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Cholesterol  2012 

Macronutrient Intake Influences the Effect of 25-Hydroxy-Vitamin D Status on Metabolic Syndrome Outcomes in African American Girls

DOI: 10.1155/2012/581432

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The objectives were to determine the effect of macronutrient modification on vitamin D status and if change in 25-hydroxy-vitamin D concentration influences components of metabolic syndrome in obese African American girls. Methods. Five-week intervention using reduced CHO (43% carbohydrate; 27% fat: SPEC) versus standard CHO (55% carbohydrate; 40% fat: STAN) eucaloric diet. Subjects were 28 obese African American females, aged 9–14 years. Dual energy X-ray absorptiometry and meal test were performed at baseline and five weeks. Results. Approximately 30% of girls had metabolic syndrome. Serum 25OHD increased in both groups at five weeks [STAN: 20.3 ± 1.1 to 22.4 ± 1.1 ( ) versus SPEC: to ( )]. The STAN group, increased 25OHD concentration over five weeks ( ), which was positively related to triglycerides ( ) and inversely associated with total cholesterol ( ) and LDL ( ). The SPEC group, had increase in 25OHD ( ), which was positively related to fasting insulin ( ) and insulin sensitivity while inversely associated with fasting glucose ( ). The contribution of vitamin D status to metabolic syndrome parameters differs according to macronutrient intake. Improvement in 25OHD may improve fasting glucose, insulin sensitivity, and LDL; however, macronutrient intake warrants consideration. 1. Introduction The steady rise in prevalence of pediatric obesity over the past three decades has been accompanied by accumulation of risk factors for metabolic syndrome (MetSyn) in childhood and adolescence. The occurrence of hypovitaminosis D (expressed as levels <20?ng/mL of circulating 25-hydroxy vitamin D (25OHD)) has been increasingly documented in the same population [1, 2]. Moreover, children/adolescents with hypovitaminosis D have been reported to experience greater instances of hypertension, hypertriglyceridemia, hyperglycemia, and low high-density lipoprotein cholesterol (HDL) [1, 3, 4]. Further, it has been proposed that elevated parathyroid hormone (PTH), consequential to chronic low vitamin D level, is mechanistically involved in the adverse perturbations of risk factors underlying MetSyn [5]. Given the emerging identification of vitamin D as an integral player in numerous metabolic pathways, it stands to reason that vitamin D status in the pediatric populace may play a role in the prevalence of metabolic disease risk factors [6, 7]. The relationship between 25OHD status and metabolic health is not equally distributed across groups. In particular, the relationship is more apparent among African American (AA) females, particularly those who are overweight/obese


[1]  T. D. Thacher and B. L. Clarke, “Vitamin D insufficiency,” Mayo Clinic Proceedings, vol. 86, no. 1, pp. 50–60, 2011.
[2]  A. A. Ginde, M. C. Liu, and C. A. Camargo Jr., “Demographic differences and trends of vitamin D insufficiency in the US population, 1988–2004,” Archives of Internal Medicine, vol. 169, no. 6, pp. 626–632, 2009.
[3]  S. Al-Musharaf, A. Al-Othman, N. M. Al-Daghri et al., “Vitamin D deficiency and calcium intake in reference to increased body mass index in children and adolescents,” European Journal of Pediatrics. In press.
[4]  J. P. Reis, D. von Mühlen, E. R. Miller III, E. D. Michos, and L. J. Appel, “Vitamin D status and cardiometabolic risk factors in the United States adolescent population,” Pediatrics, vol. 124, no. 3, pp. e371–e379, 2009.
[5]  J. Hjelmes?th, D. Hofs?, E. T. Aasheim et al., “Parathyroid hormone, but not vitamin D, is associated with the metabolic syndrome in morbidly obese women and men: a cross-sectional study,” Cardiovascular Diabetology, vol. 8, article 7, 2009.
[6]  L. S. Harkness and B. A. Cromer, “Vitamin D deficiency in adolescent females,” Journal of Adolescent Health, vol. 37, no. 1, p. 75, 2005.
[7]  K. Rajakumar, J. D. Fernstrom, M. F. Holick, J. E. Janosky, and S. L. Greenspan, “Vitamin D status and response to vitamin D3 in obese vs. Non-obese African American children,” Obesity, vol. 16, no. 1, pp. 90–95, 2008.
[8]  P. Zhou, C. Schechter, Z. Cai, and M. Markowitz, “Determinants of 25(OH)D sufficiency in obese minority children: selecting outcome measures and analytic approaches,” Journal of Pediatrics, vol. 158, no. 6, pp. 930–934.e1, 2011.
[9]  C. M. Lenders, H. A. Feldman, E. Von Scheven et al., “Relation of body fat indexes to vitamin D status and deficiency among obese adolescents,” The American Journal of Clinical Nutrition, vol. 90, no. 3, pp. 459–467, 2009.
[10]  C. M. Gordon, K. C. DePeter, H. A. Feldman, E. Grace, and S. J. Emans, “Prevalence of vitamin D deficiency among healthy adolescents,” Archives of Pediatrics and Adolescent Medicine, vol. 158, no. 6, pp. 531–537, 2004.
[11]  T. Reinehr, G. de Sousa, U. Alexy, M. Kersting, and W. Andler, “Vitamin D status and parathyroid hormone in obese children before and after weight loss,” European Journal of Endocrinology, vol. 157, no. 2, pp. 225–232, 2007.
[12]  K. Casazza, M. Cardel, A. Dulin-Keita et al., “Reduced carbohydrate diet to improve metabolic outcomes and decrease adiposity in obese peripubertal African American girls,” Journal of Pediatric Gastroenterology and Nutrition, vol. 54, no. 3, pp. 336–342, 2012.
[13]  A. L. Willig, K. Casazza, A. Dulin-Keita, F. A. Franklin, M. Amaya, and J. R. Fernandez, “Adjusting adiposity and body weight measurements for height alters the relationship with blood pressure in children,” American Journal of Hypertension, vol. 23, no. 8, pp. 904–910, 2010.
[14]  E. Breda, M. K. Cavaghan, G. Toffolo, K. S. Polonsky, and C. Cobelli, “Oral glucose tolerance test minimal model indexes of β-cell function and insulin sensitivity,” Diabetes, vol. 50, no. 1, pp. 150–158, 2001.
[15]  A. C. Ross, J. E. Manson, S. A. Abrams et al., “The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know,” Journal of Clinical Endocrinology and Metabolism, vol. 96, no. 1, pp. 53–58, 2011.
[16]  J. A. Alvarez, A. P. Ashraf, G. R. Hunter, and B. A. Gower, “Serum 25-hydroxyvitamin D and parathyroid hormone are independent determinants of whole-body insulin sensitivity in women and may contribute to lower insulin sensitivity in African Americans,” The American Journal of Clinical Nutrition, vol. 92, no. 6, pp. 1344–1349, 2010.
[17]  R. Alemzadeh, J. Kichler, G. Babar, and M. Calhoun, “Hypovitaminosis D in obese children and adolescents: relationship with adiposity, insulin sensitivity, ethnicity, and season,” Metabolism, vol. 57, no. 2, pp. 183–191, 2008.
[18]  A. J. Rovner and K. O. O'Brien, “Hypovitaminosis D among healthy children in the United States: a review of the current evidence,” Archives of Pediatrics and Adolescent Medicine, vol. 162, no. 6, pp. 513–519, 2008.
[19]  E. Rodríguez-Rodríguez, R. M. Ortega, L. G. González-Rodríguez, and A. M. López-Sobaler, “Vitamin D deficiency is an independent predictor of elevated triglycerides in Spanish school children,” European Journal of Nutrition, vol. 50, no. 5, pp. 373–378, 2011.
[20]  G. C. Major, F. Alarie, J. Doré, S. Phouttama, and A. Tremblay, “Supplementation with calcium + vitamin D enhances the beneficial effect of weight loss on plasma lipid and lipoprotein concentrations,” The American Journal of Clinical Nutrition, vol. 85, no. 1, pp. 54–59, 2007.
[21]  N. M. Al-Daghri, O. S. Al-Attas, M. S. Alokail, et al., “Hypovitaminosis D associations with adverse metabolic parameters are accentuated in patients with diabetes mellitus type 2: A BMI-independent role of adiponectin?” Journal of Endocrinological Investigation. In press.
[22]  J. C. Brand-Miller, H. J. Griffin, and S. Colagiuri, “The carnivore connection hypothesis: revisited,” Journal of Obesity, vol. 2012, Article ID 258624, 9 pages, 2012.
[23]  A. G. Pittas, J. Lau, F. B. Hu, and B. Dawson-Hughes, “Review: the role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis,” Journal of Clinical Endocrinology and Metabolism, vol. 92, no. 6, pp. 2017–2029, 2007.
[24]  Y. Pan and C. A. Pratt, “Metabolic syndrome and its association with diet and physical activity in US adolescents,” Journal of the American Dietetic Association, vol. 108, no. 2, pp. 276–286, 2008.
[25]  R. Kumar and J. R. Thompson, “The regulation of parathyroid hormone secretion and synthesis,” Journal of the American Society of Nephrology, vol. 22, no. 2, pp. 216–224, 2011.
[26]  S. A. Abrams, I. J. Griffin, K. M. Hawthorne, S. K. Gunn, C. M. Gundberg, and T. O. Carpenter, “Relationships among vitamin D levels, parathyroid hormone, and calcium absorption in young adolescents,” Journal of Clinical Endocrinology and Metabolism, vol. 90, no. 10, pp. 5576–5581, 2005.
[27]  R. P. Heaney, “Functional indices of vitamin D status and ramifications of vitamin D deficiency,” The The American Journal of Clinical Nutrition, vol. 80, no. 6, supplement, pp. 1706S–1709S, 2004.
[28]  K. M. Hill, G. P. McCabe, L. D. McCabe, C. M. Gordon, S. A. Abrams, and C. M. Weaver, “An inflection point of serum 25-hydroxyvitamin D for maximal suppression of parathyroid hormone is not evident from multi-site pooled data in children and adolescents,” Journal of Nutrition, vol. 140, no. 11, pp. 1983–1988, 2010.
[29]  F. Cosman, D. C. Morgan, J. W. Nieves et al., “Resistance to bone resorbing effects of PTH in black women,” Journal of Bone and Mineral Research, vol. 12, no. 6, pp. 958–966, 1997.
[30]  S. Cook, M. Weitzman, P. Auinger, M. Nguyen, and W. H. Dietz, “Prevalence of a metabolic syndrome phenotype in adolescents: findings from the Third National Health and Nutrition Examination Survey, 1988–1994,” Archives of Pediatrics and Adolescent Medicine, vol. 157, no. 8, pp. 821–827, 2003.
[31]  M. Rodríguez-Morán, B. Salazar-Vázquez, R. Violante, and F. Guerrero-Romero, “Metabolic syndrome among children and adolescents aged 10–18 years,” Diabetes Care, vol. 27, no. 10, pp. 2516–2517, 2004.
[32]  R. Weiss, J. Dziura, T. S. Burgert et al., “Obesity and the metabolic syndrome in children and adolescents,” The New England Journal of Medicine, vol. 350, no. 23, pp. 2362–2374, 2004.


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