Original Study

Association Between Polycystic Ovarian Syndrome, Overweight, and

Metabolic Syndrome in Adolescents
Haleh Rahmanpour MD 1,*, Leila Jamal MD 2, Seyed Nouraddin Mousavinasab PhD 1,
Abdolreza Esmailzadeh PhD 1, Kamran Azarkhish MD 1
1
Zanjan Metabolic Research Center, Zanjan University of Medical Sciences, Zanjan, Iran
2
Student of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran

a b s t r a c t
Purpose: Polycystic syndrome (PCOS) is associated with multiple metabolic abnormalities. Studies in the adolescent population are still
limited and the results have been much different. The aim of this study was to investigate the association between PCOS, overweight, and
metabolic syndrome in adolescents.
Methods: 30 PCOS adolescents were randomly selected from a PCOS population with NIH 1990 criteria and 71 adolescents from the normal
adolescents. Anthropometric, hormonal and metabolic parameters were evaluated in four sub-groups including obese and non-obese PCOS
and obese and non-obese normal adolescents.
Results: The prevalence of overweight and metabolic syndrome in adolescents with PCOS was 52% and 33.3% respectively vs 22.4%
(P 5 0.005) and 11.26% in control (normal) adolescents (P 5 0.0001). Among all subjects, including obese and non-obese adolescents with
or without PCOS, the prevalence of insulin resistance, hypercholesterolemia, central obesity, and metabolic syndrome was higher in obese
PCOS with 61.5%, 46.2%, 53.8%, and 69.2%, respectively.
Conclusions: Obesity and IR are important risk factors for metabolic syndrome in PCOS. Considering the long-term health risks, it is
necessary to identify metabolic disorders in adolescents with PCOS as early as possible.
Key Words: Metabolic abnormalities, Polycystic ovary syndrome, Adolescents

Introduction However, PCOS status could not be accurately ascertained

Polycystic ovary syndrome (PCOS) is a heterogeneous
endocrine disorder that affects 6e8% of women world-
wide.1 PCOS is associated with metabolic abnormalities,
such as dyslipidemia, obesity, and glucose intolerance,
which are also components of the metabolic syndrome
(MS).2 The prevalence of MS in adult premenopausal
women with PCOS is approximately 40%.3 There is
a growing appreciation that adolescents are at increasing
risk for type 2 diabetes mellitus and MS since the preva-
lence of obesity is increasing in this population.4e6 Data of
12- to 19-year-old adolescents included in the National
Health and Nutrition Examination Survey from 1999 to
2002 (NHANES 99-02) demonstrated that the prevalence of
the metabolic syndrome in all teens varied from 2.0% to 9.4%
of teens in the United States, depending on the denition
used. In obese teens, these prevalence rates varied from
12.4% to 44.2%.3
Since adolescents with PCOS are insulin resistant as are
their adult counterparts, they would be predicted to be at
increased risk for the MS as well.7,8 In one study using
a national database, adolescents with PCOS were found to
be at increased risk for MS in comparison with controls.9
The authors indicate no conicts of interest.
* Address correspondence to: Haleh Rahmanpour, MD, Zanjan Metabolic Research
Center, Vliasre Hospital, Sheikh Fazlollah blvd, Zanjan, Iran; phone: 98 241
7270814; Fax:98 241 7270815; Mobile:98 9122429371
E-mail address: haleh509@gmail.com (H. Rahmanpour).
1083-3188/$ - see front matter 2012 North American Society for Pediatric and Adolescent Gynecology. Published by Elsevier Inc.
doi:10.1016/j.jpag.2012.02.004
in the control subjects, MS prevalence in an adolescent
PCOS cohort was found to be at least 3-fold greater than
normal adolescents when adjusted for body mass index
(BMI).10 There is intriguing evidence that this increased risk
may be conferred not only by IR but also by hyper-
androgenemia, which is a risk factor for MS independent of
obesity and insulin resistance.11,12
In our rst study for evaluating the prevalence of PCOS in
adolescents in an Iranian population, the ndings showed
lower rate of PCOS and obesity among this group (2.9% and
8% respectively).13 Although the prevalence of PCOS in that
study was the same as the other studies in Iranian adoles-
cents,14,15 the prevalence of PCOS in Iranian women is
greater and similar to worldwide reports (i.e., 7.1e14%).16
The aim of this study was to investigate the association
between PCOS, overweight and metabolic syndrome in
adolescents of Zanjan, Iran.
Methods
In the previous study in 2009,13 50 (2.9%) PCOSs were
diagnosed among 1882 high school adolescents (14e18
years old) of Zanjan city.13 NIH 1990 criteria was used for
diagnosis and just by clinical criteria including: oligo- and/
or anovulation (i.e. #8 menstrual periods in a year or
menstrual cycles more than 35 days in length) and clinical
hyperandrogenism (i.e. hirsutism with modied Ferriman-
Gallwey scores $ 8 with or without acne). Then this
 H. Rahmanpour et al. / J Pediatr Adolesc Gynecol 25 (2012) 208e212
group was evaluated by one endocrinologist and after
ruling out other etiologies (e.g., congenital adrenal hyper-
plasia, androgen-secreting tumors, and Cushing syndrome),
they were enrolled in the PCOS group.
In the present study, six months after the rst study, all
the PCOS group members were invited to participate, i.e.,
from which 40 of them referred to us. In addition, we
randomly selected 80 adolescents from the normal
adolescents of the previous study (total of 120 adolescents).
In the new study, all the population was reevaluated con-
rming the previous diagnosis; all of the normal adoles-
cents had regular menses (an average length of the cycles
between 22 and 41 days; none or a single cycle with
a length of !22 to O41 days during the past year) without
hirsutism.
All the girls were at least 1 year post menarche at the
time of evaluation. The exclusion criteria were hypothy-
roidism, hyperprolactinemia, use of any medications known
to affect sex hormone, glucose or lipid metabolism for at
least a month and oral contraceptives for 3 months before
entering of the study. Taking these measures, 10 and 9
participants were excluded from the PCOS group and
normal group respectively. Based on the previous survey,
obesity was dened by BMI $85th percentile.13 Then the
study participants were divided into four sub-groups
including obese and non-obese PCOS and obese and non-
obese normal adolescent.
The study protocol was approved by the Institutional
Review Board of the Zanjan University of Medical Sciences.
Written informed consent was obtained from all partici-
pants and/or their parent or legal care-taker before their
participation in the study.
Study Protocols
All subjects who were enrolled in the study had a medical
history and underwent physical examination, including
height, weight waist and hip circumference, blood pressure,
modied Ferriman-Gallwey scores, and acne scores. All
measurements were done by observers trained with the
same standard protocols (allowing for comparison with
other studies)17,18; waist circumference was measured
midway between the lowest rib and the iliac crest with the
subject standing at the end of gentle expiration, and hip
circumference at the greater trochanters. Weight was
measured in kilograms and height was measured to the
nearest 0.5 cm. BMI was calculated. Blood pressure was
measured twice with mercury sphygmomanometer with
subjects seating quietly for at least 5 minutes; the readings
were averaged as the nal value. Ferriman-Gallwey scores
were assessed by at least two observers.
Since our study group consisted of virginal girls, we
could not perform trans-vaginal ultrasound. So trans-
abdominal ultrasound examination was obtained to eval-
uate the ovaries using a Toshiba Sonolayer SSA-220A
(Toshiba, Tokyo, Japan) with a mechanical 6-MHz probe.
Adolescents with regularly menstruation were scanned in
the early follicular phase (cycle days 3e5), while those with
oligomenorrhea or amenorrhea were scanned between
days 3 and 5 of spontaneous or progestin-induced
209
withdrawal bleeding. The polycystic-appearing ovary (PAO)
was dened according to the presence of increased ovarian
size and/or at least 12 follicular cysts measuring 2 to 9 mm.
After a 10-hour overnight fast, blood samples were taken
from adolescents between the rst and fth day of the
menstrual period/withdrawal bleeding in order to measure
prolactin (PRL), luteinizing hormone (LH), follicle-stimulating
hormone (FSH), free testosterone (FT), dehydroepian-
drosterone sulfate (DHEAS), 17-hydroxyprogesterone (17-
OHP), thyroid stimulating hormone (TSH), and lipid prole.
The cutoff values for abnormal serum lipid levels were
based on the National Cholesterol Education Program
Pediatric Panel Report.19 Hypertriglyceridemia, hypercho-
lesterolemia, low levels of high-density lipoprotein (HDL-
C), and high levels of low-density lipoprotein (LDL-C) were
dened by serum concentrations of triglycerides $150 mg/
dL, total cholesterol $170 mg/dL, HDL-C #35 mg/dL, and
LDL-C $110 mg/dL. The homeostasis model analysis insulin
resistance (HOMA-IR 5 fasting glucose mmol/L  fasting
insulin mIU/mL/22.5) index was used for estimating insulin
action. Cutoff value of 16 mIU/mL was used for hyper-
insulinemia based on a study in an independent cohort of
748 children and adolescents.20 MS was dened by Inter-
national Diabetes Federation criteria for MS in children and
adolescents,21,22 if they had central obesity (waist circum-
ference $ 80 cm) plus two or more of the following four
factors: (1) increased concentration of triglyceride (TG) $
150 mg/dL; (2) reduced concentration of HDL-C ! 35 mg/
dL); (3) raised blood pressure: systolic pressure $ 130 mm
Hg or diastolic pressure $ 85 mm Hg or treatment of
previously diagnosed hypertension; and (4) increased
fasting glucose level $ 100 mg/dL.
Assays
The serum levels of FSH, LH, PRL, TSH, and insulin
(Monobind, Lake Forest, CA) in serum were measured by
enzyme-linked immunosorbent assay (ELISA) (Stat Fax
2100, Awareness Technologies, Los Angeles, CA). Serum FT,
DHEAS, 17-OHP, and androstenedione were measured using
an ELISA and commercial kits (IBL, Hamburg). Serum
glucose, HDL cholesterol, total cholesterol, and TG were
measured using an enzymatic calorimetric method with an
autoanalyzer (Mindray BS-Clinical Chemistry Analyzer,
Guangzhou Shihai Medical Equipment Co, Guangdong,
China).
Statistical Analysis
All data were analyzed using SPSS version 16.0 (SPSS Inc.,
Chicago, IL). The normality of the distribution of all
continuous variables were assessed using the Kolmogorov-
Smirnov test. Continuous variables were presented as mean
and standard deviation. Means between groups were
compared with the t test and medians between them were
compared with the Mann-Whitney U test. The Pearson
chi-square test was used to analyze the differences between
the groups and obtain an odds ratio. Statistical signicance
was set at P ! 0.05.
210 H. Rahmanpour et al. / J Pediatr Adolesc Gynecol 25 (2012) 208e212

Results Table 2
Metabolic Characteristic of PCOS and Control Adolescents

The participants of this study, i.e., 30 adolescents in PCOS PCOS Normal P value
group and 71 adolescents in the normal group, were adolescent adolescent
(n 5 30) (n 5 71)
comparable in age (17.73  1.01 vs 17.69  1.29, respectively).
Waist circumference (cm) 74.3  7.26 70.31  7.91 0.02*
However, PCOS adolescents had greater BMI (P 5 0.007) and Systolic blood pressure (mm Hg) 108.17  12.06 103.1  12.22 0.059
greater level of FT (P 5 0.001). Table 1 shows the demo- Diastolic blood pressure (mm Hg) 76.67  11.24 70.83  11.43 0.02*
graphic and hormonal features of adolescents with or Fasting HDL (mg/dl) 35.53  12.54 35.38  4.32 0.94
Fasting triglyceride (mg/dl) 108.23  59.88 98.55  40.87 0.045**
without PCOS. Majority of the PCOS adolescents had Fasting cholesterol (mg/dl) 154.43  26.42 142.58  25.53 0.037**
polycystic-appearing ovaries on pelvic sonography in FBS (mg/dl) 96.6  12.32 94.39  8.21 0.565
comparison to those without PCOS (63.3% vs 7%; P 5 0.0001). Fasting insulin (mIU/liter) 10.42  6.45 8.93  5.65 0.222
HOMA - IR 2.56  1.9 2.13  1.5 0.25
Adolescents with PCOS displayed signicantly greater MS 10 (33.3%) 8 (11.26%) 0.038***
waist circumference, TG, and cholesterol levels, but there
Data are presented as mean  standard deviation or as percent, and number
were no signicant differences in fasting glucose, HOMA-IR, * t test
and HDL levels between the PCOS and the control groups. ** Mann-Whitney U test
The prevalence of MS in PCOS group was greater than the *** Chi-square test

normal group (33.3% vs 11.26% respectively; P 5 0.038). See

Table 2.
The metabolic parameters between the four sub-groups as high as 50% in a study of severely obese adolescents. Both
of this study, including obese and non-obese PCOS and BMI and waist circumference have been shown to be
obese and non-obese normal adolescents are demonstrated predictive of metabolic cardiovascular risk factors in chil-
in Table 3. There were no signicant differences between dren and adolescents.24
the non-obese adolescents either with or without PCOS Visceral adiposity is associated with IR, the primary
regarding metabolic parameters. Based on Table 3, it can be pathophysiological mechanism thought to be responsible
concluded that the frequency of impaired MS parameters for the metabolic disturbances of MS.25e27 During the past
such as hypercholesterolemia, hypertriglyceridemia, and decades, the increasing prevalence of MS in children and
raised BP were signicantly more in obese adolescents with adolescents has coincided with the rise in obesity, just as in
PCOS. adults.28 Based on the current studies, the prevalence of
The prevalence of MS in obese adolescents with PCOS obesity in PCOS is currently about 70%, 20% greater than 15
was greater than the adolescents without PCOS (69.2 vs 10.2 years ago.29 In 1999e2000, the prevalence of overweight
OR 19.8, 95% CI: 4.6e84.6) and also non-obese adolescents was 14.8% among a representative sample of American
with PCOS (69.2% vs 5.8 % OR 36, 95% CI: 3.4e373.1). females aged 2e19 years old, and in 2003e2004 the prev-
alence was 16.4%.30
Discussion
In our rst study, the prevalence of PCOS and obesity in
adolescents were 2.9% and 8% respectively, which were
In our study the prevalence of MS in PCOS group was lower than the other studies' populations. In this study, the
33.3%, almost two-fold greater than the normal adolescents NIH 1990 criteria were used for diagnosis of PCOS. It should
and 69.2% in obese PCOS, i.e. six-fold greater than the be mentioned that specialized criteria for the diagnosis of
normal group. PCOS group had greater BMI and FT level PCOS in adolescents have not been accepted to date so
which are two important risk factors for MS and cardio- instead the diagnostic criteria for adults are used in most
vascular disease in future. The prevalence of MS increased clinical practices.
with BMI in the NHANES III population with both the Cook
and the de Ferranti criteria23 and has been estimated to be
Table 3
Prevalence of Various Metabolic Abnormalities in Obese and Non-Obese
Table 1 Adolescents with and without PCOS
Endocrine Characteristic of PCOS and Control Adolescents
Non- Obese Non-obese Obese P value
PCOS adolescent Normal adolescent P value obese PCOS control control
(n 5 30) (n 5 71) PCOS N 5 13 adolescent adolescent
N 5 17 n (%) (N 5 59) (N 5 12)
Age (yr) 17.73  1.01 17.69  1.29 0.87
n (%) n (%) n (%)
BMI (kg/m2) 23.4  3.09 21.06  2.85 0.007*
BMI O85% percentile 13 (43.30%) 12 (16.90%) 0.005*** IFG 2 (11.8) 8 (61.5) 16 (27.1) 3 (25) 0.025
Weight (kg) 59.05  7.92 54.18  8.08 0.006* IR 4 (23.5) 8 (61.5) 12 (20.3) 4 (33.3) 0.025
Height (cm) 158.9  5.32 158.13  5.03 0.49 HIN 0 7 (53.8) 3 (5.1) 1 (8.3) 0.03
FreeT (ng/dl) 1.81  1.33 1.07  0.72 0.001** Hypercholesterolemia 4 (23.5) 6 (46.2) 8 (13.5) 2 (16.7) 0.061
DHEAS (ng/dl) 2.51  1.26 2.25  1.33 0.061** Hypertriglyceridemia 1 (5.8) 5 (38.5) 6 (10.1) 2 (16.7) 0.041
FSH IU/L 5.86  1.86 6.53  2.27 0.152 Low HDL 15 (88.2) 12 (92.3) 56 (94.9) 11 (91.7) 0.80
LH IU/L 9.03  6.4 5.79  6.73 0.545 Central obese 1 (5.9) 7 (53.8) 2 (3.4) 8 (66.7) 0.0001
PAO 19 (63.3%) 5 (7%) 0.0001*** Raised BP 1 (5.9) 5 (38.5) 6 (10.2) 1 (8.3) 0.03
MS 1 (5.8) 9 (69.2) 6 (10.2) 1 (8.3) 0.0001*
Abbreviation: PAO, polycystic-appearing ovaries
Data are presented as mean  standard deviation or percent (%), and number Abbreviations: IFG, impaired fasting glycemia; HIN, hyperinsulinemia; IR, insulin
* t test resistance; MS, metabolic syndrome
** Mann-Whitney U test Data are presented as % or number
*** Chi-square test * Chi-square test, in comparison of the obese-PCOS with three others
 H. Rahmanpour et al. / J Pediatr Adolesc Gynecol 25 (2012) 208e212
At present, the 2003 Rotterdam criteria are more widely
accepted than the NIH criteria, but the former tends to
expand rather than replace the latter because all women
diagnosed by the NIH 1990 criteria would also meet the
Rotterdam criteria. The risk of metabolic disturbances may
vary among different phenotypes of PCOS based on the
Rotterdam criteria.26 In other studies, adults with PCOS,
dened by NIH criteria had more severe metabolic abnor-
malities than those dened by Rotterdam criteria. The
difference in prevalence of obesity and androgen excess
may attribute to the characteristic.31e34
In our present study, obesity and PCOS alone were
attributed to lower risk of MS and the PCOS group with
normal weight had lower prevalence of IR. In previous
studies obese PCOS adolescents have been shown to have
an increased prevalence of glucose intolerance and IR.
According to Diamanti-Kandarakis, hyperandrogenemia
should be considered as the primary abnormality in PCOS.
So IR and hyperinsulinemia are superimposed upon the
pre-existing ovarian dysfunction.11 This suggests an inter-
action between hyperandrogenemia and obesity in the
expression of the metabolic phenotype in PCOS.
In comparison of the PCOS group with or without over-
weight, hyperandrogenemia has also been reported to be an
independent risk factor for MS in premenopausal women
without PCOS33 and has been associated with hyper-
insulinemia, fasting hyperglycemia, and MS in post-
menopausal women as well.35 However, data on metabolic
disturbances in adolescents with PCOS are limited and the
results seem to vary in studies of different populations.
In a study in South China, the prevalence of insulin
resistance, dyslipidemia, and MS in PCOS adolescents with
BMI O 85th percentile was 74.4%, 39.5%, and 14% vs 32.9%,
14.1%, and 0%.36 In comparison in PCOS subjects with BMI !
85th percentile, the prevalence of MS in young Korean
women with PCOS was 14.5%, nearly 3.5 times greater than
in age-matched women in Korean urban population (4.3%).
The most frequently occurring component of MS was low
HDL cholesterol (45%), and the least frequent was high
fasting serum glucose level (0.9%).37
In a Turkish study, the insulin resistance ratio in obese
adolescent with PCOS was 93.3% vs 46.6% in lean PCOS and
50% in obese controls.38 Also in another Turkish study, Vural
et al39 found greater frequency of MS and increased carotid
artery intima-media thickness in early adulthood in PCOS
patients. In their study the prevalence of MS according to
WHO guidelines in adolescents with PCOS was 11.6% vs 0 in
normal adolescents. Both in our study and in Vural et al,39
the polycystic ovarian appearance on ultrasound and in
normal adolescents was 7% and 9% respectively, which is
lower than expected.
There were several limitations with this study. First,
since the prevalence of PCOS was low in the previous study,
this resulted in a low sample size in our four sub-groups and
it made the interpretation of the results difcult. So it is
suggested that future studies be conducted with larger
sample sizes. Second, it would have been even better if we
had used HPL-MS instead of ELISA with commercial kit for
evaluating free testosterone.
211
Conclusions
The most frequently occurring components of MS in
obese PCOS group were impaired fasting glycemia and
insulin resistance (61.5%), central obesity (53.8%), and
hypercholesterolemia (46.2%), respectively.
Our data demonstrated that PCOS and obesity are two
separate risk factors for MS in adolescence that together can
have augmented effects. Interventions for weight loss such
as diet, exercise, novel interventions with insulin sensi-
tizers, and anti-androgens may reduce the risk of devel-
oping diabetes and cardiovascular disease in the PCOS
adolescents in the future. However, a question still remains
regarding which factor is more prevalent: overweight or
PCOS? This suggests the need for a much larger prospective
study.
Obesity and IR are important risk factors for MS in PCOS
adolescents. Considering the long-term health risks, it is
necessary to identify metabolic disorders in adolescents
with PCOS as early as possible.
Acknowledgments
This study was a part of Leila Jamal's thesis supported by
Metabolic Research Center of Zanjan University of Medical
Sciences (Grant No. 2010B031600058). The authors would
like to sincerely thank Seyed Muhammed Hussein Mousa-
vinasab for editing this text.
References
1. Azziz R, Woods KS, Reyna R, et al: The prevalence and features of the polycystic
ovary syndrome in an unselected population. J Clin Endocrinol Metab 2004; 89:
2745
2. Essah PA, Wickham EP, Nestler JE: The metabolic syndrome in polycystic ovary
syndrome. Clin Obstet Gynecol 2007; 50:205
3. Cook S, Auinger P, Li C, et al: Metabolic syndrome rates in United States
adolescents, from the National Health and Nutrition Examination Survey,
1999-2002. J Pediatr 2008; 152:165
4. Weiss R, Dziura J, Burgert TS, et al: Obesity and the metabolic syndrome in
children and adolescents. N Engl J Med 2004; 350:2362
5. Palmert MR, Gordon CM, Kartashov AI, et al: Screening for abnormal glucose
tolerance in adolescents with polycystic ovary syndrome. J Clin Endocrinol
Metab 2002; 87:1017
6. Sinha R, Fisch G, Teague B, et al: Prevalence of impaired glucose tolerance
among children and adolescents with marked obesity. N Engl J Med 2002;
346:802
7. Onat A, Ceyhan K, Basar O, et al: Metabolic syndrome: major impact on
coronary risk in a population with low cholesterol levels - a prospective and
cross-sectional evaluation. Atherosclerosis 2002; 165:285
8. Palmert MR, Gordon CM, Kartashov AI, et al: Screening for abnormal glucose
tolerance in adolescents with polycystic ovary syndrome. J Clin Endocrinol
Metab 2002; 87:1017
9. Talbott E, Guzick D, Clerici A, et al: Coronary heart disease risk factors in
women with polycystic ovary syndrome. Arterioscler Thromb Vasc Biol 1995;
15:821
10. Cook S, Weitzman M, Auinger P, et al: Prevalence of a metabolic syndrome
phenotype in adolescents: ndings from the third National Health and
Nutrition Examination Survey, 1988-1994. Arch Pediatr Adolesc Med 2003;
157:821
11. Diamanti-Kandarakis E: PCOS in adolescents. Best Pract Res Clin Obstet
Gynaecol 2010; 24:173
12. Coviello AD, Legro RS, Dunaif A: Adolescent girls with polycystic ovary
syndrome have an increased risk of the metabolic syndrome associated with
increasing androgen levels independent of obesity and insulin resistance. J
Clin Endocrinol Metab 2006; 91:492
13. Rahmanpour H, Heidari R, Mousavinasab SN, et al: Prevalence of polycystic
ovarian syndrome in 14-18 year old girls of Zanjan High Schools, 2008. J
ZUMS Health Serv 2008; 17:79
14. Hashemipour M, Faghihimani S, Zolfaghary B, et al: Prevalence of polycystic
ovary syndrome in girls aged 14-18 years in Isfahan, Iran. Horm Res 2004;
62:278
212 H. Rahmanpour et al. / J Pediatr Adolesc Gynecol 25 (2012) 208e212
15. Salehpour S, Esmaeilnia Shirvani H: Entezari A: Evaluation of the prevalence of
polycystic ovarian syndrome among adolescent (15-18 years old) girls in Tehran
during 2005-2006. Int J Fertil Steril 2010; 4:122
16. Tehrani FR, Simbar M, Tohidi M, et al: The prevalence of polycystic ovary
syndrome in a community sample of Iranian population: Iranian PCOS
prevalence study. Reprod Biol Endocrinol 2011; 9:39
17. van Hooff MH, Voorhorst FJ, Kaptein MB, et al: Endocrine features of polycystic
ovary syndrome in a random population sample of 14-16 year old adolescents.
Hum Reprod 1999; 14:2223
18. Korhonen S, Hippela inen M, Niskanen L, et al: Relationship of the metabolic
syndrome and obesity to polycystic ovary syndrome: a controlled,
population-based study. Am J Obstet Gynecol 2001; 184:289
19. National Cholesterol Education Panel: Report of the Expert Panel on Blood
Cholesterol Levels in Children and Adolescents. NIH Publication 91-2732.
Bethesda (MD), National Institutes of Health, 1991
20. Rodrguez-Mora n M, Guerrero-Romero F: Hyperinsulinemia in healthy children
and adolescents with a positive family history for type 2 diabetes. Pediatrics
2006; 118:e1516
21. Alberti KG, Zimmet P, Shaw J; IDF Epidemiology Task Force Consensus Group:
The metabolic syndromeea new worldwide denition. Lancet 2005; 366:1059
22. Zimmet P, Alberti G, Kaufman F, et al: The metabolic syndrome in children and
adolescents. Lancet 2007; 369:2059
23. de Ferranti SD, Gauvreau K, Ludwig DS, et al: Prevalence of the metabolic
syndrome in American adolescents: ndings from the Third National Health
and Nutrition Examination Survey. Circulation 2004; 110:2494
24. Katzmarzyk PT, Srinivasan SR, Chen W, et al: Body mass index, waist
circumference, and clustering of cardiovascular disease risk factors in
a biracial sample of children and adolescents. Pediatrics 2004; 114:e198
25. Ford ES, Giles WH, Dietz WH: Prevalence of the metabolic syndrome among US
adults: ndings from the third National Health and Nutrition Examination
Survey. JAMA 2002; 287:356
26. Reaven GM, Lithell H, Landsberg L: Hypertension and associated metabolic
abnormalitiesethe role of insulin resistance and the sympathoadrenal
system. N Engl J Med 1996; 334:374
27. Grundy SM: Hypertriglyceridemia, insulin resistance, and the metabolic
syndrome. Am J Cardiol 1999; 83:25F
28. Hedley AA, Ogden CL, Johnson CL, et al: Prevalence of overweight and
obesity among US children, adolescents, and adults, 1999-2002. JAMA
2004; 291:2847
29. Yildiz BO, Knochenhauer ES, Azziz R: Impact of obesity on the risk for polycystic
ovary syndrome. J Clin Endocrinol Metab 2008; 93:162
30. Ogden CL, Carroll MD, Curtin LR, et al: Prevalence of overweight and obesity in
the united states, 1999e2004. JAMA 2006; 295:1549
31. Fruzzetti F, Perini D, Lazzarini V, et al: Adolescent girls with polycystic ovary
syndrome showing different phenotypes have a different metabolic prole
associated with increasing androgen levels. Fertil Steril 2009; 92:626
n
32. Iba ~ ez L, Valls C, Ferrer A, et al: Additive effects of insulin-sensitizing and
anti-androgen treatment in young, nonobese women with hyperinsulinism,
hyperandrogenism, dyslipidemia, and anovulation. J Clin Endocrinol Metab
2002; 87:2870
33. Korhonen S, Hippela inen M, Vanhala M, et al: The androgenic sex hormone
prole is an essential feature of metabolic syndrome in premenopausal
women: a controlled community-based study. Fertil Steril 2003; 79:1327
34. Dieudonne MN, Pecquery R, Boumediene A, et al: Androgen receptors in human
preadipocytes and adipocytes: regional specicities and regulation by sex
steroids. Am J Physiol 1998; 274(6 Pt 1):C1645
35. Golden SH, Ding J, Szklo M, Schmidt MI, et al: Glucose and insulin components
of the metabolic syndrome are associated with hyperandrogenism in
postmenopausal women: the atherosclerosis risk in communities study. Am J
Epidemiol 2004; 160:540
36. Huang J, Ni R, Chen X, et al: Metabolic abnormalities in adolescents with
polycystic ovary syndrome in south China. Reprod Biol Endocrinol 2010;
8:142
37. Park HR, Choi Y, Lee JH, et al: The metabolic syndrome in young Korean women
with polycystic ovary syndrome. Diabetes Res Clin Pract 2007; 77(Suppl 1):
S243
38. Ozgen IT, Aydin M, Guven A, et al: Characteristics of polycystic ovarian
syndrome and relationship with ghrelin in adolescents. J Pediatr Adolesc
Gynecol 2010; 23:285
39. Vural B, Caliskan E, Turkoz E, et al: Evaluation of metabolic syndrome frequency
and premature carotid atherosclerosis in young women with polycystic ovary
syndrome. Hum Reprod 2005; 20:2409