A High‐fat vs. a Moderate‐fat Meal in Obese Boys: Nutrient Balance,Appetite, and Gastrointestinal Hormone Changes

Meal composition is a contributing factor to fat gain. In this study, we investigated the relationship between postprandial nutrient balance, satiety, and hormone changes induced by a high‐fat meal vs. a moderate‐fat meal. Ten prepubertal obese boys (BMI z‐score range: 1.3–3.0) were recruited. Two meals (energy: 590 kcal) were compared: (i) high‐fat (HF) meal: 12% protein, 52% fat, 36% carbohydrates; (ii) moderate‐fat (MF) meal: 12% protein, 27% fat, 61% carbohydrates. Pre‐ and postprandial (5 h) substrate oxidation (indirect calorimetry), appetite (visual analogue scale), biochemical parameters and gastrointestinal hormone concentrations were measured. Carbohydrate balance was significantly (P < 0.001) lower (31.3 (5.7) g/5 h vs. 66.9 (5.9) g/5 h) and fat balance was significantly (P < 0.001) higher (11.5 (3.3) g/5 h vs. ?0.7 (2.9) g/5 h) after HF than MF meal. Appetite (area under the curve (AUC)) was significantly reduced after an MF than an HF meal (494 (55) cm·300 min vs. 595 (57) cm·300 min, P < 0.05). Postprandial triglyceride concentration (AUC) was significantly (P < 0.05) higher after an HF than an MF meal: 141.1 (30.3) mmol·300 min/l vs. 79.3 (23.8) mmol·300 min/l, respectively. Peptide YY (PYY), cholecystokinin (CCK), and ghrelin concentrations (AUC) were not significantly different after an HF and MF meal. Glucagon‐like peptide‐1 (GLP‐1) was significantly (P < 0.05) higher after an HF than after an MF meal (72.3 (9.8) ng/ml vs. 22.7 (7.6) ng/ml, respectively), but it did not affect subjective appetite. In conclusion, an MF meal induced a better postprandial metabolic nutrient balance, triglyceride levels, and appetite suppression than an HF meal. Gastrointestinal hormones were not related to clinically assessed hunger suppression after both meals.     

The Influence of Higher Protein Intake and Greater Eating Frequency on Appetite Control in Overweight and Obese Men

The purpose of this study was to determine the effects of dietary protein intake and eating frequency on perceived appetite, satiety, and hormonal responses in overweight/obese men. Thirteen men (age 51 ± 4 years; BMI 31.3 ± 0.8 kg/m²) consumed eucaloric diets containing normal protein (79 ± 2 g protein/day; 14% of energy intake as protein) or higher protein (138 ± 3 g protein/day; 25% of energy intake as protein) equally divided among three eating occasions (3‐EO; every 4 h) or six eating occasions (6‐EO; every 2 h) on four separate days in randomized order. Hunger, fullness, plasma glucose, and hormonal responses were assessed throughout 11 h. No protein × eating frequency interactions were observed for any of the outcomes. Independent of eating frequency, higher protein led to greater daily fullness (P < 0.05) and peptide YY (PYY) concentrations (P < 0.05). In contrast, higher protein led to greater daily ghrelin concentrations (P < 0.05) vs. normal protein. Protein quantity did not influence daily hunger, glucose, or insulin concentrations. Independent of dietary protein, 6‐EO led to lower daily fullness (P < 0.05) and PYY concentrations (P < 0.05). The 6‐EO also led to lower glucose (P < 0.05) and insulin concentrations (P < 0.05) vs. 3‐EO. Although the hunger‐related perceived sensations and hormonal responses were conflicting, the fullness‐related responses were consistently greater with higher protein intake but lower with increased eating frequency. Collectively, these data suggest that higher protein intake promotes satiety and challenge the concept that increasing the number of eating occasions enhances satiety in overweight and obese men.     

The Effects of Consuming Frequent,Higher Protein Meals on Appetite and Satiety During Weight Loss in Overweight/Obese Men

The purpose of this study was to determine the effects of dietary protein and eating frequency on perceived appetite and satiety during weight loss. A total of 27 overweight/obese men (age 47 ± 3 years; BMI 31.5 ± 0.7 kg/m²) were randomized to groups that consumed an energy‐restriction diet (i.e., 750 kcal/day below daily energy need) as either higher protein (HP, 25% of energy as protein, n = 14) or normal protein (NP, 14% of energy as protein, n = 13) for 12 weeks. Beginning on week 7, the participants consumed their respective diets as either 3 eating occasions/day (3‐EO; every 5 h) or 6 eating occasions/day (6‐EO; every 2 h), in randomized order, for 3 consecutive days. Indexes of appetite and satiety were assessed every waking hour on the third day of each pattern. Daily hunger, desire to eat, and preoccupation with thoughts of food were not different between groups. The HP group experienced greater fullness throughout the day vs. NP (511 ± 56 vs. 243 ± 54 mm · 15 h; P < 0.005). When compared to NP, the HP group experienced lower late‐night desire to eat (13 ± 4 vs. 27 ± 4 mm, P < 0.01) and preoccupation with thoughts of food (8 ± 4 vs. 21 ± 4 mm; P < 0.01). Within groups, the 3 vs. 6‐EO patterns did not influence daily hunger, fullness, desire to eat, or preoccupation with thoughts of food. The 3‐EO pattern led to greater evening and late‐night fullness vs. 6‐EO but only within the HP group (P < 0.005). Collectively, these data support the consumption of HP intake, but not greater eating frequency, for improved appetite control and satiety in overweight/obese men during energy restriction‐induced weight loss.     

Influence of rest and exercise at a simulated altitude of 4,000 m on appetite, energy intake, and plasma concentrations of acylated ghrelin and peptide YY

The reason for high altitude anorexia is unclear but could involve alterations in the appetite hormones ghrelin and peptide YY (PYY). This study examined the effect of resting and exercising in hypoxia (12.7% O(2); ～4,000 m) on appetite, energy intake, and plasma concentrations of acylated ghrelin and PYY. Ten healthy males completed four, 7-h trials in an environmental chamber in a random order. The four trials were control-normoxia, control-hypoxia, exercise-normoxia, and exercise-hypoxia. During exercise trials, participants ran for 60 min at 70% of altitude-specific maximal oxygen consumption (Vo(2max)) and then rested. Participants rested throughout control trials. A standardized meal was consumed at 2 h and an ad libitum buffet meal at 5.5 h. Area under the curve values for hunger (assessed using visual analog scales) tended to be lower during hypoxic trials than normoxic trials (repeated-measures ANOVA, P = 0.07). Ad libitum energy intake was lower (P = 0.001) in hypoxia (5,291 ± 2,189 kJ) than normoxia (7,718 ± 2,356 kJ; means ± SD). Mean plasma acylated ghrelin concentrations were lower in hypoxia than normoxia (82 ± 66 vs. 100 ± 69 pg/ml; P = 0.005) while PYY concentrations tended to be higher in normoxia (32 ± 4 vs. 30 ± 3 pmol/l; P = 0.059). Exercise suppressed hunger and acylated ghrelin and increased PYY but did not influence ad libitum energy intake. These findings confirm that hypoxia suppresses hunger and food intake. Further research is required to determine if decreased concentrations of acylated ghrelin orchestrate this suppression.     

Increased Carbohydrate Induced Ghrelin Secretion in Obese vs. Normal‐weight Adolescent Girls

Orexigenic and anorexigenic pathways mediate food intake and may be affected by meal composition. Our objective was to determine whether changes in levels of active ghrelin and peptide YY (PYY) differ in obese vs. normal‐weight adolescent girls following specific macronutrient intake and predict hunger and subsequent food intake. We enrolled 26 subjects: 13 obese and 13 normal‐weight girls, 12–18 years old, matched for maturity (as assessed by bone age) and race. Subjects were assigned a high‐carbohydrate, high‐protein, and high‐fat breakfast in random order. Active ghrelin and PYY were assessed for 4 h after breakfast and 1 h after intake of a standardized lunch. Hunger was assessed using a standardized visual analog scale (VAS). No suppression in active ghrelin levels was noted following macronutrient intake in obese or normal‐weight girls. Contrary to expectations, active ghrelin increased in obese girls following the high‐carbohydrate breakfast, and the percent increase was higher than in controls (P = 0.046). Subsequent food intake at lunch was also higher (P = 0.03). Following the high‐fat breakfast, but not other breakfasts, percent increase in PYY was lower (P = 0.01) and subsequent lunch intake higher (P = 0.005) in obese compared with normal‐weight girls. In obese adolescents, specific intake of high‐carbohydrate and high‐fat breakfasts is associated with greater increases in ghrelin, lesser increases in PYY, and higher intake at a subsequent meal than in controls. Changes in anorexigenic and orexigenic hormones in obese vs. normal‐weight adolescents following high‐carbohydrate and high‐fat meals may influence hunger and satiety signals and subsequent food intake.     

Characteristics Associated With Fasting Appetite Hormones (Obestatin,Ghrelin, and Leptin)

Obestatin, derived from the same gene as the hunger hormone ghrelin, may reduce food intake in animals. The role of obestatin in human physiology is unclear. We evaluated cross‐sectional associations between participant characteristics and fasting levels of obestatin as well two other hormones associated with energy balance, ghrelin and leptin. Data are from the baseline visit of the Optimal Macronutrient Intake Trial to Prevent Heart Disease (OMNI‐Heart) Trial that enrolled adults with elevated blood pressure (systolic 120–159 mm Hg or a diastolic of 80–99 mm Hg) but who were otherwise healthy. Partial Spearman's correlations and linear regression models estimated the association between age, gender, BMI, physical activity, and smoking with fasting hormones. Obestatin was directly associated with ghrelin (r = 0.45, P < 0.05). On average, overweight (BMI 25–30) and obese (BMI > 30) individuals had obestatin concentrations that were 12.6 (s.d. 8.8) and 25.4 (s.d. 8.4) pg/ml lower compared to normal weight (BMI < 25) individuals, respectively (P for trend = 0.002). Overweight (BMI 25–30) and obese (BMI > 30) individuals had ghrelin concentrations that were 161.7 (s.d. 69.6) and 284.7 (s.d. 66.5) pg/ml lower compared to normal weight (BMI < 25) individuals, respectively (P for trend <0.0001). A 5 unit increase in BMI was associated with 41.3% (s.d. 4.3%) (P < 0.0001) higher leptin. Obestatin and ghrelin are directly correlated and share the same patterns of association with participant characteristics. Modifiable risk factors for chronic diseases, such as BMI, are associated with fasting levels of leptin, obestatin, and ghrelin.     

The individual and combined effects of glycemic index and protein on glycemic response, hunger, and energy intake

Although high protein and low glycemic index (GI) foods are thought to promote satiety, little is known about the effects of GI, protein, and their interaction on hunger and energy intake several hours following a mixed meal. This study investigated the long term effects of GI, protein, and their combined effects on glucose, insulin, hunger, and energy intake in healthy, sedentary, overweight, and obese adults (BMI of 30.9 ± 3.7 kg/m²). Sixteen individuals participated separately in four testing sessions after an overnight fast. The majority (75%) were non‐Hispanic Blacks. Each consumed one of four breakfast meals (high GI/low protein, high GI/high protein, low GI/low protein, low GI/high protein) in random order. Visual analog scales (VAS) and blood samples were taken at baseline, 15 min, and at 30 min intervals over 4 h following the meal. After 4 h, participants were given the opportunity to consume food ad libitum from a buffet style lunch. Meals containing low GI foods produced a smaller glucose (P < 0.002) and insulin (P = 0.0001) response than meals containing high GI foods. No main effects for protein or interactions between GI and protein were observed in glucose or insulin responses, respectively. The four meals had no differential effect on observed energy intake or self‐reported hunger, satiety, and prospective energy intake. Low GI meals produced the smallest postprandial increases in glucose and insulin. There were no effects for GI, protein, or their interaction on appetite or energy intake 4 h after breakfast.     

Effects of acute and chronic protein intake on metabolism, appetite, and ghrelin during weight loss

Objective: This study evaluated the effects of acute and chronic consumption of higher dietary protein on energy expenditure, macronutrient use, appetite, and appetite‐regulating hormones during weight loss in women. Research Methods and Procedures: Thirty‐eight women chronically consuming a 750 kcal/d energy‐deficit diet with a protein content of 30% (higher protein‐chronic diet, HP‐CD, n = 21) or 18% (normal protein‐chronic diet, NP‐CD, n = 17) for 9 weeks were tested. On separate days, metabolic, appetite, and hormonal responses were measured over 4 hours when the women consumed a higher protein‐acute meal (HP‐AM) (30% of energy as protein) or a normal protein‐acute meal (NP‐AM) (18% of energy as protein). Results: With chronic diet groups combined, HP‐AM led to lower respiratory exchange ratio (0.829 ± 0.005 vs. 0.843 ± 0.008; p < 0.05), lower carbohydrate oxidation (p < 0.05), and higher fat oxidation (p < 0.05) compared with NP‐AM. HP‐AM also led to reduced self‐reported postprandial hunger (p < 0.001) and desire to eat (p < 0.001) and lower postprandial ghrelin (252 ± 16 vs. 274 ± 18 ng/mL · 240 minutes, p < 0.05) compared with NP‐AM. No differences in postprandial energy expenditure (PPEE) occurred between meals. When combining acute meals, respiratory exchange ratio was lower (p < 0.05) and protein oxidation (p < 0.001) was higher in the HP‐CD vs. NP‐CD. An acute meal‐by‐chronic diet interaction was observed with PPEE such that HP‐AM led to greater PPEE in the HP‐CD vs. NP‐CD (28.7 ± 2.7 vs. 19.9 ± 2.7 kcal/min for 195 minutes; p < 0.05). Conclusions: During weight loss, thermogenesis and protein use appear to be influenced by chronic protein intake, while appetite and ghrelin are more responsive to acute protein intake.     

The internal circadian clock increases hunger and appetite in the evening independent of food intake and other behaviors

Objective:

Despite the extended overnight fast, paradoxically, people are typically not ravenous in the morning and breakfast is typically the smallest meal of the day. We assessed whether this paradox could be explained by an endogenous circadian influence on appetite with a morning trough, while controlling for sleep/wake and fasting/feeding effects.

Design and Methods:

Twelve healthy non‐obese adults (six males; age, 20‐42 years) were studied throughout a 13‐day laboratory protocol that balanced all behaviors, including eucaloric meals and sleep periods, evenly across the endogenous circadian cycle. Participants rated their appetite and food preferences by visual analog scales.

Results:

There was a large endogenous circadian rhythm in hunger, with the trough in the biological morning (8 AM) and peak in the biological evening (8 PM; peak‐to‐trough amplitude = 17%; P = 0.004). Similarly‐phased significant endogenous circadian rhythms were present in appetites for sweet, salty and starchy foods, fruits, meats/poultry, food overall, and for estimates of how much food participants could eat (amplitudes 14‐25%; all P < 0.05).

Conclusions:

In people who sleep at night, the intrinsic circadian evening peak in appetite may promote larger meals before the fasting period necessitated by sleep, whereas the circadian morning trough would theoretically facilitate the extended overnight fast. Furthermore, the circadian decline in hunger across the night would theoretically counteract the fasting‐induced hunger increase that could otherwise disrupt sleep.     

Exercise-induced suppression of acylated ghrelin in humans.

Ghrelin is an orexigenic hormone secreted from endocrine cells in the stomach and other tissues. Acylation of ghrelin is essential for appetite regulation. Vigorous exercise induces appetite suppression, but this does not appear to be related to suppressed concentrations of total ghrelin. This study examined the effect of exercise and feeding on plasma acylated ghrelin and appetite. Nine male subjects aged 19-25 yr participated in two, 9-h trials (exercise and control) in a random crossover design. Trials began at 0800 in the morning after an overnight fast. In the exercise trial, subjects ran for 60 min at 72% of maximum oxygen uptake between 0800 and 0900. After this, they rested for 8 h and consumed a test meal at 1100. In the control trial, subjects rested for 9 h and consumed a test meal at 1100. Area under the curve values for plasma acylated ghrelin concentration (assessed from venous blood samples) were lower over the first 3 h and the full 9 h of the exercise trial compared with the control trial: 317+/-135 vs. 510+/-186 pg.ml(-1).3 h and 917+/-342 vs. 1,401+/-521 pg.ml(-1).9 h (means+/-SE) respectively (P<0.05). Area under the curve values for hunger (assessed using a visual scale) were lower over the first 3 h of the exercise trial compared with the control trial (P=0.013). These findings demonstrate that plasma acylated ghrelin concentration and hunger are suppressed during running.     

Mode of consumption plays a role in alleviating hunger and thirst

While studying the effect of structure on satiety, effects of mode of consumption, additional water to drink, and thirst have been neglected. The objective was to assess effects of structure, mode of consumption of food, and additional drinking of water on fullness and thirst. In study 1, 20 subjects (BMI 22.5 ± 0.5 kg/m(2); age 21.4 ± 3 years) underwent consumption conditions; SEW: solids to eat + 750 ml water to drink; LEW: liquefied soup to eat including 500 ml water + 250 ml water separately to drink; LDW: the same as LEW but served as drinks; SE, LE, and LD: the same as previous but without water to drink. In study 2, a subset of subjects underwent consumption conditions: solid carbohydrate, solid protein, solid fat: the same as SEW, but for each macronutrient separately; liquefied carbohydrate, liquefied protein, liquefied fat: the same as LEW, but for each macronutrient separately. Appetite, insulin concentration, glucose concentration, and ghrelin concentration were measured. Eating, independent of structure, suppressed desire to eat more than drinking (P < 0.01). Drinking water separately vs. water consumption in the food suppressed thirst more (P < 0.001). Regarding protein, satiety was higher in the solid vs. liquefied condition, while blood parameters were not significantly different. Only after drinking a meal most subjects (80%) wanted to consume more of the same meal, in order to alleviate hunger (63%) or quench thirst (37%). We conclude that mode of consumption plays a role in alleviating hunger and thirst. Subjects required further consumption after drinking the meal, motivated by hunger or thirst, showing that drinking a meal causes confusion that may imply a risk of overconsumption.     

A solid high-protein meal evokes stronger hunger suppression than a liquefied high-protein meal

Hunger is a potential problem for compliance with an energy-restricted diet. Relatively high-protein meal-replacement products have been shown to diminish this problem; they are available as liquid and solid meals, yet their physical state can affect hunger suppression. The objective was to investigate the differences in appetite profile and physiological parameters after consumption of a single-macronutrient, subject-specific, high-protein meal in liquefied vs. solid form, controlled for energy density, weight, and volume. Ten male subjects (age: 21.1 ± 3.9 years; BMI: 22.4 ± 1.2 kg/m2) were offered lunch subject-specifically as 15% of daily energy requirement (DER), consisting of solid (steamed chicken breast + 750 ml water) or liquefied protein (steamed chicken breast blended in 500 ml water + 250 ml water). Appetite profiles, insulin, glucose, and ghrelin were measured over 3 h. Comparing the solid vs. liquefied condition, oral exposure time did not differ between conditions (19.2 ± 0.4 and 18.8 ± 0.6 min, respectively; P = 0.13). Area under the curve (AUC) effects were observed for thirst; statistically significant condition × time interactions and statistically significant differences at several time points were observed for desire to eat (condition × time P < 0.05; 31 ± 6 mm vs. 53 ± 8 mm; P < 0.04 at 115 min) and thirst (condition × time P < 0.01; 27 ± 8 mm vs. 41 ± 8 mm; P < 0.05 at 30 min and 23 ± 6 mm vs. 41 ± 8 mm; P < 0.02 at 70 min) to be lower, while hunger suppression (79 ± 3 mm and 52 ± 10 mm; P < 0.03 at 20 min and 61 ± 7 mm and 44 ± 8 mm; P < 0.03 at 115 min) was higher in the solid condition. Glucose, insulin, and ghrelin concentration curves were similar for both conditions. In conclusion, solid protein evokes a stronger suppression of hunger and desire to eat than liquefied protein.     

Low-dose pramlintide reduced food intake and meal duration in healthy, normal-weight subjects

Objective: We previously reported that a single preprandial injection (120 μg) of pramlintide, an analog of the β‐cell hormone amylin, reduced ad libitum food intake in obese subjects. To further characterize the meal‐related effects of amylin signaling in humans, we studied a lower pramlintide dose (30 μg) in normal‐weight subjects. Research Methods and Procedures: In a randomized, double‐blind, placebo‐controlled, cross‐over study, 15 healthy men (age, 24 ± 7 years; BMI, 22.2 ± 1.8 kg/m²) underwent a standardized buffet meal test on two occasions. After an overnight fast, subjects received a single subcutaneous injection of pramlintide (30 μg) or placebo, followed immediately by a standardized pre‐load meal. After 1 hour, subjects were offered an ad libitum buffet meal, and total caloric intake and meal duration were measured. Results: Compared with placebo, pramlintide reduced total caloric intake (1411 ± 94 vs. 1190 ± 117 kcal; Δ, ?221 ± 101 kcal; ?14 ± 9%; p = 0.05) and meal duration (36 ± 2 vs. 31 ± 3 minutes; Δ, ?5.1 ± 1.4 minutes; p < 0.005). Visual analog scale profiles of hunger trended lower and fullness higher during the first hour after pramlintide administration. In response to the buffet, hunger and fullness changed to a similar degree after pramlintide and placebo, despite subjects on pramlintide consuming 14% fewer kilocalories. Visual analog scale nausea ratings remained near baseline, without differences between treatments. Plasma peptide YY, cholecystokinin, and ghrelin concentrations did not differ with treatment, whereas glucagon‐like peptide‐1 concentrations after meals were lower in response to pramlintide than to placebo. Discussion: These observations add support to the concept that amylin agonism may have a role in human appetite control.     

The Impact of Food Viscosity on Eating Rate,Subjective Appetite,Glycemic Response and Gastric Emptying Rate

Understanding the impact of rheological properties of food on postprandial appetite and glycemic response helps to design novel functional products. It has been shown that solid foods have a stronger satiating effect than their liquid equivalent. However, whether a subtle change in viscosity of a semi-solid food would have a similar effect on appetite is unknown. Fifteen healthy males participated in the randomized cross-over study. Each participant consumed a 1690 kJ portion of a standard viscosity (SV) and a high viscosity (HV) semi-solid meal with 1000 mg acetaminophen in two separate sessions. At regular intervals during the three hours following the meal, subjective appetite ratings were measured and blood samples collected. The plasma samples were assayed for insulin, glucose-dependent insulinotropic peptide (GIP), glucose and acetaminophen. After three hours, the participants were provided with an ad libitum pasta meal. Compared with the SV meal, HV was consumed at a slower eating rate (P = 0.020), with postprandial hunger and desire to eat being lower (P = 0.019 and P<0.001 respectively) while fullness was higher (P<0.001). In addition, consuming the HV resulted in lower plasma concentration of GIP (P<0.001), higher plasma concentration of glucose (P<0.001) and delayed gastric emptying as revealed by the acetaminophen absorption test (P<0.001). However, there was no effect of food viscosity on insulin or food intake at the subsequent meal. In conclusion, increasing the viscosity of a semi-solid food modulates glycemic response and suppresses postprandial satiety, although the effect may be short-lived. A slower eating rate and a delayed gastric emptying rate can partly explain for the stronger satiating properties of high viscous semi-solid foods.     

Appetite and endocrine regulators of energy balance after 2 days of energy restriction: insulin, leptin, ghrelin, and DHEA-S

Using a double‐blind, placebo‐controlled crossover design, the effects of 48 h near complete energy restriction on endocrine regulators of appetite and satiety were assessed. Twelve men and one woman participated in this controlled, 2‐day diet intervention study. One experimental trial was completed in a calorie deprived state (CAL‐DEP; <10% of estimated energy requirements) and others in a fed condition (carbohydrate only and carbohydrate and fat; data were pooled and compared to CAL‐DEP). Test meals containing prescribed energy intake and indistinguishable in sensory characteristics were provided during each trial. Glucose, insulin, leptin, ghrelin, cortisol, dehydroepiandrosterone‐sulfate (DHEA‐S), and satiety were repeatedly assessed. Mean glucose, insulin, and leptin concentrations were lower (P < 0.0001) for CAL‐DEP compared to the fully fed (FED) state. Ghrelin and DHEA‐S were higher (P < 0.0001) for CAL‐DEP relative to FED. Cortisol levels declined each day regardless of diet (P < 0.0001) but were 32% higher (P < 0.01) at the conclusion of the session for CAL‐DEP compared to FED. Satiety was 25% lower (P < 0.0001) for CAL‐DEP relative to FED and decreased (P < 0.0001) over time regardless of diet. In the FED state, insulin (r = 0.55), glucose (r = 0.76), cortisol (r = ?0.59), and DHEA‐S (r = ?0.62) were associated (P < 0.05) with satiety, but not during CAL‐DEP. These findings show that 2 days of severe energy restriction alter several endocrine regulators of appetite independent of perception of increased hunger suggesting a physiological mechanism to explain overeating following acute periods of severe energy restriction.     

Ghrelin improves disturbed myocardial energy metabolism in rats with heart failure induced by isoproterenol

To explore the effects of ghrelin on disturbed myocardial energy metabolism during chronic heart failure (CHF). Rats were subcutaneously injected with isoproterenol (ISO) for 10 days with or without ghrelin for another 10 days. Enzyme immunoassay was to measure ghrelin concentrations. Compared with the control group, ISO‐treated rats showed suppressed cardiac function with high ghrelin/GHS‐R expressions. These rats also showed the decreases in food consumption and weight. The decreased levels of plasma glucose and myocardial glucogen, but the high lactate in blood and myocardium showed myocardial metabolic disturbance. Compared with the group given ISO alone, the rats with ghrelin (20 and 100 µg/kg/day) improved cardiac dysfunction and increased food intake by 13.5 and 14.2% (both P < 0.01), and rate of weight gain by 95% (P < 0.05) and 1.71‐fold (P < 0.01), respectively. The plasma glucose were increased by 49.7 and 50.8% (both P < 0.01), and myocardial glucogen, by 40.5 and 51.7% (both P < 0.01), but blood lactate decreased by 1.56‐ and 1.96‐fold (both P < 0.01), and myocardial lactate by 32.1 and 48.7% (both P < 0.05), respectively. Their MCT1 mRNA and protein expressions increased. The myocardial ghrelin/GHS‐R pathway can be upregulated during CHF. The ghrelin can attenuate cardiac dysfunction and energy metabolic disturbance in CHF rats. Copyright © 2010 European Peptide Society and John Wiley & Sons, Ltd.     

Ghrelin response to protein and carbohydrate meals in relation to food intake and glycerol levels in obese subjects

Obese subjects have lower basal and an attenuated decrease of postprandial plasma ghrelin following carbohydrate-rich meals, while the response to protein is unknown. Therefore, plasma ghrelin levels were examined after ingestion of satiating amounts of a protein- or carbohydrate-rich meal in relation to food and energy intake and hunger/satiety ratings in 30 obese subjects followed 240 min later by ad lib sandwiches. Food intake and hunger/satiety ratings were identical while energy intake was significantly greater after bread (861 +/- 62.7 vs. 441 +/- 50.4 kcal, p < 0.001). Second meal food and energy intake were not different. Ghrelin decreased after bread, but increased by 50 pg/ml (p < 0.001) after meat. The corresponding increase of insulin was 55 vs. 9 microU/ml (p < 0.001). Glycerol levels decreased significantly less after the protein meal compared to carbohydrates. After protein glycerol was significantly correlated to the rise of ghrelin but not insulin. These data demonstrate that, in obese subjects, protein has no different satiating effect than carbohydrate despite divergent ghrelin levels. Energy intake corresponds to energy density of the respective food items. Ghrelin response to both meals is qualitatively similar but quantitatively attenuated compared to normal weight subjects. The relationship between ghrelin and glycerol would support recent observations of a possible role of ghrelin in fat metabolism.     

Loneliness predicts postprandial ghrelin and hunger in women

Loneliness is strongly linked to poor health. Recent research suggests that appetite dysregulation provides one potential pathway through which loneliness and other forms of social disconnection influence health. Obesity may alter the link between loneliness and appetite-relevant hormones, one unexplored possibility. We examined the relationships between loneliness and both postmeal ghrelin and hunger, and tested whether these links differed for people with a higher versus lower body mass index (BMI; kg/m²). During this double-blind randomized crossover study, women (N = 42) ate a high saturated fat meal at the beginning of one full-day visit and a high oleic sunflower oil meal at the beginning of the other. Loneliness was assessed once with a commonly used loneliness questionnaire. Ghrelin was sampled before the meal and postmeal at 2 and 7 h. Self-reported hunger was measured before the meal, immediately postmeal, and then 2, 4, and 7 h later. Lonelier women had larger postprandial ghrelin and hunger increases compared with less lonely women, but only among participants with a lower BMI. Loneliness and postprandial ghrelin and hunger were unrelated among participants with a higher BMI. These effects were consistent across both meals. These data suggest that ghrelin, an important appetite-regulation hormone, and hunger may link loneliness to weight gain and its corresponding negative health effects among non-obese people.     

Low-dose ghrelin infusion--evidence against a hormonal role in food intake

Ghrelin is the only peripheral orexigenic peptide of gastrointestinal origin. Its preprandial increase is supposed to initiate food intake. This assumption is based on studies with intravenously infused ghrelin in rather high doses and the correlation between ghrelin levels and hunger sensations. As yet it is unclear whether or not low dose ghrelin resulting in physiological and moderately supraphysiological plasma levels has an effect on hunger sensations, the wish for food intake and / or the quantity of the meal consumed. We examined 20 normal-weight males (age 25±1.7 years, BMI 24±0.5 kg/m(2)) in a prospective double-blind randomized fashion. On two different days they obtained a ghrelin infusion 1 ng/kg/min or intravenous saline starting one hour after a standardized meal. Hunger and satiety ratings were documented by visual analogue scales. A second meal was served on demand and consumed until feeling satiated. Time point of the second meal as well as ingested calories were registered. Prior to the start of i.v. ghrelin the postprandial decrease of active plasma ghrelin by 30 pg/ml was comparable. In the controls the postprandial reduction was significant until 210 min compared to basal. With i.v. ghrelin basal levels were reached within 10 min. The maximal rise was twice basal. No effect was observed on hunger and satiety ratings. The time period between the meals and the food quantity of the second meal were similar. During ghrelin infusion glucose and growth hormone but not insulin and cortisol levels were significantly higher after the second meal compared to saline. The present data demonstrate for the first time the effect of a low dose ghrelin infusion on food intake. Neither physiological nor moderably supraphysiological ghrelin levels were associated with any change of the various food intake parameters determined. These data do not favour a hormonal role of peripheral ghrelin in the regulation of food intake.     

Meal size and frequency: effect on potentiation of the thermal effect of food by prior exercise

Prior exercise potentiates the thermic effect of a carbohydrate meal. The purpose of this study was to determine if meal size or feeding pattern influences this response. Two groups of healthy, normal-weight young women exercised for 45 min on a cycle ergometer at 70% of maximal aerobic capacity. Once aerobic capacity returned to pre-exercise baseline, the thermic effect of food (TEF) was determined by indirect calorimetry over a 2-h period. One group of subjects ingested a 2510-kJ meal and the other a 5020-kJ meal. As a control, subjects ingested the test meal without prior exercise. In addition, subjects ingesting the 5020–kJ meal were studied for an additional 2 h. In a separate trial, these subjects ingested a 5020-kJ meal in two equal portions after a bout of exercise, the second portion 120 min after the first. TEF was less for the 2510-kJ meal compared with the 5020-kJ meal for both the control [mean (SE), 76 (17) vs 158 (19) kJ · 2h^–1,P < 0.01), and prior exercise [124 (23) vs 197 (24) kJ · 2h^–1,P<0.01) trials. However, the same increment in TEF resulted from the prior bout of exercise [48 (9) vs 40 (8) kJ · 2h^– for 2510-and 5020-kJ meals, respectively). TEF was 31 % lower when the 5020-kJ meal was given in two portions compared with one [281 (30) vs 369 (41) kJ · 4h^–1, P < 0.05]. No difference in TEF was found between the first and second 2510-kJ portion. The results suggest that potentiation of TEF by prior exercise is not influenced by caloric density or energy content of the meal. Rather, meal volume and hence meal frequency is a greater determinant of postexercise TEF.