Physiological Evidence for the Involvement of Peptide YY in the Regulation of Energy Homeostasis in Humans*

Obesity and Diabetes Clinical Research Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, AZ 85016, USA.
Obesity (Impact Factor: 3.73). 10/2006; 14(9):1562-70. DOI: 10.1038/oby.2006.180
Source: PubMed


To explore the potential role of the endogenous peptide YY (PYY) in the long-term regulation of body weight and energy homeostasis.
Fasting and postprandial plasma PYY concentrations were measured after an overnight fast and 30 to 180 minutes after a standardized meal in 29 (21 men/8 women) non-diabetic subjects, 16 of whom had a follow-up visit 10.8 +/- 1.4 months later. Ratings of hunger and satiety were collected using visual analog scales. Resting metabolic rate (RMR) (15-hour RMR) and respiratory quotient (RQ) were assessed using a respiratory chamber.
Fasting PYY concentrations were negatively correlated with various markers of adiposity and negatively associated with 15-hour RMR (r = -0.46, p = 0.01). Postprandial changes in PYY (area under the curve) were positively associated with postprandial changes in ratings of satiety (r = 0.47, p = 0.01). The maximal PYY concentrations achieved after the meal (peak PYY) were negatively associated with 24-hour RQ (r = -0.41, p = 0.03). Prospectively, the peak PYY concentrations were negatively associated with changes in body weight (r = -0.58, p = 0.01).
Our data indicate that the endogenous PYY may be involved in the long-term regulation of body weight. It seems that this long-term effect was not exclusively driven by the modulation of food intake but also by the control of energy expenditure and lipid metabolism.

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Available from: Pablo Enriori, Oct 14, 2014
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    • "This effect is mediated through the Y2 receptor (Batterham et al., 2002) and has been documented in diverse conditions and several species, including rodents and humans (Table 1). Basal levels are lower and the meal-induced release of PYY 3–36 is blunted in obese individuals (Alvarez Bartolomé et al., 2002; Batterham et al., 2003; le Roux et al., 2006; Guo et al., 2006; Sodowski et al., 2007). Also, PYY overexpression protects against diet-induced obesity (Boey et al., 2008). "
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    ABSTRACT: The gastrointestinal hormone peptide tyrosine tyrosine 3-36 (PYY3-36) has attained broad recognition with respect to its involvement in energy homeostasis and the control of food intake. It is mainly secreted by distal intestinal enteroendocrine L-cells in response to eating and exerts both neurally mediated paracrine and endocrine effects on various target organs. In addition to its gastrointestinal effects, PYY3-36 has long been known to inhibit food intake. Recent closer examination of the effects of PYY3-36 revealed that this gut-derived peptide also influences a wide spectrum of behavioral and cognitive functions that are pivotal for basic processes of perception and judgment, including central information processing, salience learning, working memory, and behavioral responding to novelty. Here, we review the effects of PYY3-36 that go beyond food intake and provide a conceptual framework suggesting that several apparently unrelated behavioral actions of PYY3-36 may actually reflect different manifestations of modulating the central dopamine system. Copyright © 2014. Published by Elsevier Inc.
    Full-text · Article · Dec 2014 · Frontiers in Neuroendocrinology
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    • "Because baseline differences in BMI were found between the two groups, we controlled for these in all of our analyses using BMI as a covariate. Controlling for baseline differences in BMI was important since relationships between PYY and BMI have previously been demonstrated in the literature [7] [28] and eating behaviors, such as elevated dietary restraint and disinhibition have been demonstrated to be associated with obesity [5]. For PYY, sample size was based on the detection of a meaningful difference of 5 pmol/L and an SD of 23 pmol/L following a meal in women with high disinhibition compared to women with normal disinhibition, based on a previously published report [2]. "
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    ABSTRACT: Acylated Ghrelin and Peptide YY (PYY3-36) are involved in appetite-regulation and energy homeostasis. These gastrointestinal hormones provide peripheral signals to the central nervous system to regulate appetite and short term food intake, and interact with leptin and insulin to regulate energy balance. Dietary restraint is an eating behavior phenotype manifest as a conscious cognitive control of food intake in order to achieve or sustain a desired body weight. The purpose of the current study was to determine if college-aged women (18 to 25 years) with different eating behavior phenotypes, i.e., high vs normal dietary restraint, differ with respect to circulating concentrations of gastrointestinal hormones during and following a test meal. We hypothesized that women with high dietary cognitive restraint [High CR (score ≥ 13, n=13)] would have elevated active ghrelin and PYY3-36 concentrations after a test meal compared to women with normal dietary cognitive restraint [Normal CR (score < 13, n=30)]. Gastrointestinal hormones were assessed before (-15 and 0 min) and after (10, 15, 20, 30, 60, 90, 120 and 180 min) the consumption of a mixed composition meal (5.0 kcal per kg/body weight). In contrast to our hypothesis, mean PYY3-36 concentrations (p=0.042), peak PYY3-36 concentrations (p=0.047), and PYY3-36 area under the curve (p=0.035) were lower in the High CR group compared to the Normal CR group after controlling for body mass index. No group differences were observed with respect to acylated ghrelin before or after the meal. In conclusion, PYY3-36 concentrations were suppressed in the women with High CR compared to the women with Normal CR. While the current study is cross-sectional and cause/effect of high dietary restraint and suppressed PYY3-36 concentrations cannot be determined, we speculate that these women with high cognitive restraint may be prone to weight gain or weight re-gain related to the suppressed circulating PYY after a meal. Further investigations need to explore the relationship between dietary cognitive restraint, circulating PYY, and weight gain.
    Full-text · Article · Jul 2013 · Physiology & Behavior
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    • "This can, according to the authors, create a state of chronic hunger and contribute to opportunistic eating characteristic of the disinhibition trait. Moreover, the magnitude of the postprandial PYY peak was shown to predict changes in body weight over a period of 6 months, with those presenting with lower postprandial PYY peaks being at increased risk for weight gain (Guo et al., 2006). Our finding of a tendency towards lower postprandial PYY levels in individuals with high disinhibition levels therefore reinforces the previous argument. "
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    ABSTRACT: The impact of eating behaviours on circulating levels of appetite-regulating hormones remains largely unknown. The aims of this study were to assess the role of restraint and disinhibition on fasting/postprandial peptide YY (PYY) plasma levels and subjective feelings of appetite in normal-weight individuals and to determine whether the effect was energy load dependent. 33 participants (12 men) were classified as restrained/unrestrained and low/high in disinhibition based on Three Factor Eating Questionnaire-18R and Dutch Eating Behaviour Questionnaire. The impact of restraint/disinhibition on PYY plasma levels and feelings of appetite was measured, after a 500kcal and 1000kcal breakfast, using a randomised crossover design. Restraint did not impact on either fasting or postprandial PYY plasma levels, but participants with high disinhibition had a tendency towards a blunted postprandial PYY response. Moreover, restrained eaters reported lower ratings of prospective food consumption postprandially, and a tendency towards higher fullness/lower hunger. In conclusion, circulating PYY is unaffected by restrained eating behaviour, despite being associated with increased fullness and reduced hunger in the fed state. High levels of disinhibition tend to be associated with a blunted PYY response and this may contribute towards the susceptibility to overconsumption and increased risk of weight gain characteristic of this trait.
    Full-text · Article · Oct 2010 · Appetite
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