A lesser postprandial suppression of plasma ghrelin in Prader–Willi syndrome is associated with low fasting and a blunted postprandial PYY response

Giménez-Palop, Olga; Giménez-Pérez, Gabriel; Mauricio, Dı́dac; González-Clemente, José-Miguel; Potau, Neus; Berlanga, Eugenio; Trallero, Roser; Laferrère, Blandine; Caixàs, Assumpta

doi:10.1111/j.1365-2265.2006.02707.x

Cited by 50 publications

(45 citation statements)

References 65 publications

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“…Despite overall higher levels of ghrelin in PWS, these subjects still exhibited normal postprandial suppression of ghrelin in our study, consistent with results reported in 3 studies of children with PWS (Haqq et al, 2003, Paik et al, 2006and Paik et al, 2007b and another of adults (Gimenez-Palop et al, 2007). Future trials are needed to elucidate the role of ghrelin in PWS using specific ghrelin antagonists, currently in development.…”

Section: Discussionsupporting

confidence: 90%

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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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Section: Discussionsupporting

confidence: 90%

“…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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“…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: 80%

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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“…( Bizzarri et al, 2010;Cummings et al, 2002b;Gimenez-Palop et al, 2007;Goldstone et al, 2005;Haqq et al, 2003a;Paik et al, 2004). Levels of fasting ghrelin may also even be higher in PWS patients than in lean controls (Bizzarri et al, 2010;Choe et al, 2005a;Cummings et al, 2002b;Delparigi et al, 2002;Gimenez-Palop et al, 2007).…”

Section: Ghrelin and Prader-willi Syndromementioning

confidence: 99%

“…Levels of fasting ghrelin may also even be higher in PWS patients than in lean controls (Bizzarri et al, 2010;Choe et al, 2005a;Cummings et al, 2002b;Delparigi et al, 2002;Gimenez-Palop et al, 2007). Postprandial levels of ghrelin do fall in patients with PWS though they remain elevated compared to non-PWS obese controls, with conflicting results as to whether the magnitude of the decrease in ghrelin is blunted (Gimenez-Palop et al, 2007;Goldstone et al, 2005;Haqq et al, 2003b). In addition, the age-related decline in ghrelin is blunted in PWS infants and children (Haqq et al, 2008).…”

Section: Ghrelin and Prader-willi Syndromementioning

confidence: 99%

Ghrelin in obesity and endocrine diseases

Scerif

Goldstone

Korbonits

2011

Molecular and Cellular Endocrinology

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A lesser postprandial suppression of plasma ghrelin in Prader–Willi syndrome is associated with low fasting and a blunted postprandial PYY response

Abstract: In PWS, the low decrease in postprandial ghrelin levels could be related to the low fasting PYY concentrations and their blunted postprandial response.

Cited by 50 publications

References 65 publications

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

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

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

Ghrelin in obesity and endocrine diseases

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