Ghrelin, Peptide YY, Glucose-Dependent Insulinotropic Polypeptide, and Hunger Responses to a Mixed Meal in Anorexic, Obese, and Control Female Adolescents

Imperial College London, Londinium, England, United Kingdom
Journal of Clinical Endocrinology & Metabolism (Impact Factor: 6.21). 05/2005; 90(4):2161-8. DOI: 10.1210/jc.2004-1251
Source: PubMed


To determine whether peptide YY (PYY), ghrelin, glucose-dependent insulinotropic polypeptide (GIP), and satiety responses to food intake are impaired in anorexia or obesity, we studied 30 female adolescents with anorexia nervosa [body mass index (BMI) 16.3 kg/m2], obesity (BMI 34.3 kg/m2), or normal weight (BMI 20.2 kg/m2). PYY, ghrelin, GIP, insulin, and glucose concentrations and four markers of satiety were measured for 240 min after a mixed meal. The area under the curve for glucose was similar in obese (OB) and normal-weight control (C) subjects but was 15% lower in anorexic (AN) subjects. The area under the curve for insulin was 47% lower in AN and 87% higher in OB subjects, compared with C subjects. After the meal, PYY increased significantly in C (+41%, P < 0.05) but not in AN or OB adolescents. Ghrelin concentrations were highest in AN subjects and lowest in the OB group, compared with C subjects and fell significantly by 25% in all three groups. GIP concentrations were lower in AN subjects throughout the test and increased in all three groups after the mixed meal. AN adolescents reported being less hungry than OB and C adolescents. There was a negative correlation between fasting ghrelin (but not PYY or GIP) and BMI and insulin (r2= 0.33) and a positive correlation between the decrease in hunger 15 min after the meal and PYY concentrations at 15 min (r2= 0.20). In conclusion, the blunted PYY response to a meal in OB adolescents suggests that PYY plays a role in the pathophysiology of obesity. Ghrelin is unlikely to play a causal role in anorexia nervosa or obesity. The lower GIP observed in AN subjects despite a similar caloric intake may appropriately prevent an excessive insulin response in these patients.

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    • "In AN women, baseline plasma PYY 3–36 levels were reported to be normal (Stock et al., 2005), increased (Misra et al., 2006) or reduced (Germain et al., 2007, 2010), whereas plasma PYY 3–36 response to energy intake was reported to be time delayed (Stock et al., 2005) or increased and not completely restored after weight gain (Nakahara et al., 2007). Initial studies in BN reported normal CSF and plasma levels of PYY in both symptomatic and 1-year recovered patients with bulimia (Gendall et al., 1999). "
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    ABSTRACT: A large body of literature suggests the occurrence of a dysregulation in both central and peripheral modulators of appetite in patients with anorexia nervosa (AN) and bulimia nervosa (BN), but at the moment, the state or trait-dependent nature of those changes is far from being clear. It has been proposed, although not definitively proved, that peptide alterations, even when secondary to malnutrition and/or to aberrant eating behaviours, might contribute to the genesis and the maintenance of some symptomatic aspects of AN and BN, thus affecting the course and the prognosis of these disorders. This review focuses on the most significant literature studies that explored the physiology of those central and peripheral peptides, which have prominent effects on eating behaviour, body weight and energy homeostasis in patients with AN and BN. The relevance of peptide dysfunctions for the pathophysiology of eating disorders is critically discussed. Copyright © 2014 John Wiley & Sons, Ltd and Eating Disorders Association.
    Full-text · Article · Sep 2014 · European Eating Disorders Review
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    • "Perceived hunger and fullness were assessed by self-report (adapted from (Flint, Raben, Blundell, & Astrup, 2000; Stock et al., 2005)) during the breakfast meal test. Participants responded to each of the two questions prior to breakfast and at 15, 60, 90, 120, 180, and 240 minutes after each meal by marking a visual analog scale (VAS) ranging from zero mm (lowest) to 100 mm (highest). "
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    ABSTRACT: To test the hypothesis that a breakfast meal with high carbohydrate/low fat results in an earlier increase in postprandial glucose and insulin, a greater decrease below baseline in postprandial glucose, and an earlier return of appetite, compared to a low carbohydrate/high fat meal. Overweight but otherwise healthy adults (n=64) were maintained on one of two eucaloric diets: high carbohydrate/low fat (HC/LF; 55:27:18% kcals from carbohydrate: fat: protein) versus low carbohydrate/high fat (LC/HF; 43:39:18% kcals from carbohydrate: fat: protein). After 4 weeks of acclimation to the diets, participants underwent a meal test during which circulating glucose and insulin and self-reported hunger and fullness, were measured before and after consumption of breakfast from their assigned diets. The LC/HF meal resulted in a later time at the highest and lowest recorded glucose, higher glucose concentrations at 3 and 4 hours post-meal, and lower insulin incremental area under the curve. Participants consuming the LC/HF meal reported lower appetite 3 and 4 hours following the meal, a response that was associated with the timing of the highest and lowest recorded glucose. Modest increases in meal arbohydrate content at the expense of fat content may facilitate weight gain over the long-term by contributing to an earlier rise and fall of postprandial glucose concentrations and an earlier return of appetite.
    Full-text · Article · May 2014 · Appetite
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    • "Postprandial decrease of ghrelin levels is further dependent on meal calorie value and composition; for example, the decrease is lower after fat-based meals compared with carbohydrate- or protein-based meals [10, 11]. Basic ghrelin levels respond in a compensatory manner to the energy deficit/excess: low ghrelin levels are observed in obesity, whereas high levels in anorexia (Figure 2) [12, 13]. A lower decrease in ghrelin levels in relation to fasting values is observed in postprandial obese individuals [14]. "
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    ABSTRACT: Obesity, influencing the increase of incidence of type 2 diabetes, cardiovascular complications and cancer is a growing medical problem worldwide. The feelings of hunger and satiety are stimulated by the "gut-brain axis", where a crucial role is played by gastrointestinal hormones: glucagon-like peptide 1, glucose-dependent insulinotropic polypeptide, pancreatic polypeptide, peptide YY, oxyntomodulin, cholecystokinin and ghrelin. These hormones affect not only the functioning of the digestive tract, but also might have effects on insulin secretion and are mediators which affect brain areas involved in the regulation of food intake. The effect of their actions can be antagonistic as well as an additive or synergistic, and their secretion is dependent on many factors, such as dietary nutrients or the energy state of the body. Changes in circulating gut hormones concentrations result in activation of various pathways primarily within the hypothalamus and brain stem areas, which modulate feeding behaviour and a number of metabolic processes.
    Full-text · Article · May 2014 · Przegląd Gastroenterologiczny
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