Abstract
Background
Subjects with Prader–Willi syndrome (PWS) have a higher fat mass and a lower fat-free mass compared to subjects with essential obesity. However, few data are presently available on the segmental body composition (BC) of PWS subjects.
Aim
To evaluate whether women with PWS and women with essential obesity, matched for age and percent body fat, differ in segmental fat distribution and surrogate markers of cardiometabolic disease (CMD).
Subjects and methods
35 women with PWS and 50 women with essential obesity were matched for age and percent body fat using coarsened exact matching. BC was measured by dual-energy X-ray absorptiometry. Oral glucose tolerance testing and measurements of cholesterol, triglycerides, C-reactive protein, and blood pressure were performed. Comparisons between PWS and obese women were performed using generalized linear models.
Results
Trunk fat was lower in PWS than in obese women on both absolute [−7.3 (95 % confidence interval −9.4 to −5.2) kg] and relative [−4.1 (−6.9 to −1.4) % of body fat] grounds. PWS and obese women had similar surrogate markers of CMD, with the exception of HDL-cholesterol, which was higher in PWS women.
Conclusion
Trunk fat is lower in obese women with PWS than in those with essential obesity. Surrogate markers of CMD are, however, mostly similar in the two groups.
Similar content being viewed by others
References
Cassidy SB, Schwartz S, Miller JL et al (2012) Prader–Willi syndrome. Genet Med 14:10–26
Brambilla P, Bosio L, Manzoni P et al (1997) Peculiar body composition in patients with Prader–Labhart–Willi syndrome. Am J Clin Nutr 65:1369–1374
Theodoro MF, Talebizadeh Z, Butler MG (2006) Body composition and fatness patterns in Prader–Willi syndrome: comparison with simple obesity. Obesity 14:1685–1690
Forbes GB (1997) A distinctive obesity: body composition provides the clue. Am J Clin Nutr 65:1540–1541
Després J-P (2012) Body fat distribution and risk of cardiovascular disease: an update. Circulation 126:1301–1313
Whittington JE, Holland AJ, Webb T et al (2001) Population prevalence and estimated birth incidence and mortality rate for people with Prader–Willi syndrome in one UK health region. J Med Genet 38:792–798
Goldstone AP, Thomas EL, Brynes AE et al (2001) Visceral adipose tissue and metabolic complications of obesity are reduced in Prader–Willi syndrome female adults: evidence for novel influences on body fat distribution. J Clin Endocrinol Metab 86:4330–4338
Thomas EL, Saeed N, Hajnal JV et al (1998) Magnetic resonance imaging of total body fat. J Appl Physiol 85:1778–1785
Sode-Carlsen R, Farholt S, Rabben KF et al (2010) Body composition, endocrine and metabolic profiles in adults with Prader–Willi syndrome. Growth Horm IGF Res 20:179–184
l’Allemand D, Eiholzer U, Schlumpf M, et al (2000) Cardiovascular risk factors improve during 3 years of growth hormone therapy in Prader–Willi syndrome. Eur J Pediatr 159:835–842
Kennedy L, Bittel DC, Kibiryeva N et al (2006) Circulating adiponectin levels, body composition and obesity-related variables in Prader–Willi syndrome: comparison with obese subjects. Int J Obes Relat Metab Disord 30:382–387
Viardot A, Sze L, Purtell L et al (2010) Prader–Willi syndrome is associated with activation of the innate immune system independently of central adiposity and insulin resistance. J Clin Endocrinol Metab 95:3392–3399
Bedogni G, Grugni G, Tringali G et al (2014) Assessment of fat-free mass from bioelectrical impedance analysis in obese women with Prader–Willi syndrome. Ann Hum Biol 26:1–5 [Epub ahead of print]
Bedogni G, Grugni G, Nobili V et al (2014) Is non-alcoholic fatty liver disease less frequent among women with Prader–Willi syndrome. Obes Facts 7:71–76
Bedogni G, Gastaldelli A, Tiribelli C et al (2014) Relationship between glucose metabolism and non-alcoholic fatty liver disease severity in morbidly obese women. J Endocrinol Invest 37:739–744
Blackwell M, Iacus S, King G et al (2009) CEM: coarsened exact matching in Stata. Stata J 9:524–546
Hind K, Oldroyd B (2013) In-vivo precision of the GE Lunar iDXA densitometer for the measurement of appendicular and trunk lean and fat mass. Eur J Clin Nutr 67:1331–1333
Wallace TM, Levy JC, Matthews DR (2004) Use and abuse of HOMA modeling. Diabetes Care 27:1487–1495
Matsuda M, DeFronzo RA (1999) Insulin sensitivity indices obtained from oral glucose tolerance testing: comparison with the euglycemic insulin clamp. Diabetes Care 22:1462–1470
Gastaldelli A, Ferrannini E, Miyazaki Y et al (2004) Beta-cell dysfunction and glucose intolerance: results from the san antonio metabolism (SAM) study. Diabetologia 47:31–39
Iacus SM, King G, Porro G (2011) Multivariate matching methods that are monotonic imbalance bounding. J Am Stat Assoc 106:345–361
Wells JCK (2012) Sexual dimorphism in body composition across human populations: associations with climate and proxies for short- and long-term energy supply. Am J Hum Biol 24:411–419
Lohman TG, Going SB (2006) Body composition assessment for development of an international growth standard for preadolescent and adolescent children. Food Nutr Bull 27:S314–S325
Sode-Carlsen R, Farholt S, Rabben KF et al (2010) One year of growth hormone treatment in adults with Prader–Willi syndrome improves body composition: results from a randomized, placebo-controlled study. J Clin Endocrinol Metab 95:4943–4950
Sode-Carlsen R, Farholt S, Rabben KF et al (2012) Growth hormone treatment in adults with Prader–Willi syndrome: the Scandinavian study. Endocrine 41:191–199
Oto Y, Tanaka Y, Abe Y et al (2014) Exacerbation of BMI after cessation of growth hormone therapy in patients with Prader–Willi syndrome. Am J Med Genet A 164A:671–675
Tanaka Y, Abe Y, Oto Y et al (2013) Characterization of fat distribution in Prader–Willi syndrome: relationships with adipocytokines and influence of growth hormone treatment. Am J Med Genet A 161A:27–33
Grugni G, Crinò A, Bedogni G et al (2013) Metabolic syndrome in adult patients with Prader–Willi syndrome. Nutr Metab Cardiovasc Dis 23:1134–1140
Brambilla P, Crinò A, Bedogni G et al (2011) Metabolic syndrome in children with Prader–Willi syndrome: the effect of obesity. Nutr Metab Cardiovasc Dis 21:269–276
Faienza MF, Ventura A, Lauciello R et al (2012) Analysis of endothelial protein C receptor gene and metabolic profile in Prader–Willi syndrome and obese subjects. Obesity 20:1866–1870
Acknowledgments
The study was supported by Progetti di Ricerca Corrente, Istituto Auxologico Italiano, Verbania and Milan, Italy.
Conflict of interest
The authors declare that they have no conflict of interest.
Ethical approval
All the procedures performed in this study were approved by the Ethical Committee of the Istituto Auxologico Italiano (Piancavallo, Verbania, Italy) and were in accordance with the 1964 Helsinki declaration and the Additional Protocol to the European Convention of Human Rights and Medicine, concerning Biomedical Research 2005.
Informed consent
Written informed consent was obtained from the PWS patients and their parents or guardians. Written consent was also obtained from the women with essential obesity.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Bedogni, G., Grugni, G., Tringali, G. et al. Does segmental body composition differ in women with Prader–Willi syndrome compared to women with essential obesity?. J Endocrinol Invest 38, 957–961 (2015). https://doi.org/10.1007/s40618-015-0266-y
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s40618-015-0266-y