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CC BY 4.0 · Journal of Child Science 2020; 10(01): e187-e195
DOI: 10.1055/s-0040-1718896
Original Article

Measurement of Serum Chemerin, Oxidized LDL, and Vitamin D Levels in Prader–Willi Syndrome: A Cross-Sectional Study in Pediatric Egyptian Patients

Manal M. Thomas
1   Clinical Genetics Department, Center of Scientific Excellence, National Research Centre, Cairo, Egypt
,
Moushira E. Zaki
2   Department of Biological Anthropology, National Research Centre, Cairo, Egypt
,
Eman Youness
2   Department of Biological Anthropology, National Research Centre, Cairo, Egypt
,
Khaled Hamed
1   Clinical Genetics Department, Center of Scientific Excellence, National Research Centre, Cairo, Egypt
,
Azzah A. Khedr
3   Human Genetics and Genome Research Division, Human Cytogenetics Department, National Research Centre, Cairo, Egypt
,
Phoebe M. Abd El-Massieh
4   Human Genetics and Genome Research Division, Oro-dental Genetics Department, National Research Centre, Cairo, Egypt
,
Sara M. Abdo
5   Biochemistry Division, Chemistry Department, Faculty of Science, Helwan University, Cairo, Egypt
,
Hala T. El-Bassyouni
1   Clinical Genetics Department, Center of Scientific Excellence, National Research Centre, Cairo, Egypt
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Abstract

Prader–Willi syndrome (PWS) is the commonest genetic cause of obesity. Oxidative stress and chronic low-grade inflammation play a crucial role in the pathogenesis of obesity. Alterations of vitamin D (25-OHD) levels are commonly encountered with obesity. The aim of this study was to analyze serum chemerin, oxidized low-density lipoprotein (ox-LDL), and 25-OHD values in pediatric PWS patients in comparison with obese healthy children and nonobese control groups, highlighting possible correlations with body mass index (BMI) and obesity. Twenty-six PWS Egyptian patients and 26 obese healthy individuals referred to the outpatient clinic of the Clinical Genetics Department, National Research Centre, Cairo, Egypt, and 20 control patients with matching age and sex were enrolled in the study. Patients were clinically diagnosed and confirmed by routine cytogenetic and fluorescence in-situ hybridization analysis. Anthropometric measurements were performed, and BMI was calculated by weight/height2 (kg/m2), and BMI z score was also determined. Serum chemerin, ox-LDL, and vitamin D were determined by enzyme-linked immunosorbent assay. Chemerin levels, which reflected chronic inflammation, were significantly elevated as compared with obese and nonobese controls (p ≤ 0.0001). Concerning oxidative damage, children with PWS showed higher Ox-LDL levels compared with obese and nonobese controls (p < 0.0001). Vitamin D levels were significantly lower in PWS patients compared with obese and nonobese controls (p ≤ 0.0001). Our data showed that obesity in PWS is associated with oxidative stress and chronic low-grade inflammation. Ox-LDL is a good indicator of oxidative stress, and chemerin could be used as a biomarker for the chronic inflammatory state. Furthermore, vitamin D supplementation is recommended in PWS patients

Keywords

PWS - chemerin - oxidized LDL - 25 hydroxy vitamin D - BMI


Publication History

Received: 10 July 2020

Accepted: 16 September 2020

Article published online:
02 November 2020

© 2020. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/).

Georg Thieme Verlag KG
Stuttgart · New York

 

  • References

  • 1 OMIM. (Online Mendelian Inheritance in Man). 2018. McKusick- Nathans Institute for Genetic Medicine, John Hopkins University (Baltimore, MD) and National Center for Biotechnology Information National Library of Medicine (Bethesda, MD); WorldWideWebURL: http://www.ncbi.nlm.nih.gov/omim. Accessed July 20, 2019
    Google Scholar
  • 2 Lionti T, Reid SM, White SM, Rowell MM. A population-based profile of 160 Australians with Prader-Willi syndrome: trends in diagnosis, birth prevalence and birth characteristics. Am J Med Genet A 2015; 167A (02) 371-378
    CrossrefPubMedGoogle Scholar
  • 3 Butler MG, Weaver DD, Meaney FJ. Prader-Willi syndrome: are there population differences?. Clin Genet 1982; 22 (05) 292-294
    CrossrefPubMedGoogle Scholar
  • 4 Angulo MA, Butler MG, Cataletto ME. Prader-Willi syndrome: a review of clinical, genetic, and endocrine findings. J Endocrinol Invest 2015; 38 (12) 1249-1263
    CrossrefPubMedGoogle Scholar
  • 5 El-Bassyouni HT, Hassan N, Mahfouz I, Abd-Elnaby AE, Mostafa MI, Tosson AMS. Early detection and management of Prader-Willi syndrome in Egyptian Patients. J Pediatr Genet 2019; 8 (04) 179-186
    Article in Thieme ConnectPubMedGoogle Scholar
  • 6 Butler MG, Miller JL, Forster JL. Prader-Willi syndrome - clinical genetics, diagnosis and treatment approaches: an update. Curr Pediatr Rev 2019; 15 (04) 207-244
    CrossrefPubMedGoogle Scholar
  • 7 Butler MG, Lee PDK, Whitman BY. Management of Prader-Willi Syndrome. 3rd edition.. New York, NY: Springer Verlag Inc; 2006
    CrossrefGoogle Scholar
  • 8 Cassidy SB, Driscoll DJ. Prader-Willi syndrome. Eur J Hum Genet 2009; 17 (01) 3-13
    CrossrefPubMedGoogle Scholar
  • 9 Cassidy SB, Schwartz S, Miller JL, Driscoll DJ. Prader-Willi syndrome. Genet Med 2012; 14 (01) 10-26
    Google Scholar
  • 10 Salah EM, El-Bassyouni HT, Kholoussi S, Marwa S, Kandeel WA. Behavioral problems, biochemical and anthropometric characteristics of patients with Prader-Willi syndrome. Middle East J Med Genet 2015; 4: 63-69
    CrossrefPubMedGoogle Scholar
  • 11 Butler MG. Single gene and syndromic causes of obesity: Illustrative examples. Prog Mol Biol Transl Sci 2016; 140: 1-45
    CrossrefPubMedGoogle Scholar
  • 12 Alves C, Franco RR. Prader-Willi syndrome: endocrine manifestations and management. Arch Endocrinol Metab 2020; 64 (03) 223-234
    CrossrefPubMedGoogle Scholar
  • 13 Butler MG, Manzardo AM, Forster JL. Prader-Willi syndrome: clinical genetics and diagnostic aspects with treatment approaches. Curr Pediatr Rev 2016; 12 (02) 136-166
    CrossrefPubMedGoogle Scholar
  • 14 Irizarry KA, Bain J, Butler MG. et al. Metabolic profiling in Prader-Willi syndrome and nonsyndromic obesity: sex differences and the role of growth hormone. Clin Endocrinol (Oxf) 2015; 83 (06) 797-805
    CrossrefPubMedGoogle Scholar
  • 15 Heksch R, Kamboj M, Anglin K, Obrynba K. Review of Prader-Willi syndrome: the endocrine approach. Transl Pediatr 2017; 6 (04) 274-285
    CrossrefPubMedGoogle Scholar
  • 16 Dalle-Donne I, Rossi R, Colombo R, Giustarini D, Milzani A. Biomarkers of oxidative damage in human disease. Clin Chem 2006; 52 (04) 601-623
    CrossrefPubMedGoogle Scholar
  • 17 Weinbrenner T, Schröder H, Escurriol V. et al. Circulating oxidized LDL is associated with increased waist circumference independent of body mass index in men and women. Am J Clin Nutr 2006; 83 (01) 30-35 , quiz 181–182
    CrossrefPubMedGoogle Scholar
  • 18 Linna MS, Ahotupa M, Kukkonen-Harjula K, Fogelholm M, Vasankari TJ. Co-existence of insulin resistance and high concentrations of circulating oxidized LDL lipids. Ann Med 2015; 47 (05) 394-398
    CrossrefPubMedGoogle Scholar
  • 19 Holvoet P, Lee DH, Steffes M, Gross M, Jacobs Jr DR. Association between circulating oxidized low-density lipoprotein and incidence of the metabolic syndrome. JAMA 2008; 299 (19) 2287-2293
    CrossrefPubMedGoogle Scholar
  • 20 Holvoet P, Jenny NS, Schreiner PJ, Tracy RP, Jacobs DR. Multi-Ethnic Study of Atherosclerosis. The relationship between oxidized LDL and other cardiovascular risk factors and subclinical CVD in different ethnic groups: the Multi-Ethnic Study of Atherosclerosis (MESA). Atherosclerosis 2007; 194 (01) 245-252
    CrossrefPubMedGoogle Scholar
  • 21 Rondinone CM. Adipocyte-derived hormones, cytokines, and mediators. Endocrine 2006; 29 (01) 81-90
    CrossrefPubMedGoogle Scholar
  • 22 Panagiotakos DB, Pitsavos C, Yannakoulia M, Chrysohoou C, Stefanadis C. The implication of obesity and central fat on markers of chronic inflammation: the ATTICA study. Atherosclerosis 2005; 183 (02) 308-315
    CrossrefPubMedGoogle Scholar
  • 23 Zaki ME, Youness E, Gadelhak M. et al. DNA damage and neutrophil elastase in children with Prader-Willi syndrome. Biomed Pharmacol J 2019; 12: 1967-1974
    CrossrefPubMedGoogle Scholar
  • 24 Goralski KB, McCarthy TC, Hanniman EA. et al. Chemerin, a novel adipokine that regulates adipogenesis and adipocyte metabolism. J Biol Chem 2007; 282 (38) 28175-28188
    CrossrefPubMedGoogle Scholar
  • 25 Zabel BA, Kwitniewski M, Banas M, Zabieglo K, Murzyn K, Cichy J. Chemerin regulation and role in host defense. Am J Clin Exp Immunol 2014; 3 (01) 1-19
    PubMedGoogle Scholar
  • 26 Saneei P, Salehi-Abargouei A, Esmaillzadeh A. Serum 25-hydroxy vitamin D levels in relation to body mass index: a systematic review and meta-analysis. Obes Rev 2013; 14 (05) 393-404
    CrossrefPubMedGoogle Scholar
  • 27 Walker GE, Ricotti R, Roccio M. et al. Pediatric obesity and vitamin D deficiency: a proteomic approach identifies multimeric adiponectin as a key link between these conditions. PLoS One 2014; 9 (01) e83685
    CrossrefPubMedGoogle Scholar
  • 28 Cediel G, Corvalán C, Aguirre C, de Romaña DL, Uauy R. Serum 25-Hydroxyvitamin D associated with indicators of body fat and insulin resistance in prepubertal Chilean children. Int J Obes 2016; 40 (01) 147-152
    CrossrefPubMedGoogle Scholar
  • 29 Fintini D, Grugni G, Bocchini S. et al. Genetic Obesity Study Group of the Italian Society of Pediatric Endocrinology and Diabetology (ISPED). Disorders of glucose metabolism in Prader-Willi syndrome: results of a multicenter Italian cohort study. Nutr Metab Cardiovasc Dis 2016; 26 (09) 842-847
    CrossrefPubMedGoogle Scholar
  • 30 WHO AnthroPlus for personal computers Manual: Software for assessing growth of the world’s children and adolescents. Geneva: WHO, 2009. Accessed July 3, 2020 at: http://www.who.int/growthref/tools/en/
  • 31 Pinkel D, Gray JW, Trask B, van den Engh G, Fuscoe J, van Dekken H. Cytogenetic analysis by in situ hybridization with fluorescently labeled nucleic acid probes. Cold Spring Harb Symp Quant Biol 1986; 51 (Pt 1): 151-157
    CrossrefPubMedGoogle Scholar
  • 32 Verma RS, Babu A. Tissue culture techniques and chromosome preparation. In: Verma RS, Babu A. , eds. Human Chromosomes Principles and Technique. 2nd edition.. New York: McGraw-Hill; 1995: 6-71
    Google Scholar
  • 33 Haaf T. Fluorescence in situ hybridization. In: Meyers RA. , ed. Encyclopedia of Analytic Chemistry. Genetic Diagnosis of Prader–Willi Syndrome. Chichester, UK: John Wiley & sons Ltd; 2000: 4984-5006
    Google Scholar
  • 34 Wielders JP, Wijnberg FA. Preanalytical stability of 25(OH)-vitamin D3 in human blood or serum at room temperature: solid as a rock. Clin Chem 2009; 55 (08) 1584-1585
    CrossrefPubMedGoogle Scholar
  • 35 Rocha CF, Paiva CLA. Prader-Willi-like phenotypes: a systematic review of their chromosomal abnormalities. Genet Mol Res 2014; 13 (01) 2290-2298
    CrossrefPubMedGoogle Scholar
  • 36 Tsuyusaki Y, Yoshihashi H, Furuya N. et al. 1p36 deletion syndrome associated with Prader-Willi-like phenotype. Pediatr Int 2010; 52 (04) 547-550
    CrossrefPubMedGoogle Scholar
  • 37 D'Angelo CS, Kohl I, Varela MC. et al. Obesity with associated developmental delay and/or learning disability in patients exhibiting additional features: report of novel pathogenic copy number variants. Am J Med Genet A 2013; 161A (03) 479-486
    CrossrefPubMedGoogle Scholar
  • 38 Afifi HH, El-Ruby MO, El-Bassyouni HT. et al. The most encountered groups of genetic disorders in Giza Governorate, Egypt. Bratisl Lek Listy 2010; 111 (02) 62-69
    Google Scholar
  • 39 Khedr AA, Meguid NA, Mohamed AM. et al. Genetic diagnosis of Prader–Willi syndrome. Middle East J Med Genet 2016; 5: 45-53
    CrossrefPubMedGoogle Scholar
  • 40 Khan MJ, Gerasimidis K, Edwards CA, Shaikh MG. Mechanisms of obesity in Prader-Willi syndrome. Pediatr Obes 2018; 13 (01) 3-13
    CrossrefPubMedGoogle Scholar
  • 41 Anichini C, Lotti F, Longini M. et al. Antioxidant effects of potassium ascorbate with ribose therapy in a case with Prader Willi syndrome. Dis Markers 2012; 33 (04) 179-183
    CrossrefPubMedGoogle Scholar
  • 42 Bondia-Pons I, Ryan L, Martinez JA. Oxidative stress and inflammation interactions in human obesity. J Physiol Biochem 2012; 68 (04) 701-711
    CrossrefPubMedGoogle Scholar
  • 43 Kelly AS, Jacobs Jr DR, Sinaiko AR, Moran A, Steffen LM, Steinberger J. Relation of circulating oxidized LDL to obesity and insulin resistance in children. Pediatr Diabetes 2010; 11 (08) 552-555
    CrossrefPubMedGoogle Scholar
  • 44 Zhao SP, Wu J, Zhang DQ, Ye HJ, Liu L, Li JQ. Fenofibrate enhances CD36 mediated endocytic uptake and degradation of oxidized low density lipoprotein in adipocytes from hypercholesterolemia rabbit. Atherosclerosis 2004; 177 (02) 255-262
    CrossrefPubMedGoogle Scholar
  • 45 Chui PC, Guan HP, Lehrke M, Lazar MA. PPARgamma regulates adipocyte cholesterol metabolism via oxidized LDL receptor 1. J Clin Invest 2005; 115 (08) 2244-2256
    CrossrefPubMedGoogle Scholar
  • 46 Marseglia L, Manti S, D'Angelo G. et al. Oxidative stress in obesity: a critical component in human diseases. Int J Mol Sci 2014; 16 (01) 378-400
    CrossrefPubMedGoogle Scholar
  • 47 Ferretti G, Bacchetti T, Masciangelo S, Grugni G, Bicchiega V. Altered inflammation, paraoxonase-1 activity and HDL physicochemical properties in obese humans with and without Prader-Willi syndrome. Dis Model Mech 2012; 5 (05) 698-705
    CrossrefPubMedGoogle Scholar
  • 48 Hassan NE, El-Masry SA, Abu Shady MM. et al. Relation of circulating oxidized LDL with fat distribution and insulin resistance among obese school students. RJMMS 2013; 8: 16-22
    PubMedGoogle Scholar
  • 49 Moreno-Indias I, Oliva-Olivera W, Omiste A. et al. Adipose tissue infiltration in normal-weight subjects and its impact on metabolic function. Transl Res 2016; 172: 6-17.e3
    CrossrefPubMedGoogle Scholar
  • 50 Sell H, Divoux A, Poitou C. et al. Chemerin correlates with markers for fatty liver in morbidly obese patients and strongly decreases after weight loss induced by bariatric surgery. J Clin Endocrinol Metab 2010; 95 (06) 2892-2896
    CrossrefPubMedGoogle Scholar
  • 51 Perumalsamy S, Aqilah Mohd Zin NA, Widodo RT, Wan Ahmad WA, Vethakkan SRDB, Huri HZ. Chemokine like receptor-1 (CMKLR-1) receptor: a potential therapeutic target in management of chemerin induced type 2 diabetes mellitus and cancer. Curr Pharm Des 2017; 23 (25) 3689-3698
    CrossrefPubMedGoogle Scholar
  • 52 Sell H, Laurencikiene J, Taube A. et al. Chemerin is a novel adipocyte-derived factor inducing insulin resistance in primary human skeletal muscle cells. Diabetes 2009; 58 (12) 2731-2740
    CrossrefPubMedGoogle Scholar
  • 53 Chakaroun R, Raschpichler M, Klöting N. et al. Effects of weight loss and exercise on chemerin serum concentrations and adipose tissue expression in human obesity. Metabolism 2012; 61 (05) 706-714
    CrossrefPubMedGoogle Scholar
  • 54 Helfer G, Wu QF. Chemerin: a multifaceted adipokine involved in metabolic disorders. J Endocrinol 2018; 238 (02) R79-R94
    CrossrefPubMedGoogle Scholar
  • 55 Lehrke M, Becker A, Greif M. et al. Chemerin is associated with markers of inflammation and components of the metabolic syndrome but does not predict coronary atherosclerosis. Eur J Endocrinol 2009; 161 (02) 339-344
    CrossrefPubMedGoogle Scholar
  • 56 Rourke JL, Dranse HJ, Sinal CJ. Towards an integrative approach to understanding the role of chemerin in human health and disease. Obes Rev 2013; 14 (03) 245-262
    CrossrefPubMedGoogle Scholar
  • 57 Stejskal D, Karpisek M, Hanulova Z, Svestak M. Chemerin is an independent marker of the metabolic syndrome in a Caucasian population–a pilot study. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2008; 152 (02) 217-221
    CrossrefPubMedGoogle Scholar
  • 58 Ross AW, Helfer G, Russell L, Darras VM, Morgan PJ. Thyroid hormone signalling genes are regulated by photoperiod in the hypothalamus of F344 rats. PLoS One 2011; 6 (06) e21351
    CrossrefPubMedGoogle Scholar
  • 59 Khoo J, Dhamodaran S, Chen D-D, Yap S-Y, Chen RY-T, Tian RH-H. Exercise-induced weight loss is more effective than dieting for improving adipokine profile, insulin resistance, and inflammation in obese men. Int J Sport Nutr Exerc Metab 2015; 25 (06) 566-575
    CrossrefPubMedGoogle Scholar
  • 60 Faramarzi M, Banitalebi E, Nori S, Farzin S, Taghavian Z. Effects of rhythmic aerobic exercise plus core stability training on serum omentin, chemerin and vaspin levels and insulin resistance of overweight women. J Sports Med Phys Fitness 2016; 56 (04) 476-482
    Google Scholar
  • 61 Buechler C, Feder S, Haberl EM, Aslanidis C. Chemerin isoforms and activity in obesity. Int J Mol Sci 2019; 20 (05) 1128
    CrossrefPubMedGoogle Scholar
  • 62 Becker M, Rabe K, Lebherz C. et al. Expression of human chemerin induces insulin resistance in the skeletal muscle but does not affect weight, lipid levels, and atherosclerosis in LDL receptor knockout mice on high-fat diet. Diabetes 2010; 59 (11) 2898-2903
    CrossrefPubMedGoogle Scholar
  • 63 Rouger L, Denis GR, Luangsay S, Parmentier M. ChemR23 knockout mice display mild obesity but no deficit in adipocyte differentiation. J Endocrinol 2013; 219 (03) 279-289
    CrossrefPubMedGoogle Scholar
  • 64 Gruben N, Aparicio Vergara M, Kloosterhuis NJ. et al. Chemokine-like receptor 1 deficiency does not affect the development of insulin resistance and nonalcoholic fatty liver disease in mice. PLoS One 2014; 9 (04) e96345
    CrossrefPubMedGoogle Scholar
  • 65 Tam CS, Clément K, Baur LA, Tordjman J. Obesity and low-grade inflammation: a paediatric perspective. Obes Rev 2010; 11 (02) 118-126
    CrossrefPubMedGoogle Scholar
  • 66 Catrysse L, van Loo G. Inflammation and the metabolic syndrome: the tissue-specific functions of NF-kappaB. Trends Cell Biol 2017; 27 (06) 417-429
    CrossrefPubMedGoogle Scholar
  • 67 Huang J-Y, Zhou QL, Huang C-H. et al. Neutrophil elastase regulates emergency myelopoiesis preceding systemic inflammation in diet-induced obesity. J Biol Chem 2017; 292 (12) 4770-4776
    CrossrefPubMedGoogle Scholar
  • 68 Weigert J, Neumeier M, Wanninger J. et al. Systemic chemerin is related to inflammation rather than obesity in type 2 diabetes. Clin Endocrinol (Oxf) 2010; 72 (03) 342-348
    CrossrefPubMedGoogle Scholar
  • 69 Coimbra S, Brandão Proença J, Santos-Silva A, Neuparth MJ. Adiponectin, leptin, and chemerin in elderly patients with type 2 diabetes mellitus: a close linkage with obesity and length of the disease. BioMed Res Int 2014; 2014: 701915
    CrossrefPubMedGoogle Scholar
  • 70 Zhuang XH, Sun FD, Chen SH. et al. Circulating chemerin levels are increased in first-degree relatives of type 2 diabetic patients. Clin Lab 2014; 60 (06) 983-988
    PubMedGoogle Scholar
  • 71 Catalán V, Gómez-Ambrosi J, Rodríguez A. et al. Increased levels of chemerin and its receptor, chemokine-like receptor-1, in obesity are related to inflammation: tumor necrosis factor-α stimulates mRNA levels of chemerin in visceral adipocytes from obese patients. Surg Obes Relat Dis 2013; 9 (02) 306-314
    CrossrefPubMedGoogle Scholar
  • 72 Fatima SS, Rehman R, Baig M, Khan TA. New roles of the multidimensional adipokine: chemerin. Peptides 2014; 62: 15-20
    CrossrefPubMedGoogle Scholar
  • 73 Mariani F, Roncucci L. Chemerin/chemR23 axis in inflammation onset and resolution. Inflamm Res 2015; 64 (02) 85-95
    CrossrefPubMedGoogle Scholar
  • 74 Fintini D, Pedicelli S, Bocchini S. et al. 25OH vitamin D levels in pediatric patients affected by Prader-Willi syndrome. J Endocrinol Invest 2018; 41 (06) 739-742
    CrossrefPubMedGoogle Scholar
  • 75 Ameri P, Giusti A, Boschetti M, Murialdo G, Minuto F, Ferone D. Interactions between vitamin D and IGF-I: from physiology to clinical practice. Clin Endocrinol (Oxf) 2013; 79 (04) 457-463
    CrossrefPubMedGoogle Scholar
  • 76 Savanelli MC, Scarano E, Muscogiuri G. et al. Cardiovascular risk in adult hypopituitaric patients with growth hormone deficiency: is there a role for vitamin D?. Endocrine 2016; 52 (01) 111-119
    CrossrefPubMedGoogle Scholar
  • 77 Samuel L, Borrell LN. The effect of body mass index on optimal vitamin D status in U.S. adults: the National Health and Nutrition Examination Survey 2001-2006. Ann Epidemiol 2013; 23 (07) 409-414
    CrossrefPubMedGoogle Scholar
  • 78 Walsh JS, Evans AL, Bowles S. et al. Free 25-hydroxyvitamin D is low in obesity, but there are no adverse associations with bone health. Am J Clin Nutr 2016; 103 (06) 1465-1471
    CrossrefPubMedGoogle Scholar
  • 79 Walsh JS, Bowles S, Evans AL. Vitamin D in obesity. Curr Opin Endocrinol Diabetes Obes 2017; 24 (06) 389-394
    CrossrefPubMedGoogle Scholar
  • 80 Wamberg L, Christiansen T, Paulsen SK. et al. Expression of vitamin D-metabolizing enzymes in human adipose tissue – the effect of obesity and diet-induced weight loss. Int J Obes 2013; 37 (05) 651-657
    CrossrefPubMedGoogle Scholar
  • 81 Di Nisio A, De Toni L, Sabovic I. et al. Impaired release of vitamin D in dysfunctional adipose tissue: new cues on vitamin D supplementation in obesity. J Clin Endocrinol Metab 2017; 102 (07) 2564-2574
    CrossrefPubMedGoogle Scholar
  • 82 Brunetti G, Grugni G, Piacente L. et al. Analysis of circulating mediators of bone remodeling in Prader-Willi syndrome. Calcif Tissue Int 2018; 102 (06) 635-643
    CrossrefPubMedGoogle Scholar
  • 83 Purtell L, Viardot A, Campbell LV. Vitamin D levels in primary growth hormone deficiency disorder Prader-Willi syndrome. Endocrine 2016; 53 (02) 619-620
    CrossrefPubMedGoogle Scholar
  • 84 Rubin DA, Nowak J, McLaren E, Patiño M, Castner DM, Dumont-Driscoll MC. Nutritional intakes in children with Prader-Willi syndrome and non-congenital obesity. Food Nutr Res 2015; 59: 29427
    CrossrefPubMedGoogle Scholar