Hindawi Publishing Corporation
Volume 2012, Article ID 581432, 8 pages
25-Hydroxy-Vitamin D Status on Metabolic SyndromeOutcomes
AnnaL.Newton,1LynaeJ. Hanks,1AmbikaP. Ashraf,2ElizabethWilliams,1
Michelle Davis,1andKrista Casazza1
1Department of Nutrition Sciences, University of Alabama at Birmingham, 1675 University Boulevard, WEBB 439 Birmingham,
AL 35294-3360, USA
2Division of Pediatric Endocrinology, Department of Medicine, University of Alabama at Birmingham, Birmingham,
AL 35294-3360, USA
Correspondence should be addressed to Krista Casazza, firstname.lastname@example.org
Received 29 February 2012; Revised 23 April 2012; Accepted 23 April 2012
Academic Editor: Roya Kelishadi
Copyright © 2012 Anna L. Newton et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
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 (P < 0.05) versus SPEC: 16.1 ± 1.0 to 16.8 ± 1.0 (P = 0.05)]. The
STAN group, increased 25OHD concentration over five weeks (P < 0.05), which was positively related to triglycerides (P < 0.001)
and inversely associated with total cholesterol (P < 0.001) and LDL (P < 0.001). The SPEC group, had increase in 25OHD
(P = 0.05), which was positively related to fasting insulin (P < 0.001) and insulin sensitivity while inversely associated with fasting
glucose (P < 0.05). The contribution of vitamin D status to metabolic syndrome parameters differs according to macronutrient
The steady rise in prevalence of pediatric obesity over the
risk factors for metabolic syndrome (MetSyn) in childhood
and adolescence. The occurrence of hypovitaminosis D
(expressed as levels <20ng/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 experi-
ence 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 . Given
the emerging identification of vitamin D asan 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
[8–11]. Although greater prevalence of hypovitaminosis
D among obese AA may be in part attributed to skin
pigmentation and sequestering of vitamin D in adipose
tissue, differences in classical endocrine effects (e.g., PTH
may modify the relationship between vitamin D bioavail-
ability and underlying metabolic pathways. It is known
that 25OHD level is dependent on intestinal absorption of
dietary vitamin D, the extent to which vitamin D may exert
effects on metabolic factors is at least in part dependent
upon macronutrient profile of the diet. The metabolic
response to dietary composition, specifically carbohydrate
quantity of a meal, influences the postprandial cascade of
events (increased glucose, insulin, lipogenesis, glycogenesis,
etc.). Vitamin D has been independently associated with
these processes, and the fact that vitamin D insufficiency
stimulates secretion of PTH cannot be ignored. Data from
this group has demonstrated that the physiological response
to macronutrient concentration of the diet differs among
racial groups ; however, to our knowledge there has been
profile to vitamin D involvement with metabolic compo-
nents. Accordingly, the independent and interactive contri-
bution of diet and vitamin D status (and consequent PTH
level) on metabolic risk warrants investigation, particularly
among obese adolescents.
Understanding the extent to which macronutrient com-
position influences vitamin D bioavailability may be partic-
ularly important during growth and development. Adoles-
cence characterizes a time when risk factors for MetSyn can
be identified, and modification of the dietary profile repre-
sents a strategy in which intervention may have the greatest
directive impact. Therefore, the objective of this study was
to determine the effect of macronutrient modifications on
vitamin D status and if change in 25OHD concentration
would influence components of MetSyn in obese AA girls.
Further, as AA females are a population group that are
at increased metabolic risk, this study seeks to evaluate
the effect of macronutrient modification on associations
of vitamin D concentrations and potential influence of
PTH in AA adolescent females to parameters of MetSyn
(fat distribution, insulin sensitivity, glucose tolerance, lipid
concentrations, and blood pressure).
Participants included 28 overweight/obese AA girls aged 9–
14 years. Obesity was defined as greater than 95th sex- and
criteria were medical diagnosis and/or taking medications
known to affect body composition, metabolism, and cardiac
function. Participants were recruited through newspaper
advertisements, flyers posted at various community part-
nerships, and by word-of-mouth. The nature, purpose,
and possible risks of the study were carefully explained
to each participant and guardian(s), and informed assent
and consent, respectively were obtained. The protocol was
approved by the Institutional Review Board for human
subjects at the University of Alabama at Birmingham (UAB).
All measurements were performed at the Participant and
Clinical Interactions Resources (PCIRs) and the Department
of Nutrition Sciences at UAB between 2008 and 2009.
2.1. Protocol. This study was part of a 16-week intervention
comparing the effectiveness of a reduced CHO (43% carbo-
hydrate: SPEC) versus a standard CHO (55% carbohydrate:
STAN) diet on weight loss and metabolic health. Included
data were derived from the initial five-week eucaloric phase,
during which time the goal was for participants to maintain
their baseline weight while consuming respective diets.
Participants were block-randomized to one of the two diets
which they remained on for the duration of the study. All
food was provided, with the amount determined according
to calculated individual needs determined by resting energy
expenditure (REE; assessed via indirect calorimetry) multi-
plied by a 1.2 activity factor (averaging about 2000kcal/d).
At baseline, participants attended two visits. The first
visit entailed a physical examination by the study pedia-
trician, questionnaires on typical diet and regular physical
activity, and a full-body dual energy X-ray absorptiometry
(DXA) scan. At the second visit, participants reported to
the PCIR in the morning in the fasted state for metabolic
testing. After 30minutes of rest, REE was assessed, and a
liquid mixed-meal test (LMMT) was performed. To ensure
weight stability, participants were weighed twice per week at
food pickup to evaluate the caloric prescription throughout
the five-week eucaloric phase. Weight changes exceeding
two kilograms from baseline resulted in caloric modification
in effort to maintain weight. Participants were asked to
maintain their regular level of physical activity. At the
duration of five weeks, the DXA scan, indirect calorimetry,
and LMMT were repeated.
2.2. Diets. The SPEC diet comprised 42% of energy from
CHO and 40% of energy from fat, whereas the STAN
diet comprised 55% of energy from CHO and 27% of
energy from fat. Both diets contained a similar content of
protein (about 18%). Baseline energy levels for all diets
were 1600kcal with the addition of 100 to 400kcal snack
per day. All diets included culturally- and age-appropriate
foods with no inclusion of supplements or formulas, and
noncaloric fluid intake of ≥64 fluid ounces per day was
recommended. All meals were prepared and packaged in
the research kitchen at the UAB PCIR. A trained registered
dietitian coded and entered data from each diet into the
computerized Nutrition Data System for Research (NDSR).
2.3. Anthropometrics. The same registered dietitian obtained
anthropometric measurements for all participants. Partic-
ipants were weighed (Scale-Tronix 6702W; Scale-Tronix,
Carol Stream, IL, USA) to the nearest 0.1kg in minimal
clothing without shoes. Height was also recorded without
shoes using a digital stadiometer (Heightronic 235; Mea-
surement Concepts, Snoqualmie, WA, USA). BMI percentile
and obesity status (≥95th percentile) was calculated using
sex- and age-specific CDC growth charts based on these
2.4. Body Composition and Fat Mass Index. Body com-
position was measured by DXA using GE Lunar Prodigy
densitometer (GE LUNAR Radiation Corp., Madison, WI,
flat on their backs with arms at their sides. Due to size
limitations, participants not fitting within the scanning box
were right-sided hemiscanned with the left side estimated as
per instrument protocol. Fat mass index calculated as total
body fat divided by height was used as a covariate .
2.5. Liquid Mixed Meal Test/Insulin Sensitivity. Insulin
response to a standardized meal was determined from an
index of insulin sensitivity and secretion through frequent
blood sampling following ingestion of a LMMT (Carnation
Instant Breakfast prepared with whole milk). To perform
the LMMT, a flexible intravenous catheter was placed in
the antecubital space of the left arm. The “dose” for the
liquid meal test was obtained according to amount of lean
body mass (LBM) of the participant (1.75g CHO/kg LBM).
Participants were required to consume the meal within five
minutes. Blood was drawn at baseline (three samples over
15minutes) prior to initiation of meal consumption at time
“zero.” Subsequent blood samples were drawn every five
time 40 to 180minutes, and at 210 and 240minutes. Using
the obtained measures, the insulin sensitivity index (SI) was
calculated by oral glucose model .
2.6. Assay of Metabolites. Glucose was measured in 12μL
sera with the glucose oxidase method using a SIRRUS
analyzer (interassay CV 2.56%). Insulin was analyzed using
a TOSOH 1800 Automated Immunoassay Analyzer. Assay
interassay CV is 6.0%. Triglycerides (TGs) were assessed with
the glyceryl phosphate method. HDL was analyzed using
a two-reagent system involving stabilization of low-density
lipoprotein cholesterol (LDL), very low-density lipoprotein
cholesterol (VLDL), and chylomicrons using cyclodextrin
and dextrin sulfate, and subsequent enzymatic-colorimetric
detection of HDL. 25OHD and PTH concentration was
obtained from fasting sera drawn and assayed in the UAB
Core Laboratory with liquid chromatography/tandem mass
spectrometry technique and a two-site radiometric assay,
2.7. Statistical Analysis. Differences at baseline in descrip-
tive characteristics between girls in the two diet groups
were examined using t-tests. The differences between diet
groups regarding metabolic parameters were evaluated using
ANOVA to allow for inclusion of covariates (pubertal stage,
fat mass index, and baseline measures). Multivariate linear
regression (Model A) was used to analyze the contribution
of the change in 25OHD concentration over five weeks
to individual components of metabolic syndrome. Due to
the intricate relationship with PTH, for each component
that was observed to be associated with 25OHD, a second
regression model (Model B) was analyzed with inclusion of
PTH as a covariate. To conform to the assumptions of linear
regression, all statistical models were evaluated for residual
normality and logarithmic transformations were performed
Table 1: Baseline descriptive characteristics.
(n = 28)
12.4 ± 0.3
4.4 ± 0.2
159.5 ± 1.5
89.6 ± 4.6
98.0 ± 0.3
46.1 ± 1.4
38.6 ± 2.4
43.9 ± 1.0
46.0 ± 2.2
(n = 15)
12.5 ± 0.4
4.4 ± 0.3
159.3 ± 2.0
93.8 ± 7.5
98.1 ± 0.3
48.1 ± 1.7
41.1 ± 3.6
47.4 ± 3.4
(n = 13)
12.4 ± 0.5
4.4 ± 0.3
160.3 ± 2.3
85.1 ± 4.8
97.9 ± 0.5
43.9 ± 2.3
35.2 ± 2.7
44.2 ± 2.3
Trunk fat (%)
Total fat (kg)
Percent fat (%)
Total lean (kg)
Energy intake (kcal/d)
∗Indicate significant difference between diet groups (P < 0.05).
STAN: standard diet (55% calories from carbohydrate).
SPEC: specialized diet (43% calories from carbohydrate).
Table 2: Circulating 25OHD levels at baseline and five weeks in the
presence or absence of MetSyn.
∗Indicates significant difference between baseline and five weeks (P < 0.05).
Abbreviations: standard error (SE).
when appropriate. All data were analyzed using SAS 9.2
software. Subsequently, models were evaluated by presence
or absence of MetSyn. MetSyn was defined as meeting the
IDF criteria for at least three of the components and was
coded as zero for absence and one for presence. In addition,
interaction terms were created (diet by change in 25OHD)
and included in regression models to test the moderation
by diet and change in 25OHD of relationships between
Descriptive characteristics and body composition at baseline
in the total sample and by diet group are presented in
Table 1. There were no differences between groups across
variables, with the exception of percent body fat, which was
significantly higher in the STAN diet group versus the SPEC
diet group. At baseline, 29% of participants met the criteria
for MetSyn, and individual components are illustrated at
baseline and five weeks in Figure 1. Differences between diet
groups were observed at baseline for circulating 25OHD and
all lipid parameters [TG, LDL, HDL, and total cholesterol
(tot chol)], and at five weeks for circulating 25OHD and TG.
Diet group evaluations related to MetSyn components
are illustrated in Figure 2. Among those consuming the
STAN diet, significant differences were observed from base-
line to five weeks for circulating 25OHD (P < 0.05) and
all lipid parameters (P < 0.001), except HDL. A significant
Trunk fat (%)
Trunk fat (%)
Figure 1: Components of metabolic syndrome at baseline and five weeks.∗Indicates significant difference between diet groups (P < 0.5).
Abbreviations: circulating vitamin D (25OHD), triglycerides (TGs), cholesterol (Chol), high-density lipoprotein (HDL), low-density
lipoprotein (LDL), fasting glucose (Glu), insulin sensitivity (SI), and insulin (Ins).
Trunk fat (%)
STAN five weeks
Trunk fat (%)
SPEC five weeks
Figure 2: Diet group evaluations related to MetSyn components.∗Indicates significant differences between baseline and five weeks (P <
0.05). Abbreviations: circulating vitamin D (25OHD), triglycerides (TGs), cholesterol (Chol), high-density lipoprotein (HDL), low-density
lipoprotein (LDL), fasting glucose (Glu), insulin sensitivity (SI), and insulin (Ins).
increase was revealed for circulating 25OHD and TG with
a decrease in total chol and LDL across the five-week
period. Among those consuming the SPEC diet, a significant
increase in circulating 25OHD and insulin (P
and P < 0.001, resp.) from baseline to five weeks was
distinguished. Although an increase in circulating 25OHD
was observed for both diet groups, circulating 25OHD levels
versus those with no MetSyn (Table 2). Similarly, greater
PTH concentrations were observed in those presenting with
MetSyn than those without MetSyn at both baseline and
five weeks (P < 0.001). Further, individuals meeting criteria
for MetSyn displayed no increase in circulating 25OHD
The contribution of change in circulating 25OHD
(ΔOHD) over the five weeks to MetSyn components is
presented in Table 3. Two models were used to assess
Table 3: The contribution of ΔOHD over the five weeks to MetSyn components represented by two models. Model A illustrates the
independent contribution of ΔOHD to metabolic parameters and Model B presents the inclusion of both ΔOHD and PTH as independent
REG Model A
Trunk fat (kg)
REG Model B
∗Indicates significant difference (P < 0.05).
aValues represent beta coefficient and standard error.
Abbreviations: insulin sensitivity (SI), low-density lipoprotein (LDL), high-density lipoprotein (HDL), parathyroid hormone (PTH), and change in 25OHD
−0.06 ± 0.43
−0.04 ± 0.06
−1.53 ± 0.60∗
−0.33 ± 0.38
0.67 ± 0.44
0.18 ± 0.12
0.68 ± 0.36
−0.03 ± 0.07
0.11 ± 0.37
−2.33 ± 1.01∗
0.66 ± 0.26∗
0.99 ± 2.54
−0.47 ± 0.89
4.71 ± 3.46
0.35 ± 0.35
−2.31 ± 1.04∗
0.66 ± 0.22∗
1.10 ± 2.62
4.62 ± 3.62
0.29 ± 0.07∗
0.00 ± 0.01
−0.13 ± 0.15
−0.27 ± 0.07∗
−0.14 ± 0.26
−0.11 ± 0.05∗
0.31 ± 0.55
−0.20 ± 0.85
the relationship. Model A illustrates the independent con-
tribution of ΔOHD to metabolic parameters, and Model B
presents the inclusion of both ΔOHD and PTH as indepen-
dent variables. Among those consuming the STAN diet, an
inverse relationship between ΔOHD and LDL (P < 0.05) was
observed (Model A); in Model B, the association remained
significant (P < 0.05). However, in this model a marginal
association between ΔOHD and fasting glucose (P = 0.07)
was observed as well as an independent contribution of PTH
to fasting glucose concentration (P < 0.001). Additionally,
a significant positive association between PTH and TG
(P < 0.01) was observed. Among those consuming the
SPEC diet, ΔOHD (Model A) was inversely associated with
fasting glucose (P < 0.05) and positively associated with SI
(P < 0.05); in Model B, these relationships remained, and
an inverse relationship between PTH and SI was observed,
whereas there was no relationship between PTH and fasting
At five weeks, 32% of participants met the criteria
for MetSyn. There was no difference in those meeting
criteria between diet groups; however, when the interaction
term (ΔOHD × diet) was evaluated, those individuals who
presented with MetSyn at five weeks displayed significantly
positive associations between the interaction term and TG
(P < 0.001), HDL (P < 0.01), LDL (P < 0.01), and
systolic blood pressure (SysBP; P < 0.01). SI and insulin were
inversely associated with the interaction term (P < 0.01) in
those individuals who did not present with MetSyn at five
weeks. After five weeks, there was an increase in circulating
25OHD among those without MetSyn, yet no change was
observed in those with MetSyn (Figure 3). Further, 25OHD
concentration among those with MetSyn was at a level that
would be deemed insufficient based on currently accepted
Figure 3: Circulating 25OHD levels at baseline and five weeks in
the presence or absence of MetSyn.
Vitamin D’s emerging role as an integral component of
metabolism is accompanied by the occurrence of risk
factors for metabolic disease early in life and displays a
critical conduit to which dietary intervention may facilitate
improved metabolic outcomes. The objective of this study
was to determine the effect of macronutrient modifications
in the absence of weight loss on vitamin D status and
if ΔOHD concentration would influence components of
MetSyn in AA adolescent females. For those consuming a
reduced carbohydrate diet, ΔOHD was inversely associated
with fasting glucose and positively associated with SI. These
relationships were maintained with inclusion of PTH. Clus-
tering of metabolic parameters occurred such that glucose-
related parameters in those without MetSyn, and lipid-
related components in those with MetSyn were significantly
associated with an interaction of diet and ΔOHD. These
D may exert on alterations in the biological response to
macronutrients lending itself to further exploration.
Numerous studies in children have suggested metabolic
effects of 25OHD on several markers of glucose (e.g., fasting
glucose, insulin concentrations, and HOMA score) [16–19]
and lipid metabolism (e.g., TG, HDL, and LDL) [18, 19].
In this sample, the interaction term (diet and ΔOHD) was
positively associated with lipid profile among those meeting
the criteria for MetSyn. Similarly, an independent effect of
vitamin D on lipid profile was suggested by a weight-loss
intervention study that found vitamin D supplementation
resulted in improved lipid profile in the supplementation
. Additionally, Al-Daghri and colleagues observed an
association between total cholesterol and LDL and 25OHD
which was apparent among adults with Type 2 Diabetes,
but not in those without. Further, there was a reversal of
MetSyn manifestations with vitamin D status correction
. From a physiologic standpoint, metabolic response to
diet and potential relation with vitamin D status is an area
in need of further exploration. The differential impact of the
interaction between macronutrient composition and ΔOHD
is of particular interest in light of the lack of consensus
regarding optimal 25OHD concentration as it relates to
vitamin D recommendations.
It has been suggested that a reduction in carbohydrate
intake requires increased insulin resistance to maintain
glucose homeostasis, particularly during reproductive devel-
opment . Among the SPEC diet group, glucose concen-
tration increased to a greater extent in those with a lesser
increase in 25OHD, respectively insulin sensitivity decreased
to a greater extent in those with a lesser increase in 25OHD.
It is plausible that vitamin D mediates the effect of reduced
carbohydrate intake through its direct action on pancreatic
β-cell function . Conversely, in the STAN diet group,
in which carbohydrate intake reflected that which is more
typical of the adolescent population , manifestations
of altered 25OHD concentration were apparent in lipid
parameters. LDL concentration increased to a greater extent
in those with a lesser increase in 25OHD. Although cross-
of 25OHD concentration on LDL, vitamin D’s function
in lipid metabolism remains uncertain. The confluence of
macronutrient composition adds further complexity. The
relationship observed in this study is clear, and our findings
suggest that effect of dietary composition on 25OHD
bioavailability warrant consideration.
complicated by its reciprocal association with PTH; in addi-
tion, several of the proposed predictors of MetSyn are also
known to be associated with PTH. Not surprisingly, in those
meeting criteria, as opposed to those not meeting the criteria
for MetSyn, PTH concentrations were significantly greater
at both baseline and five weeks of this study. Many [25–
27], but not all , studies report an inverse relationship
between 25OHD and PTH. Moreover, AA generally present
with lower 25OHD concentrations and higher PTH relative
to European American counterparts [16, 26, 29, 30]. The
relationship between vitamin D and PTH is influenced by
various factors during growth and development, including
dietary macronutrient composition, supported by findings
reported herein. Independent of the positive association
with vitamin D, an inverse relationship was found between
PTH and SI, only apparent in those consuming the reduced
carbohydrate, specialized diet. This may be translated into
independent pathways of both PTH and vitamin D in
linkage with MetSyn. It has been recently reported that PTH
concentration, but not 25OHD, contributed to MetSyn in
obese adults . Support is provided for the postulation
that influence by each of these factors diverges according to
This study had many strengths as well as evident limi-
tations. Comprehensive phenotyping using robust measures
of body composition is a major strength. The provision of
food to each participant is an additional advantage because
it ensured some degree of dietary control. Despite these
strengths, it is important to evaluate certain shortcomings
of this investigation. In noninstitutionalized subjects, dietary
adherence is difficult to ascertain; beyond monitoring for
weight change, the consumption of additional foods other
than those provided cannot be certain. Also, the modest
sample size and inclusion of only one racial group limits
generalizability to other populations. Each participant was
in the >99% BMI percentile, which may limit the ability to
detect changes in outcome measures across body habitus.
Finally, it is important to note that the short duration of
the intervention may limit ability to identify the long-term
effects of the diet on vitamin D.
Initiation and progression to MetSyn encompasses pertur-
bations in glucose and lipid metabolism and is exacerbated
by overweight/obesity, with AA females experiencing dis-
proportionate incidence. Similar to what has been reported
in other studies [7, 30–32], 29% of girls in this study
presented with MetSyn and 25OHD was observed to be
significantly lower and deemed insufficient in those pre-
senting with MetSyn. Additionally, our results support the
effect of macronutrient composition on the contribution of
circulating 25OHD to parameters associated with MetSyn.
Our findings also indicate that improvement in circulating
25OHD concentrations may normalize glucose parameters
associated with initiation and progression to MetSyn. Addi-
tionally, though the mechanistic response of PTH to diet
is unclear, its reciprocal relationship with vitamin D may
mediate the effects of a reduced carbohydrate diet. This
investigation builds upon previous findings which imply
unique metabolic characteristics of peripubertal AA females.
In this context and considering the consistent reports of
vitamin D insufficiency among this group, our findings may
help inform recommendation efforts.
The authors report no conflict of interest.
This research was supported by R00DK083333 (K. Casazza);
CA-47888 (L. J. Hanks); P30 DK056336 UAB Nutrition
Obesity Research Center; UAB Diabetes Research Center
Human Physiology Core P60DK079626, Thrasher Research
 T. D. Thacher and B. L. Clarke, “Vitamin D insufficiency,”
Mayo Clinic Proceedings, vol. 86, no. 1, pp. 50–60, 2011.
 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.
 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.
 J. P. Reis, D. von M¨ uhlen, E. R. Miller III, E. D. Michos, and L.
the United States adolescent population,” Pediatrics, vol. 124,
no. 3, pp. e371–e379, 2009.
 J. Hjelmesæth, D. Hofsø, 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,
 L. S. Harkness and B. A. Cromer, “Vitamin D deficiency in
adolescent females,” Journal of Adolescent Health, vol. 37, no.
1, p. 75, 2005.
 K. Rajakumar, J. D. Fernstrom, M. F. Holick, J. E. Janosky, and
in obese vs. Non-obese African American children,” Obesity,
vol. 16, no. 1, pp. 90–95, 2008.
 P. Zhou, C. Schechter, Z. Cai, and M. Markowitz, “Deter-
minants 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.
 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.
 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.
 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.
 K. Casazza, M. Cardel, A. Dulin-Keita et al., “Reduced car-
bohydrate 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.
 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.
 E. Breda, M. K. Cavaghan, G. Toffolo, K. S. Polonsky, and C.
β-cell function and insulin sensitivity,” Diabetes, vol. 50, no. 1,
pp. 150–158, 2001.
 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.
 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.
 R. Alemzadeh, J. Kichler, G. Babar, and M. Calhoun, “Hypovi-
taminosis D in obese children and adolescents: relationship
with adiposity, insulin sensitivity, ethnicity, and season,”
Metabolism, vol. 57, no. 2, pp. 183–191, 2008.
 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.
 E. Rodr´ ıguez-Rodr´ ıguez, R. M. Ortega, L. G. Gonz´ alez-
Rodr´ ıguez, and A. M. L´ opez-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.
 G. C. Major, F. Alarie, J. Dor´ e, 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.
 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.
 J. C. Brand-Miller, H. J. Griffin, and S. Colagiuri, “The
vol. 2012, Article ID 258624, 9 pages, 2012.
 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,
 Y. Pan and C. A. Pratt, “Metabolic syndrome and its associa-
tion with diet and physical activity in US adolescents,” Journal
of the American Dietetic Association, vol. 108, no. 2, pp. 276–
 R. Kumar and J. R. Thompson,“The regulation ofparathyroid
hormone secretion and synthesis,” Journal of the American
Society of Nephrology, vol. 22, no. 2, pp. 216–224, 2011.
Gundberg, and T. O. Carpenter, “Relationships among vita-
min D levels, parathyroid hormone, and calcium absorption
in young adolescents,” Journal of Clinical Endocrinology and
Metabolism, vol. 90, no. 10, pp. 5576–5581, 2005.
 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.
 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.
 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.
 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–
 M. Rodr´ ıguez-Mor´ an, B. Salazar-V´ azquez, 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.
 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,