Human distribution and release of a putative new gut hormone, peptide YY

Adrian, Thomas E.; Ferri, Gian-Luca; Bacarese-Hamilton, A.J.; Füeßl, Hermann S.; Polak, Julia M.; Bloom, Stephen R.

doi:10.1016/0016-5085(85)90211-2

Cited by 999 publications

(635 citation statements)

References 12 publications

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“…The L-cell is found at its highest density in the colonic epithelium (39) and secretes the anorexigenic hormones peptide tyrosine tyrosine (PYY) and glucagon-like peptide (GLP)-1 (27) . PYY is released into the circulation after food intake, with levels rising to a plateau after 1-2 h and remaining elevated for up to 6 h (40) . Intravenous infusion of PYY to both lean and obese human subjects has been demonstrated to reduce energy intake (41,42) , and this anorexigenic effect is thought be exerted via neuropeptide Y inhibition and POMC activation in the hypothalamic ARC (41,43) .…”

Section: Scfa Receptors and Anorectic Gut Hormone Releasementioning

confidence: 99%

Control of appetite and energy intake by SCFA: what are the potential underlying mechanisms?

2014

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In recent years, there has been a renewed interest in the role of dietary fibre in obesity management. Much of this interest stems from animal and human studies which suggest that an increased intake of fermentable fibre can suppress appetite and improve weight management. A growing number of reports have demonstrated that the principal products of colonic fermentation of dietary fibre, SCFA, contribute to energy homeostasis via effects on multiple cellular metabolic pathways and receptor-mediated mechanisms. In particular, over the past decade it has been identified that a widespread receptor system exists for SCFA. These G-protein-coupled receptors, free fatty acid receptor (FFAR) 2 and FFAR3 are expressed in numerous tissue sites, including the gut epithelium and adipose tissue. Investigations using FFAR2-or FFAR3-deficient animal models suggest that SCFAmediated stimulation of these receptors enhances the release of the anorectic hormones peptide tyrosine tyrosine and glucagon-like peptide-1 from colonic L cells and leptin from adipocytes. In addition, the SCFA acetate has recently been shown to have a direct role in central appetite regulation. Furthermore, the SCFA propionate is a known precursor for hepatic glucose production, which has been reported to suppress feeding behaviour in ruminant studies through the stimulation of hepatic vagal afferents. The present review therefore proposes that an elevated colonic production of SCFA could stimulate numerous hormonal and neural signals at different organ and tissue sites that would cumulatively suppress short-term appetite and energy intake.Colonic fermentation: SCFA: Appetite: Gut hormone: Obesity Recent longitudinal studies highlight that adults increase body weight gradually through middle age, with an average annual weight gain of approximately 0·5 kg (1,2) . This accumulation of body weight has resulted in an increased prevalence of obesity and its associated co-morbidities, as obesity incidence rates are now above 20 % in most Western countries and represent a major public health burden (3) . As a result, interventions that can be safely applied at the population level to prevent long-term weight gain would have major benefits to public health. It has been suggested that gradual adult weight gain can be the result of only a small habitual positive energy balance of 209·2-418·4 kJ/d (50-100 kcal/d) (4) . Consequently, an improved understanding of the hormonal and neuronal signals that control appetite regulation may facilitate the development of novel dietary strategies that supress energy intake and oppose a positive energy balance and long-term weight gain.Epidemiological and experimental studies have consistently highlighted an inverse association between dietary fibre intake and body weight gain (5)(6)(7) . Furthermore, an increased intake of dietary fibre has been associated with improved appetite regulation (8) , thus making high-fibre diets an attractive strategy to reduce obesity levels. The current definition of dietary fibre (9) encompasses a ...

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Section: Scfa Receptors and Anorectic Gut Hormone Releasementioning

confidence: 99%

Control of appetite and energy intake by SCFA: what are the potential underlying mechanisms?

2014

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“…PYY and ghrelin-like immunoreactivity was measured using established radioimmunoassays. [33][34][35][36] The ghrelin antibody used in this assay crossreacted with both acylated and des-acylated ghrelin. All samples were assayed in duplicate and within one assay to eliminate interassay variation.…”

Section: Experimental Protocolmentioning

confidence: 99%

Neural representations of hunger and satiety in Prader–Willi syndrome

et al. 2005

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Objective: To investigate the neural basis of the abnormal eating behaviour in Prader-Willi syndrome (PWS), using brain imaging. We predicted that the satiety response in those with PWS would be delayed and insensitive to food intake. Design and participants: The design of this study was based on a previous investigation of the neural activation associated with conditions of fasting and food intake in a nonobese, non-PWS group. The findings were used to generate specific hypotheses regarding brain regions of interest for the current study, in which 13 adults with PWS took part (mean7s.d. age ¼ 2976; BMI ¼ 31.575.1; IQ ¼ 7178, six were female). Measurements: Regional cerebral blood flow was measured using positron emission tomography in three sessions: one following an overnight fast and two following disguised energy controlled meals of similar volume and appearance -one of 1674 kJ (400 kcal) and another of 5021 kJ (1200 kcal). Subjective ratings of hunger, fullness and desire to eat, and blood plasma levels of glucose, insulin, leptin, ghrelin and PYY were measured before and after each imaging session. Results: The neural representation of hunger, after an overnight fast, was similar to that found in nonobese individuals in the control study. In contrast, after food intake, the patterns of neural activation previously associated with satiety were not found, even after the higher-energy load. Lateral and medial orbitofrontal cortical activation was associated with consumption of the 400-and 1200-kcal meals, respectively. The medial orbitofrontal activation, however, was only found in those who had shown a large percentage change in fullness ratings following the higher-energy meal. Conclusion: We conclude that there is a dysfunction in the satiety system in those with PWS. These findings suggest that brain regions associated with satiety are insensitive even to high-energy food intake in those with the syndrome. This may be the neural basis of the hyperphagia seen in PWS.

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“…7,8 PYY 1À36 is secreted by cells localized in distal small intestine and colon in response, and in proportion, to the calorie content of a meal. 9 Cleavage by the enzyme dipeptidyl-peptidase IV yields the circulating form most abundant after a meal, PYY . 10,11 In the fasting state, PYY is the dominating form.…”

Section: Introductionmentioning

confidence: 99%

“…10,11 In the fasting state, PYY is the dominating form. 9 While PYY and NPY 12 can activate NPY receptors Y1, Y2 and Y5, PYY 3-36 is a selective agonist for the Y2 receptor. 13 Y2R is a seven transmembrane domain G-protein-coupled presynaptic inhibitory autoreceptor, 14 which is highly expressed in NPY neurons within the hypothalamic arcuate nucleus, a key brain area regulating appetite.…”

Section: Introductionmentioning

confidence: 99%

Common neuropeptide Y2 receptor gene variant is protective against obesity among Swedish men

et al. 2005

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Background: Gut hormones and their receptors are considered important in the control of feeding behavior. The gut hormone peptide-YY (PYY) has anorexic effects via the inhibitory neuropeptide Y2 receptor (Y2R) highly expressed in orexigenic NPY/ AGRP neurons within the arcuate nucleus, a major integrator of appetite control in the hypothalamus. Design: Genetic case-control association study of single nucleotide polymorphisms (SNPs) in Y2R and PYY. Subjects: Swedish Caucasians comprising 148 lean, 129 overweight/obese and 226 morbidly obese men. Measurements: Genotypes of the common, silent and conserved SNP Y2R 585T4C and the common SNP PYY Arg72Thr, as well as various obesity-related clinical parameters. Results: Obese men had a lower allele and homozygosity frequency of the common allele 585T4C:T which was particularly evident comparing morbidly obese with lean men (P ¼ 0.002), and analyzing dependence between continuous body mass index (BMI) and genotype (P ¼ 0.002). In agreement, systolic blood pressure tended to be lower in those homozygous for allele T, which was not explained by the BMI -genotype dependence. We found no association to obesity for the PYY Arg72Thr polymorphism, which is located nearby the essential carboxy terminal. Conclusion: A common and conserved variant of the PYY and NPY receptor Y2R is less prevalent among obese compared to among lean Swedish men. This suggests that the common Y2R variant is protective against obesity. Our findings further implicate Y2R in food intake regulation.

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Human distribution and release of a putative new gut hormone, peptide YY

Cited by 999 publications

References 12 publications

Control of appetite and energy intake by SCFA: what are the potential underlying mechanisms?

Control of appetite and energy intake by SCFA: what are the potential underlying mechanisms?

Neural representations of hunger and satiety in Prader–Willi syndrome

Common neuropeptide Y2 receptor gene variant is protective against obesity among Swedish men

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