Ghrelin levels in young children with Prader-Willi syndrome

Erdie-Lalena, Christine; Holm, Vanja A.; Kelly, P.; Frayo, R. Scott; Cummings, David E.

doi:10.1016/j.jpeds.2006.04.011

Cited by 52 publications

(45 citation statements)

References 56 publications

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“…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. 42 The findings from these studies suggest that hyperghrelinaemia does not precede or coincide with the development of hyperphagia in PWS children.…”

Section: Ghrelinsupporting

confidence: 93%

“…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. 23,24,29,30,34,38,45,48 Similar discrepancies have been seen for glucagon with fasting levels reported as low in one study of PWS children (410 years) and adults, 25 but normal fasting and post-prandial glucagon levels in another adult study.…”

Section: Discussionmentioning

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: Ghrelinsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

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

et al. 2012

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“…Some studies have shown elevated ghrelin levels in PWS infants and children and thus it appears that hyperghrelinemia may precede hyperphagia in PWS, though this has not been universally seen in all studies (Erdie-Lalena et al, 2006;Feigerlova et al, 2008;Haqq et al, 2008). Neonatal transgenic deletion PWS mice die from severe neonatal hypoglycemia due to depletion of liver glycogen stores, and ghrelin levels increase reciprocally with the falling glucose levels (Stefan et al, 2005) Although it has been hypothesised that hyperphagia in PWS may be partly explained by rapid gastric emptying due to increased gastric motility caused by elevated ghrelin levels, in fact patients with PWS have delayed gastric emptying (Choe et al,…”

mentioning

confidence: 98%

Ghrelin in obesity and endocrine diseases

Scerif

Goldstone

Korbonits

2011

Molecular and Cellular Endocrinology

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“…13 In a small study of nine nonhyperphagic children with PWS (17-60 months of age), similar levels of circulating ghrelin as in the eight control children matched for BMI, age, and sex were found. 14 By contrast, in a larger and younger study cohort of 40 children and adolescents with PWS (range: 0.2-17.2 years, median age: 3.6 years), ghrelin levels were significantly elevated in the PWS group at any age compared with 84 age and BMI-matched controls. 15 In fact, the highest ghrelin levels in PWS were found in the youngest children.…”

Section: Hypogonadismmentioning

confidence: 72%