![]() ![]() This methodological issue is important in the design of studies to examine postprandial effects of macronutrients, for which it is essential to measure effects after controlled iso-energetic meals. ![]() ![]() However, when foods varying in fat and carbohydrate are delivered under controlled, isoenergetic conditions in fixed amounts, the effects on appetite are very similar, although not always identical ( 30). However, the effect of these 2 nutrients is more apparent when foods are consumed under ad libitum conditions, when high-fat foods tend to lead to high-fat hyperphagia ( 28) or “passive overconsumption” ( 29). Fat is often regarded as having a much weaker action on satiety than carbohydrate ( 27). Research on the nutritional aspects of appetite control has focused considerable attention on the effects of fat and carbohydrate ( 26). GLP-1 and PYY are 2 of many satiety hormones released throughout the gastrointestinal tract eg, cholecystokinin and others are also thought to play a role in satiety ( 25). In contrast, only one study has shown the greatest increase in PYY after carbohydrate consumption ( 24). Ingestion of fat has been shown to produce the greatest release of PYY, followed by protein and then carbohydrate ( 22, 23). ![]() PYY infusion has previously been shown to reduce food intake in normal-weight ( 6) and obese humans ( 21), and repeated administration to rodents has been shown to attenuate weight gain ( 6). The role of GLP-1 as an incretin indicates a greater response to ingested carbohydrates ( 20). Studies have shown reduced postprandial GLP-1 release in severely obese subjects, which normalizes with weight loss ( 18), but others have failed to replicate these findings ( 19). GLP-1 is a potent incretin, that is, a stimulator of insulin release, and peripheral administration of GLP-1 inhibits appetite in animals and humans ( 17). Infusion of GLP-1 has been shown to reduce hunger levels and energy intake ( 16). GLP-1 is secreted from the same gut endocrine cells that synthesize PYY in the distal small and large intestine and therefore is released into the circulation after a meal ( 15). In contrast to ghrelin, GLP-1 and PYY are released into the circulation after a meal and are reduced during periods of fasting. Other authors have argued that ghrelin suppression is dependent on the energy content of the meal consumed ( 14) and not on the proportion of macronutrients. In other research, ghrelin has been shown to be suppressed more by carbohydrates than by fat ( 12, 13) however, this is not always the case. Furthermore, there was no association between area under the curve ghrelin levels and energy intake at either the lunch or dinner meals or with the subjects' chosen intermeal interval. However, the actual correlation between the variables was not reported. Ghrelin has also been described as a meal initiator on the basis of a study in which ghrelin and hunger sensations were measured in relation to food intake and revealed an overlap between the 2 variables in the interval between meals ( 2). Exogenous administration of ghrelin has been shown to stimulate appetite and food intake in rats and humans ( 4, 8– 11). Ghrelin has been described as the “hunger hormone” ( 7) with episodic changes in profiles of hunger sensations and levels being similar throughout the day: increasing during fasting and decreasing after food intake. Ghrelin is the only known circulating orexigenic hormone and should be considered separately from the anorexigenic, satiety-related hormones. Episodic hormones are those that change throughout the day, particularly before and after meals. Much research has been conducted on 3 peptides, ghrelin, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), that fluctuate episodically and are believed to have contrasting actions on appetite control ( 5, 6). The second strategy has been less commonly used. Most studies using the former strategy have demonstrated an action of the peptides on appetite and food intake, but the effect may depend on the attainment of supraphysiological peptide levels. Research strategies involve either the exogenous administration of appetite-related peptides with the subsequent measurement of postadministration action ( 3, 4) or the monitoring of physiological concentrations of peptides in the blood after specific nutrient loads or controlled meals. The most interest has focused on the episodic peptides and their relationship with hunger and the short-term (meal-to-meal) control of appetite ( 2). In the context of obesity, there is considerable interest in the role of gut peptides on appetite control ( 1). ![]()
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