Effects of oatmeal and corn flakes cereal breakfasts on satiety, gastric emptying, glucose, and appetite-related hormones.

OBJECTIVE: The extent to which different types of breakfasts affect appetite and food intake is unclear. To assess the satiety effects of a high-fiber cereal, we compared oatmeal, isocaloric corn flakes, and water. SUBJECTS/METHODS: Thirty-six subjects (18 lean, 18 overweight) were assigned to three conditions in a randomized sequence on different days. Ratings of hunger and fullness were obtained concurrently with blood samples for measuring concentrations of glucose, insulin, glucagon, leptin, and acetaminophen (gastric emptying tracer). Appetite was assessed by calculating the area under the curve (AUC) for fullness and hunger, and by measuring food intake of an ad libitum lunch meal at 180 min. RESULTS: Lunch meal intake was lowest after consuming oatmeal (p < 0.00001), which was lower for overweight subjects than lean subjects (p = 0.007). Fullness AUC was greatest (p = 0.00001), and hunger AUC lowest (p < 0.001) after consuming oatmeal. At 180 min, blood glucose was lowest after the corn flakes (p = 0.0001). Insulin AUC was greater for both cereals than water (p < 0.00001). Leptin AUC and glucagon AUC values did not differ between conditions. Acetaminophen concentrations peaked latest after consuming oatmeal (p = 0.046), reflecting slower gastric emptying. CONCLUSIONS: Satiety was greater and ad libitum test meal intake lower after consuming oatmeal than after corn flakes, especially in the overweight subjects.

Skipping breakfast leads to weight loss but also elevated cholesterol compared with consuming daily breakfasts of oat porridge or frosted cornflakes in overweight individuals: a randomised controlled trial.

Eating breakfast may reduce appetite, body weight and CVD risk factors, but the breakfast type that produces the greatest health benefits remains unclear. We compared the effects of consuming a high-fibre breakfast, a non-fibre breakfast, or no-breakfast control on body weight, CVD risk factors and appetite. A total of thirty-six overweight participants (eighteen men and eighteen women) (mean age 33·9 (sd 7·5) years, mean BMI 32·8 (sd 4·7) kg/m(2)) were randomly assigned to consume oat porridge (n = 12), frosted cornflakes (n = 12) or a water control (n = 12) breakfast daily for 4 weeks. Appetite ratings were collected on the first day and weekly thereafter. Before and after the intervention, body weight, composition, blood pressure and resting energy expenditure (REE) were measured and a fasting blood sample was collected. Across the 4 weeks, fullness was higher and hunger was lower in the oat porridge group compared with the control group (P < 0·05). Mean weight change over the intervention was significantly different in the control group (-1·18 (sd 1·16) kg) compared with both the cornflakes (-0·12 (sd 1·34) kg) and oat porridge (+0·26 (sd 0·91) kg) groups (P < 0·05). However, the control group also showed elevated total cholesterol concentrations relative to the cornflakes and oat porridge groups (P < 0·05). There were no differences between groups in changes in body composition, blood pressure, REE or other CVD risk factors. In conclusion, although skipping breakfast led to weight loss, it also resulted in increased total cholesterol concentrations compared with eating either oat porridge or frosted cornflakes for breakfast.

Ghrelin levels after a cold pressor stress test in obese women with binge eating disorder.

OBJECTIVE: Ghrelin, a peptide hormone secreted mainly by the stomach, increases appetite and food intake. Surprisingly, ghrelin levels are lower in obese individuals with binge eating disorder (BED) than in obese non-BED individuals. Acute psychological stress has been shown to raise ghrelin levels in animals and humans. Our aim was to assess ghrelin levels after a cold pressor test (CPT) in women with BED. We also examined the relationship between the cortisol stress response and changes in ghrelin levels. METHODS: Twenty-one obese (mean [standard deviation] body mass index = 34.9 [5.8] kg/m(2)) women (10 non-BED, 11 BED) underwent the CPT, hand submerged in ice water for 2 minutes. Blood samples were drawn for 70 minutes and assayed for ghrelin and cortisol. RESULTS: There were no differences between the groups in ghrelin levels at baseline (-10 minutes). Ghrelin rose significantly after the CPT (F = 2.4, p = .024) peaking at 19 minutes before declining (F = 17.9, p < .001), but there were no differences between the BED and non-BED groups. Area under the curve for ghrelin was not related to ratings of pain, stress, hunger, or desire to eat after CPT. In addition, there were no observed relationships between the area under the curves for ghrelin or cortisol after stress. CONCLUSIONS: Although there were no differences between BED groups, there was a significant rise in ghrelin in obese humans after a stressor, consistent with other recent reports suggesting a stress-related role for ghrelin.

Cortisol, hunger, and desire to binge eat following a cold stress test in obese women with binge eating disorder.

OBJECTIVE: Increased basal cortisol levels have been found in bulimia nervosa. After stress, increased cortisol levels have been associated with increased food intake in healthy women. Therefore, we assessed cortisol, hunger, and desire to binge eat after a cold pressor test (CPT) among women with binge eating disorder (BED). METHODS: Twenty-two obese (body mass index [BMI] = 36.7 +/- 6.5 SD) females (11 non-BED, 11 BED) completed the Zung depression scale and underwent the CPT, hand submerged in ice water for 2 minutes. Over 60 minutes, periodic ratings of hunger and desire to binge eat were obtained, just before blood draws for cortisol, as well as insulin. On a separate day, participants had a 1-mg oral dexamethasone suppression test (DST). RESULTS: The BED group had higher depression scores than the non-BED (p = .04), but depression was not a significant covariate for the cortisol response or to DST. After controlling for contraceptive use (n = 3), the BED group had higher basal cortisol than the non-BED group (p = .03), but cortisol did not differ after DST (p = .40). The BED group had nearly significant greater cortisol AUC after the CPT (p = .057) after controlling for insulin AUC and contraceptive use (p = .057). The BED group also had greater AUC for hunger (p = .03) and desire to binge eat (p = .02) after the CPT. CONCLUSION: These findings support our hypothesis of a hyperactive HPA-axis in BED, which may contribute to greater hunger and binge eating.

Peripheral and central signals in the control of eating in normal, obese and binge-eating human subjects.

The worldwide increase in the incidence of obesity is a consequence of a positive energy balance, with energy intake exceeding expenditure. The signalling systems that underlie appetite control are complex, and the present review highlights our current understanding of key components of these systems. The pattern of eating in obesity ranges from over-eating associated with binge-eating disorder to the absence of binge-eating. The present review also examines evidence of defects in signalling that differentiate these sub-types. The signalling network underlying hunger, satiety and metabolic status includes the hormonal signals leptin and insulin from energy stores, and cholecystokinin, glucagon-like peptide-1, ghrelin and peptide YY3-36 from the gastrointestinal tract, as well as neuronal influences via the vagus nerve from the digestive tract. This information is routed to specific nuclei of the hypothalamus and brain stem, such as the arcuate nucleus and the solitary tract nucleus respectively, which in turn activate distinct neuronal networks. Of the numerous neuropeptides in the brain, neuropeptide Y, agouti gene-related peptide and orexin stimulate appetite, while melanocortins and alpha-melanocortin-stimulating hormone are involved in satiety. Of the many gastrointestinal peptides, ghrelin is the only appetite-stimulating hormone, whereas cholecystokinin, glucagon-like peptide-1 and peptide YY3-36 promote satiety. Adipose tissue provides signals about energy storage levels to the brain through leptin, adiponectin and resistin. Binge-eating has been related to a dysfunction in the ghrelin signalling system. Moreover, changes in gastric capacity are observed, and as gastric capacity is increased, so satiety signals arising from gastric and post-gastric cues are reduced. Understanding the host of neuropeptides and peptide hormones through which hunger and satiety operate should lead to novel therapeutic approaches for obesity; potential therapeutic strategies are highlighted.

Gastric capacity, test meal intake, and appetitive hormones in binge eating disorder.

Binge eating disorder (BED), characterized by ingestion of very large meals without purging afterwards, is found in a subset of obese individuals. We showed previously that stomach capacity is greater in obese than in lean subjects, and in this study, we investigated capacity in obese individuals with BED. We also determined ad-libitum intake of a test meal until extremely full. Furthermore, we measured various appetitive hormones (insulin, leptin, glucagon, CCK, ghrelin) and glucose before a fixed meal and for 120 min afterwards. An acetaminophen tracer was used to assess gastric emptying rate. We compared three groups of overweight women: 11 BED, 13 BE (subthreshold BED), and 13 non-binge-eating normals. The BED individuals had the largest stomach capacity as assessed by either maximum volume tolerated (P=.05) or by gastric compliance to pressure (P=.02) using an intragastric balloon. Although test meal intake did not differ between groups, it correlated (P=.03) with gastric capacity. The BED group showed a tendency (P=.06) to have greater area under the curve (AUC) and had higher values at 5 and 60 min (P<.05) for insulin compared to normals. Moreover, the BED subjects had lower ghrelin baselines premeal, and lower AUC for ghrelin, which then declined less postmeal than for the normals (P<.05). None of the other blood values differed, including glucose, leptin glucagon, and CCK, as well as acetaminophen, reflecting gastric emptying. The lower ghrelin in BED, although contrary to what was expected, is consistent with lower ghrelin in obesity, and suggests down-regulation of ghrelin by overeating. The lack of differences in CCK is consistent with the lack of differences in gastric emptying rate, given that CCK is released when nutrients reach the intestine. The results show that BED subjects have a large gastric capacity as well as abnormalities in meal-related ghrelin and insulin patterns that may be factors in binge eating.

Obese patients have inadequate protein intake related to protein intolerance up to 1 year following Roux-en-Y gastric bypass.

BACKGROUND: Inadequate protein intake is a concern following Roux-en-Y gastric bypass (RYGBP). The small gastric pouch and bypass restrict energy intake and may lead to insufficient protein intake and absorption, and excess loss of lean tissue. METHODS: We evaluated protein intake in 93 (77 F, 16 M) morbidly obese individuals (BMI = 52.0 +/- 12.9 [SD]) who underwent RYGBP at our medical center. Participants completed 24-hr food recalls and received nutritional counseling at 3, 6, and 12 months following surgery. RESULTS: Daily energy intake (kcal/day) increased from 849 +/- 329 (SD) at 3 months to 1,101 +/- 400 at 12 months (P = .009). Protein intake also increased (g/day) from 45.6 +/- 14.2 at 3 months to 58.5 +/- 17.1 at 12 months (P = .04), and as a percentage of goal protein intake from 55.1% +/- 23.0 at 3 months to 73.5% +/- 38.0 at 12 months (P = .02). Although energy and protein intake increased significantly over the 12-month period, protein intake at 12 months remained significantly lower (P = .01) than the daily recommended guidelines (1.5 g/kg IBW) for a low-energy restrictive diet. Energy intake did not differ in those who reported food intolerances at 3 months (P = .77) or 6 months (P = .65), but was lower in them at 12 months (trend, P = .06). Also at 12 months, protein intake (P = .02) and percentage of protein intake goal (P = .04) were significantly lower in those with protein intolerance. CONCLUSIONS: These results suggest that postoperative patients consume insufficient amounts of protein, possibly mediated by protein intolerance. Protein supplementation following RYGBP deserves further consideration.