Circulating adiponectin levels, body composition and obesity-related variables in Prader–Willi syndrome: comparison with obese subjects

Kennedy, Laurence; Bittel, Douglas C.; Kibiryeva, Nataliya; Kalra, Satya P.; Torto, Rita; Butler, Merlin G.

doi:10.1038/sj.ijo.0803115

Cited by 78 publications

(67 citation statements)

References 33 publications

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“…In another genetic syndrome with a predisposition to obesity, Prader Willi Syndrome (PWS), the association between leptin and total body fat had an increased slope in subjects with PWS compared to controls, similar to our findings in DS (22). In two other studies, however, no difference in leptin levels were observed between subjects with PWS and controls (23,24), even after adjusting for adiposity (22). Thus, there are conflicting data about PWS as a possible syndromic model of increased leptin resistance.…”

Section: Discussionsupporting

confidence: 89%

Leptin Levels among Prepubertal Children with Down Syndrome Compared with Their Siblings

Magge

O'Neill

Shults

et al. 2008

The Journal of Pediatrics

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Objectives-To compare levels of leptin and other obesity-related hormones between prepubertal children with Down syndrome (DS), a population at high obesity risk, and unaffected siblings, to better understand the pathophysiology of obesity in children with DS.Study design-Cross-sectional study of 35 children with DS and 33 control siblings, ages 4 to 10 years, with a fasting blood sample, and anthropometric measurements to estimate body composition. Generalized estimating equations were used to account for the lack of independence between siblings.Results-In addition to having higher body mass index (BMI) and percent body fat, children with DS had higher leptin levels than unaffected siblings, even after adjustment for age, sex, race, and ethnicity (difference: 5.8 ng/ml, 95% CI: 2.4-9.3, p=0.001), and further adjustment for percent body fat (difference: 2.7 ng/ml, 95% CI: 0.08-5.4, p=0.04). Leptin and percent body fat were positively associated in both groups (p<0.0001), but with a significantly greater positive association in the DS group, suggesting a significant effect modification (p<0.0001).Conclusions-This group of children with DS had increased leptin for percent body fat than their unaffected siblings. This difference may contribute to the increased risk for obesity in children with DS. KeywordsObesity; Body Mass Index; Pediatrics; Body composition; Adiposity Individuals with Down syndrome (DS) are at increased risk for several endocrinologic conditions, including hypothyroidism, growth retardation, diabetes mellitus, and obesity (3, 4). The reason for the increased risk of obesity in this population is unclear, but several mechanisms have been suggested, including a decreased resting metabolic rate (5,6) and

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Section: Discussionsupporting

confidence: 89%

Leptin Levels among Prepubertal Children with Down Syndrome Compared with Their Siblings

Magge

O'Neill

Shults

et al. 2008

The Journal of Pediatrics

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“…Interestingly, the two groups were also matched for central adiposity and insulin resistance without specific selection of control subjects. Although our PWS cohort might seem unusual, as a lower visceral fat mass and preserved insulin sensitivity has been reported previously (Brambilla et al, 1997, Goldstone et al, 2001, Goldstone et al, 2004, Goldstone et al, 2005, Talebizadeh and Butler, 2005, Kennedy et al, 2006, Theodoro et al, 2006, Haqq et al, 2010and Sode-Carlsen et al, 2010, other investigators recently reported similar observations to ours, i.e. obese children and adults with PWS having the same amount of visceral fat mass, the same degree of insulin resistance and a similar prevalence of metabolic syndrome compared to carefully weight-matched obese subjects Butler, 2005 andBrambilla et al, 2010).…”

Section: Discussionsupporting

confidence: 86%

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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“…There were no significant effects (i.e., significant positive or negative correlations (data not shown) observed for genetic subtypes (15qll-q13 deletion or maternal disomy 15) and CRP concentrations which is consistent with our previous report of adiponectin levels in PWS. 29 Additionally, we saw no significant correlations between CRP levels for body mass index (BMI), percentage of fat, weight, age, or waist to hip ratios (see Table 2). …”

Section: Resultsmentioning

confidence: 98%

“…In addition, there are only scattered reports of cerebrovascular accidents in the PWS population including a report of a teenager with PWS and type 2 diabetes mellitus and a vaso-occlusive stroke with revascularization of the middle cerebral arteries. 22 Since ischemic vascular disease is commonly linked to obesity in the general population, [23][24][25] the low number of reports or prevalence of these conditions in PWS is surprising and may be due to underreporting or perhaps to lower than expected occurrence of dyslipidemia and insulin-resistance, 26,27 higher adiponectin levels, 28,29 or lower CRP levels than commonly seen in the general obese population.…”

mentioning

confidence: 99%

C-reactive protein levels in subjects with Prader-Willi syndrome and obesity

Butler

Bittel²,

Kibiryeva³

et al. 2006

Genetics in Medicine

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Purpose: Prader-Willi syndrome is characterized by infantile hypotonia, feeding difficulties, hypogonadism, small hands and feet, mental deficiency, behavioral problems, and hyperphagia leading to obesity in early childhood. To date there have been no studies examining the associated risk of cardiovascular disease related to obesity in Prader-Willi syndrome, nor of circulating biomarkers such as C-reactive protein known to be predictive of cardiovascular disease. Therefore, we have measured the levels of C-reactive protein in a descriptive study of a cohort of Prader-Willi syndrome and comparison subjects. Methods: An immunoassay was used to quantify C-reactive protein in plasma samples from subjects with Prader-Willi syndrome and obesity and compared to anthropometric and body composition data. Results: The mean circulating C-reactive protein concentration for 28 subjects with Prader-Willi syndrome (13 females, 15 males; mean age 24.6 Ϯ 11.6 years; mean body mass index 35.9 Ϯ 11.9) was 10.3 Ϯ 8.8 mg/L. The mean C-reactive protein concentration for 22 nonsyndromic obese subjects (16 females, 6 males; mean age 32.3 Ϯ 12.2 years; mean body mass index 36.6 Ϯ 10.7) was 8.8 Ϯ 10.9 mg/L. The reported mean value for C-reactive protein was 2.6 Ϯ 3.0 mg/L from 100 healthy adults. Conclusions: The mean C-reactive protein values were similar between the subjects with Prader-Willi syndrome and obesity but significantly higher in Prader-Willi syndrome and obese subjects relative to normative data. Increased levels of C-reactive protein

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Circulating adiponectin levels, body composition and obesity-related variables in Prader–Willi syndrome: comparison with obese subjects

Cited by 78 publications

References 33 publications

Leptin Levels among Prepubertal Children with Down Syndrome Compared with Their Siblings

Leptin Levels among Prepubertal Children with Down Syndrome Compared with Their Siblings

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

C-reactive protein levels in subjects with Prader-Willi syndrome and obesity

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