Children with Prader–Willi syndrome exhibit more evident meal-induced responses in plasma ghrelin and peptide YY levels than obese and lean children

Bizzarri, Carla; Rigamonti, Antonello E.; Luce, Antonella; Cappa, Marco; Cella, Silvano G.; Berini, J.; Sartório, Alessandro; Müller, Eugenio E.; Salvatoni, Alessandro

doi:10.1530/eje-09-1033

Cited by 58 publications

(69 citation statements)

References 39 publications

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“…While fasting or post-prandial insulin levels have sometimes been reported as low in human PWS children, 44,58 this has not been found in the current study and others. 28,39,41,45,48 In addition low fasting and postprandial insulin levels in PWS children and adults may be related more to preserved insulin sensitivity than reduced insulin secretion, as supported by reduced hypertriglyceridaemia and altered levels of related adipocytokines, such as increased plasma adiponectin in PWS.…”

Section: Discussioncontrasting

confidence: 89%

“…PYY Fasting PYY levels in PWS did decline with age (more steeply than in controls) and eating code in our study. However, we found overall normal fasting PYY levels in PWS children under 5 years compared with the controls, in agreement with other studies in children over 4 or 11 years 41,44 and adults. 38,43,59 One study has reported elevated fasting PYY levels in PWS children over 7 years.…”

Section: Ghrelinsupporting

confidence: 93%

“…26,27,32,34,36 --38,40,43 --48 Levels of ghrelin do fall after food intake in children and adults with PWS but remain elevated compared with the controls relative to their obesity. 37,38,40,43,44 In our current study, we were unable to demonstrate any elevation of plasma ghrelin levels in PWS children under 5 years, unadjusted or when correcting for age, BMI, fasting insulin or insulin resistance. This finding is in agreement with previous studies of PWS children aged under 3 or 5 years, 39,42,46 although it should be noted that one of these studies did not find hyperghrelinaemia in PWS children over 3 years and adults either.…”

Section: Ghrelincontrasting

confidence: 77%

“…38,43,59 One study has reported elevated fasting PYY levels in PWS children over 7 years. 45 Post-prandial PYY levels have generally been found to be normal in PWS children and adults, 38,41,44 though one study found decreased post-prandial levels. 43 Similarly fasting plasma levels of the anorexigenic gut hormone GLP-1 that is cosecreted from intestinal L-cells with PYY appear normal in PWS children and adults, 10,34,38,48 and post-prandial GLP-1 levels are normal in PWS adults PWS.…”

Section: Ghrelinmentioning

confidence: 99%

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Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrome

et al. 2012

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OBJECTIVE: Prader --Willi syndrome (PWS) is a genetic neurodevelopmental disorder with several nutritional phases during childhood proceeding from poor feeding, through normal eating without and with obesity, to hyperphagia and life-threatening obesity, with variable ages of onset. We investigated whether differences in appetite hormones may explain the development of abnormal eating behaviour in young children with PWS. SUBJECTS: In this cross-sectional study, children with PWS (n ¼ 42) and controls (n ¼ 9) aged 7 months --5 years were recruited. Mothers were interviewed regarding eating behaviour, and body mass index (BMI) was calculated. Fasting plasma samples were assayed for insulin, leptin, glucose, peptide YY (PYY), ghrelin and pancreatic polypeptide (PP). RESULTS: There was no significant relationship between eating behaviour in PWS subjects and the levels of any hormones or insulin resistance, independent of age. Fasting plasma leptin levels were significantly higher (mean±s.d.: 22.6±12.5 vs 1.97 ± 0.79 ng ml À1 , P ¼ 0.005), and PP levels were significantly lower (22.6 ± 12.5 vs 69.8 ± 43.8 pmol l À1 , Po0.001) in the PWS group compared with the controls, and this was independent of age, BMI, insulin resistance or IGF-1 levels. However, there was no significant difference in plasma insulin, insulin resistance or ghrelin levels between groups, though PYY declined more rapidly with age but not BMI in PWS subjects. CONCLUSION: Even under the age of 5 years, PWS is associated with low levels of anorexigenic PP, as in older children and adults. Hyperghrelinaemia or hypoinsulinaemia was not seen in these young children with PWS. Change in these appetite hormones was not associated with the timing of the transition to the characteristic hyperphagic phase. However, abnormal and/or delayed development or sensitivity of the effector pathways of these appetitive hormones (for example, parasympathetic and central nervous system) may interact with low PP levels, and later hyperghrelinaemia or hypoinsulinaemia, to contribute to hyperphagia in PWS.

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Section: Discussioncontrasting

confidence: 89%

Section: Ghrelinsupporting

confidence: 93%

Section: Ghrelincontrasting

confidence: 77%

Section: Ghrelinmentioning

confidence: 99%

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Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrome

et al. 2012

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“…Some have found that adults and children with PWS have lower fasting and postprandial PYY levels than controls (Butler et al, 2004 andGimenez-Palop et al, 2007), while others reported no difference (Goldstone et al, 2005 andPaik et al, 2007a) or increased PYY levels (Bizzarri et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

In adults with Prader–Willi syndrome, elevated ghrelin levels are more consistent with hyperphagia than high PYY and GLP-1 levels

et al. 2011

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ObjectivePrader-Willi syndrome (PWS) is a leading genetic cause of obesity, characterized by hyperphagia, endocrine and developmental disorders. It is suggested that the intense hyperphagia could stem, in part, from impaired gut hormone signaling. Previous studies produced conflicting results, being confounded by differences in body composition between PWS and control subjects. Design Fasting and postprandial gut hormone responses were investigated in a cross-sectional cohort study including 10 adult PWS, 12 obese subjects matched for percentage body fat and central abdominal fat, and 10 healthy normal weight subjects. Methods PYY [total], PYY , GLP-1[active] and ghrelin [total] were measured by ELISA or radioimmunoassay. Body composition was assessed by dual energy X-ray absorptiometry. Visual analog scales were used to assess hunger and satiety. Results In contrast to lean subjects (p < 0.05), PWS and obese subjects were similarly insulin resistant and had similar insulin levels. Ghrelin[total] levels were significantly higher in PWS compared to obese subjects before and during the meal (p < 0.05). PYY meal responses were higher in PWS than in lean subjects (p = 0.01), but not significantly different to obese (p = 0.08), with an additional non-significant trend in PYY[total] levels. There were no significant differences in self-reported satiety between groups, however PWS subjects reported more hunger throughout (p = 0.003), and exhibited a markedly reduced mealinduced suppression of hunger (p = 0.01) compared to lean or obese subjects. Conclusions Compared to adiposity-matched control subjects, hyperphagia in PWS is not related to a lower postprandial GLP-1 or PYY response. Elevated ghrelin levels in PWS are consistent with increased hunger and are unrelated to insulin levels.

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Ghrelin Appetite Hormone in Health and Disease

Çaylak

2012

Encyclopedia of Life Sciences

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Ghrelin is a 28‐amino‐acid appetite hormone and has numerous physiological roles in appetite modulation, glucose and lipid metabolisms, gastrointestinal, cardiovascular, reproductive, pulmonary and bone systems or immune modulation and cell proliferation. Recent studies implicate ghrelin in the pathogenesis of many diseases, including obesity, Prader–Willi syndrome, cachexia, Anorexia nervosa, cardiovascular diseases, reproductive disorders, diabetes and inflammatory bowel disease. Understanding the pharmacology and physiology of ghrelin agonists and antagonists and investigation of the role of appetite hormones in the regulation of food intake in humans will allow us to find potential therapeutic managements for the treatment of many of those diseases. Key Concepts: Ghrelin, a 28 amino‐acid peptide hormone that was discovered as an endogenous ligand for the growth hormone secretagogue‐receptor (GHS‐R), has two circulating forms: acylated and desacyl. The acylated form is essential for ghrelin's biological activity through GHS‐R. It is produced primarily in the stomach, hypothalamus, pituitary, intestine, kidney, heart, lung, gonads and placenta. Ghrelin is peripheral circulating appetite hormone, acts as a physiological hunger signal. Its secretion and blood levels rise during fasting and fall after eating. It stimulates appetite and increases food intake via secretion of GH. Repeated administration of ghrelin results in decreased energy expenditure; thus, increasing body fat and weight. Ghrelin have major biological functions in glucose and lipid metabolism and main physiological systems such as gastrointestinal, cardiovascular, reproductive, pulmonary, bone and immune. Ghrelin appears to be involved in the pathophysiological mechanisms of several human disorders, including obesity, Prader–Willi syndrome, cachexia, Anorexia nervosa, cardiovascular diseases, reproductive disorders, diabetes and inflammatory bowel disease.

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Children with Prader–Willi syndrome exhibit more evident meal-induced responses in plasma ghrelin and peptide YY levels than obese and lean children

Cited by 58 publications

References 39 publications

Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrome

Appetite hormones and the transition to hyperphagia in children with Prader-Willi syndrome

In adults with Prader–Willi syndrome, elevated ghrelin levels are more consistent with hyperphagia than high PYY and GLP-1 levels

Ghrelin Appetite Hormone in Health and Disease

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