to insulin resistance.

Effect of cheese on intestinal transit time and other indicators of bowel function in residents of a retirement home.

Effects of increased intake of cheese on intestinal transit time and other indicators of bowel function were studied in 21 retirement home residents (18 women and 3 men; age, 68-87 years). The study was divided into four succeeding periods: 1) 1-week basal period (usual diet); 2)3-week cheese period (extra cheese was offered as such on bread or used in cooking); 3) 3-week no-cheese period (all cheese on bread was replaced with cured meats and cold cuts, and no cheese was used in cooking); 4) 3-week follow-up period (usual diet). During the last week of each period a questionnaire was filled out on fecal frequencies, consistency of feces (soft, normal, hard), and occurrence of abdominal pain and flatulence. Use of laxative medications and therapeutic foods (prunes) was registered. Eleven of the 21 subjects collected fecal samples for the determination of fecal wet weight and intestinal transit time by means of radiopaque Sitzmark capsules. Intakes of cheese, fiber-containing foods, and fluids by these 11 subjects during meals offered in the cafeteria were recorded on a prefilled questionnaire. In spite of a 10-fold increase in the intake of cheese no change in intestinal transit time, fecal frequency, fecal wet weight, consistency of feces, and occurrence of gastrointestinal symptoms was observed. The use of laxative medication was higher during the cheese period, but no change in the combined use of laxative medication and therapeutic foods (prunes) was observed.(ABSTRACT TRUNCATED AT 250 WORDS)