Sloth B, Holst JJ, Flint A, Gregersen NT, Astrup A. Effects of PYY1-36 and PYY3-36 on appetite, energy intake, energy expenditure, glucose and fat metabolism in obese and lean subjects. produced reduced EI, lower ratings of well-being, increases in FFA, postprandial glucose (only 0.8 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 PYY3-36) and insulin concentrations, as well as heart rate and EE (only 0.8 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 PYY3-36). PYY1-36 at 1.6 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 produced increased heart rate and postprandial insulin response. Ratings of appetite were opposite with infusions of 0.8 and 1.6 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 PYY1-36 and seemed to depend on subjects being lean or obese. PYY3-36 caused increased thermogenesis, lipolysis, postprandial insulin and glucose responses, suggestive of increased sympathoadrenal activity. PYY1-36 had no effect on EI and no clear effects on appetite but resulted in increased heart rate and postprandial insulin response. However, highest tolerable dose of PYY1-36 was probably not reached in the present study. Peptide YY; free fatty acids; insulin sensitivity; arcuate nucleus; neuropeptide Y receptors THE IMBALANCE BETWEEN energy intake (EI) and energy expenditure (EE) that produces the obese state may partly be a consequence of an inadequate appetite regulation. Hence, scientific interest in recent years has concentrated on both the secretion and function of different gastrointestinal hormones, and on the appetite regulatory centers of the brain, including the arcuate nucleus which is considered a key brain area (22).Peptide YY (PYY) is a 36-amino acid peptide released postprandially from the endocrine L cells in the distal gastrointestinal tract in proportion to the calorie and fat content of the ingested meal (1,8,18). PYY is part of the neuropeptide Y (NPY) protein family and exists in human blood in two forms: the intact PYY , in which the NH 2 -terminal Tyr-Pro dipeptide has been removed by dipeptidyl aminopeptidase IV (DPP IV) cleavage (12, 13). PYY 1-36 binds to and activates the Y1, Y2, and Y5 NPY receptor subtypes, whereas PYY 3-36 preferentially binds to the inhibitory presynaptic Y2 receptor, which is highly expressed in NPY neurons in the appetite regulatory center in the arcuate nucleus (27).Infusion of PYY 3-36 at doses producing supraphysiological plasma concentrations has been shown to result in a dosedependent decrease in subsequent food intake (8, 18). The highest suppression of food intake has been demonstrated with doses of 0.8 pmol⅐kg Ϫ1 ⅐min Ϫ1 and amounted to a decrease of between 25 and 34%, with the highest reduction in lean subjects (4,5,8,18) and a somewhat lower reduction in obese subjects (4). The differences in EI were observed either during the subsequent ad libitum meal or during the first 12 h after the infusion. In the context of appetite-suppressant effect in humans, the quantitative effect of PYY is of a magnitude not previously reported in connection with anorectic drugs (sibutramine etc.), and PYY receptors therefore constitute a very promising drug target for obesi...

Background: Video game playing has been linked to obesity in many observational studies. However, the influence of this sedentary activity on food intake is unknown. Objective: The objective was to examine the acute effects of sedentary video game play on various components of energy balance. Design: With the use of a randomized crossover design, 22 healthy, normal-weight, male adolescents (mean 6 SD age: 16.7 6 1.1 y) completed two 1-h experimental conditions, namely video game play and rest in a sitting position, followed by an ad libitum lunch. The endpoints were spontaneous food intake, energy expenditure, stress markers, appetite sensations, and profiles of appetite-related hormones. Results: Heart rate, systolic and diastolic blood pressures, sympathetic tone, and mental workload were significantly higher during the video game play condition than during the resting condition (P , 0.05). Although energy expenditure was significantly higher during video game play than during rest (mean increase over resting: 89 kJ; P , 0.01), ad libitum energy intake after video game play exceeded that measured after rest by 335 kJ (P , 0.05). A daily energy surplus of 682 kJ (163 kcal) over resting (P , 0.01) was observed in the video game play condition. The increase in food intake associated with video game play was observed without increased sensations of hunger and was not compensated for during the rest of the day. Finally, the profiles of glucose, insulin, cortisol, and ghrelin did not suggest an up-regulation of appetite during the video game play condition. Conclusion: A single session of video game play in healthy male adolescents is associated with an increased food intake, regardless of appetite sensations. The trial was registered at clinicaltrials.gov as NCT01013246.

It is unclear whether postprandial blood glucose or insulin exerts a regulatory function in short-term appetite regulation in humans. The aim of this study was to investigate, by use of meta-analysis, the role of blood glucose and insulin in short-term appetite sensation and energy intake (EI) in normal weight and overweight participants. Data from seven test meal studies were used, including 136 healthy participants (ALL) (92 normal weight (NW) and 44 overweight or obese (OW)). All meals were served as breakfasts after an overnight fast, and appetite sensations and blood samples were obtained frequently in the postprandial period. Finally, an ad libitum lunch was served. Data were analysed by fixed effects study level (SL) metaregression analysis and individual participant data (IPD) regression analysis, using STATA software. In SL analysis, postprandial insulin response was associated with decreased hunger in ALL, NW and OW (P, 0·019), and with increased satiety in NW (P¼ 0·004) and lower subsequent EI in OW (P¼ 0·022). Multivariate IPD analysis showed similar associations, but only in NW for hunger, satiety and EI (P ,0·028), and in ALL for EI (P¼ 0·016). The only association involving blood glucose was the multivariate IPD analysis showing an inverse association between blood glucose and EI in ALL (P¼ 0·032). Our results suggest that insulin, but not glucose, is associated with short-term appetite regulation in healthy participants, but the relationship is disrupted in the overweight and obese. We conclude that the postprandial insulin response may be an important satiety signal, and that central nervous system insulin resistance in overweight might explain the blunted effect on appetite.

Our aim was to examine the effects of GLP-1 and PYY3-36, separately and in combination, on energy intake, energy expenditure, appetite sensations, glucose and fat metabolism, ghrelin, and vital signs in healthy overweight men. Twenty-five healthy male subjects participated in this randomized, double-blinded, placebo-controlled, four-arm crossover study (BMI 29 ± 3 kg/m(2), age 33 ± 9 yr). On separate days they received a 150-min intravenous infusion of 1) 0.8 pmol·kg(-1)·min(-1) PYY3-36, 2) 1.0 pmol·kg(-1)·min(-1) GLP-1, 3) GLP-1 + PYY3-36, or 4) placebo. Ad libitum energy intake was assessed during the final 30 min. Measurements of appetite sensations, energy expenditure and fat oxidation, vital signs, and blood variables were collected throughout the infusion period. No effect on energy intake was found after monoinfusions of PYY3-36 (-4.2 ± 4.8%, P = 0.8) or GLP-1 (-3.0 ± 4.5%, P = 0.9). However, the coinfusion reduced energy intake compared with placebo (-30.4 ± 6.5%, P < 0.0001) and more than the sum of the monoinfusions (P < 0.001), demonstrating a synergistic effect. Coinfusion slightly increased sensation of nausea (P < 0.05), but this effect could not explain the effect on energy intake. A decrease in plasma ghrelin was found after all treatments compared with placebo (all P < 0.05); however, infusions of GLP-1 + PYY3-36 resulted in an additional decrease compared with the monoinfusions (both P < 0.01). We conclude that coinfusion of GLP-1 and PYY3-36 exerted a synergistic effect on energy intake. The satiating effect of the meal was enhanced by GLP-1 and PYY3-36 in combination compared with placebo. Coinfusion was accompanied by slightly increased nausea and a decrease in plasma ghrelin, but neither of these factors could explain the reduction in energy intake.

The ad libitum test meal used to measure spontaneous EI is reproducible, and the reproducibility does not seem to be influenced by prior standardization. However, prior diet standardization exerts a significant effect on ad libitum EI.

Our data do not support that EE is increased after RYGB. More likely, RYGB promotes weight loss by reducing appetite, partly mediated by changes in gastrointestinal hormone secretion. Furthermore, we found that the early changes in glycaemic control after RYGB is to a large extent mediated by caloric restriction.

Foods and dietary patterns that enhance satiety may provide benefit to consumers. The aim of the present review was to describe, consider and evaluate research on potential benefits of enhanced satiety. The proposal that enhanced satiety could only benefit consumers by a direct effect on food intake should be rejected. Instead, it is proposed that there is a variety of routes through which enhanced satiety could (indirectly) benefit dietary control or weight-management goals. The review highlights specific potential benefits of satiety, including: providing appetite control strategies for consumers generally and for those who are highly responsive to food cues; offering pleasure and satisfaction associated with low-energy/healthier versions of foods without feeling 'deprived'; reducing dysphoric mood associated with hunger especially during energy restriction; and improved compliance with healthy eating or weight-management efforts. There is convincing evidence of short-term satiety benefits, but only probable evidence for longer-term benefits to hunger management, possible evidence of benefits to mood and cognition, inadequate evidence that satiety enhancement can promote weight loss, and no evidence on which consumers would benefit most from satiety enhancement. The appetite-reducing effects of specific foods or diets will be much more subtle than those of pharmaceutical compounds in managing hunger; nevertheless, the experience of pharmacology in producing weight loss via effects on appetite suggests that there is potential benefit of satiety enhancement from foods incorporated into the diet to the consumer.

Many dietary factors or substances exert effects on the three components of energy balance, and one strategy for tackling weight gain could be to use the inherent properties of these substances. Here, we will review the evidence regarding nutritional factors with a potential impact on energy balance, such as wholegrain foods, dietary fiber and protein content, calcium, and certain spices. There is ample evidence to suggest that dietary protein, wholegrain, and fiber promote satiety and either reduce energy absorption or stimulate energy expenditure. Dietary calcium reduces fat absorption, and a sufficient intake may also prevent excessive hunger during weight loss diets. Chili and mustard have beneficial effects on energy balance, although the quantitative importance of this may be modest. Manipulation of diet composition with an aim to prevent weight gain and weight regain is a promising avenue of research.