DOI: 10.1177/1942602X15575355
For reprints and permission queries visit SAGE’s Web site,
2  NASN School Nurse | Month 2015
metabolic syndrome, and polycystic
ovary syndrome (PCOS). In an individual
without insul...
Month 2015  |  NASN School Nurse  3
thus far, no consensus exists, as youth
develop insulin resistance normally
during pub...
4  NASN School Nurse | Month 2015
cross the line to indicate the
midaxillary line of the body.
Standing on the SP’s right ...
Month 2015  |  NASN School Nurse  5
and waist circumference monitored at
each visit (Legro et al., 2013).
Difficulties ass...
6  NASN School Nurse | Month 2015
Recognizing that there is a problem and
acting upon it are two separate issues
when appr...
Month 2015  |  NASN School Nurse  7
Pressure in Children and Adolescents.
(2004). The fourth report on the diagnosis,
of 7

NASN School Nurse-2015-Platt-1942602X15575355(1)

Published on: Mar 3, 2016

Transcripts - NASN School Nurse-2015-Platt-1942602X15575355(1)

  • 1. DOI: 10.1177/1942602X15575355 For reprints and permission queries visit SAGE’s Web site, © 2015 The Author(s) Month 2015  |  NASN School Nurse  1 Healthy Lifestyles School nurses are well aware of the childhood obesity epidemic in the United States, as one in three youth are overweight or obese. Co-morbidities found in overweight or obese adults were not commonly found in youth three decades ago but are now increasingly “normal” as the obesity epidemic continues to evolve. This article is the second of six related articles discussing the co-morbidities of childhood obesity and discusses the complex association between obesity and insulin resistance, metabolic syndrome, and polycystic ovary syndrome. Insulin resistance increases up to 50% during puberty, which may help to explain why youth are more likely to develop co- morbidities as teens. Treatment of these disorders is focused on changing lifestyle habits, as a child cannot change his or her pubertal progression, ethnicity, or family history. School nurses and other personnel can assist youth with insulin resistance, metabolic syndrome, and polycystic ovary syndrome by supporting their efforts to make changes, reinforcing that insulin resistance is not necessarily type 2 diabetes even if the child is taking medication, and intervening with negative peer pressure. Keywords: insulin resistance; metabolic syndrome; PCOS; childhood obesity O besity continues to be a major health risk in youth, with 16.9% of the 2- to 19-year-old population in the United States meeting the criteria with a body mass index (BMI) greater than or equal to the 95th percentile when plotted on the 2000 Centers for Disease Control and Prevention (CDC) growth charts (Ogden, Carroll, Kit, & Flegal, 2012). Childhood and adolescent overweight and obesity combined have increased substantially in developed countries since 1980, with males increasing from 16.9% to 23.8%, and females increasing from 16.2% to 22.6% (Ng et al., 2014). Youth at highest risk for development of overweight- or obesity-related co-morbidities need to be identified promptly by their primary care providers (PCPs). It has been reported that a child with impaired glucose metabolism will progress to type 2 diabetes in 2.5 years, which is a much faster pace than an adult (Weiss et al., 2005). Subsequently, an overweight/obese child with a personal history of rapid weight gain or BMI ≥ the 85th percentile when plotted on the CDC growth charts should be counseled and referred to a weight management program or a pediatric registered dietitian, if available. These resources need to be identified in the local community. According to the American Diabetes Association (2014), asymptomatic youth with a BMI ≥ the 85th percentile in addition to two other risk factors (family history of type 2 diabetes, high risk race/ethnicity, clinical signs of insulin resistance, or a maternal history of gestational diabetes) should be screened for diabetes at age 10 years or at the onset of puberty. These youth should then be rescreened every 3 years. Any child with a BMI ≥ the 85th percentile with symptoms of diabetes should be further evaluated. Insulin Resistance Insulin resistance is an early risk factor for the development of several disorders that in the past occurred in adulthood and were associated with excess weight. It is a foundation that enhances the development of impaired glucose metabolism including type 2 diabetes, 575355NASXXX10.1177/1942602X15575355NASN School NurseNASN School Nurse research-article2015 Insulin Resistance, Metabolic Syndrome, and Polycystic Ovary Syndrome in Obese Youth Adrienne M. Platt, PhD, RN, CPNP at UNIV OF KANSAS MEDICAL CENTER on June 9, 2015nas.sagepub.comDownloaded from
  • 2. 2  NASN School Nurse | Month 2015 metabolic syndrome, and polycystic ovary syndrome (PCOS). In an individual without insulin resistance, “elevated glucose levels stimulate pancreatic β cells to secrete insulin and decrease glucagon production and increased glucose uptake by the muscle, liver, and adipose tissue” (Lann & LeRoith, 2007, p. 1063). Insulin resistance is caused by β cell dysfunction, which in turn leads to an insufficient first phase insulin response to glucose load (food intake). Subsequently, a postprandial hyperglycemia develops. The β cells compensate with an exaggerated second phase insulin response causing hyperinsulinemia (Gallagher, LeRoith, & Karnieli, 2011; Lann & LeRoith, 2007). Chronic high levels of insulin (hyperinsulinemia) will down-regulate insulin receptors and impair insulin sensitivity (insulin resistance), which can lead to β cell death and eventually type 2 diabetes (Lann & LeRoith, 2007). Youth are predisposed to development of insulin resistance due to excess adipose tissue, lack of physical activity, poor diet choices, genetics, and ethnicity (Santoro & Weiss, 2012). Also, as youth progress through puberty, there is a reported 25% to 50% increase in insulin resistance, which predisposes these adolescents to an even higher risk for development of impaired glucose metabolism and other alterations in health (Cree-Green, Triolo, & Nadeau, 2013; Hannon, Janosky, & Arslanian, 2006; Reinehr, Wolters, Knop, Lass, & Holl, 2015). The most noticeable clinical sign of insulin resistance is acanthosis nigricans, which is a hyperpigmentation and thickening of the skin usually first noted around the neck of an obese individual. It is also common on the skin covering the joints of the hands, in skin folds (creases of the nose, and navel area), and in the axilla (Guran, Turan, Akcay, & Bereket, 2008). Acanthosis nigricans is most noticeable in youth with a darker skin tone. It is difficult to appreciate on Caucasian youth but is usually noticeable in the axilla and on the joints of the hands if looking closely. Acanthosis can also be associated with skin tags when it is more severe. Acanthosis nigricans has been reported as a predictor of insulin resistance in obese youth (Guran et al., 2008). Another hallmark of insulin resistance is rapid weight gain, hence the rationale for early identification and referral as mentioned earlier in this article. A possible explanation may be related to parental report of “constant hunger.” If a child senses hunger more frequently than normal, he or she is more likely to eat more often. Energy balance and subsequent body weight is controlled by the central nervous system (Faulconbridge & Hayes, 2011). Satiation is caused by gastric distention and extensive satiation signals (gut-peptides) to the brain, which in turn cause the brainstem to release inhibitory signals that the stomach is full (Faulconbridge & Hayes, 2011). Leptin is a hormone (adipokine) derived from adipose tissue and is one of the hormones regulating food intake based on energy expenditure. However, in an individual with excess adipose tissue, a chronically higher leptin level at the receptor sites can cause the brain to incorrectly interpret the satiation signals (Faulconbridge & Hayes, 2011). In addition to the leptin dysfunction, the insulin signaling is ineffective in overweight and obese individuals, and the cells of the body are not able to efficiently utilize the excessive amounts of circulating glucose. A “vicious cycle develops” (Faulconbridge & Hayes, 2011, p. 738) and these children or their parents report constant hunger or a lack of satiation. “If you had eaten your dinner then you wouldn’t be hungry now” is commonly reported by parents. However, these parents may also report that the child is eating excessive portion sizes. Ghrelin is the only known peptide hormone to stimulate increased food intake and is released in the stomach and small intestine. Ghrelin is released before meals and declines rapidly after food consumption (Faulconbridge & Hayes, 2011). “Ghrelin may function by blocking the action of the anorexic hormone leptin” (Sondike, 2009, p. 277). Studies are being conducted on antagonists to ghrelin as a treatment for obesity by decreasing hunger, but none have proved to be successful thus far (Faulconbridge & Hayes, 2011; Solomou & Korbonits, 2014). In an environment with readily available high caloric foods in conjunction with less physical activity than in the past, the insulin and leptin signaling is diminished, leading to insulin resistance (Faulconbridge & Hayes, 2011). In a recent study evaluating insulin sensitivity in obese youth, it was reported that the 2-hour serum glucose results after glucose challenge was a reflection of a gradual decline in β cell function as the result approached impairment (Giannini et al., 2012). The process of developing obesity is not this straightforward and includes many other signaling pathways not discussed in this article. In summary, insulin resistance is a result of hormonal changes in response to an energy surplus, which leads to excess adipose tissue. In overweight or obese youth, it is related to a combination of lifestyle habits, ethnicity, pubertal changes, and family history. It is extremely important that healthy lifestyle habits are stressed by the primary care provider, by school personnel, and at home, as the other risk factors cannot be changed. Metabolic Syndrome The prevalence of metabolic syndrome in youth was described in 2003 (Cook, Weitzman, Auinger, Nguyen, & Dietz) after an examination of data from the National Health and Nutrition Examination Survey (NHANES) from 1988 to 1994. Adult criteria for metabolic syndrome were adapted for youth using a combination of guidelines from several organizations (American Diabetes Association, 2000; National Cholesterol Education Panel, 1991; National High Blood Pressure Education Program Working Group on Hypertension Control in Children and Adolescents, 1996). Metabolic syndrome in children and adolescents as defined by Cook et al. (2003) is when three out of five criteria are met: (see Table 1). There have been multiple attempts to define metabolic syndrome in youth and, at UNIV OF KANSAS MEDICAL CENTER on June 9, 2015nas.sagepub.comDownloaded from
  • 3. Month 2015  |  NASN School Nurse  3 thus far, no consensus exists, as youth develop insulin resistance normally during puberty, cholesterol levels can vary by age, sex, and ethnicity, and there are no standardized measures of central obesity (Weiss, Bremer, & Lustig, 2013). However, when youth meet adult criteria, it is obvious that they meet the criteria as youth for a diagnosis of metabolic syndrome. It has been reported that the principle cause of metabolic syndrome seems to be excess weight. The prevalence of metabolic syndrome was reported at 28.7% in overweight youth when compared to 0.1% in normal weight youth after examination of NHANES III data (Cook et al., 2003; Herouvi, Karanasios, Karayianni, & Karavanaki, 2013). In a more recent study of obese Italian youth (N = 1,080), the prevalence of metabolic syndrome was reported at 29.2% of the sample (Santoro et al., 2013). It was recently reported that metabolic syndrome was more frequently diagnosed in obese youth with acanthosis nigricans and a family history of type 2 diabetes and was even more likely when these youth had an elevated waist-to-hip ratio (Santoro et al., 2013). The Bogalusa Heart Study was initially funded in 1972 as a longitudinal study examining cardiovascular risk factors in youth that could predict heart disease in adulthood (Berenson, 2001). Bogalusa, Louisiana, is a rural community in the southeastern United States. The data were part of a longitudinal study and have been examined on multiple occasions. In one study published in 2012 examining the data from the Bogalusa Heart Study, it was reported that the adults with the worst cardiometabolic profiles had been overweight/obese youth with abnormal metabolic profiles (Li, Chen, Srinivasan, Xu, & Berenson, 2012). Dyslipidemia is defined as a low HDL-C of ≤ 40 mg/dL and an elevated fasting triglyceride level ≥ 110 mg/dL. In practice, a majority of youth do not present in a fasting state for their appointment. If asked to come in for laboratory testing at a later time, frequently the testing is not completed. Consequently, laboratory testing is done either fasting or as a random draw (non-fasting) as long as it is noted as such in the patient note for accurate test result interpretation. If the triglyceride level is mildly elevated when randomly drawn, it is interpreted with less vigilance than a fasting sample. If the triglyceride level reported is significantly high, the parents are notified to bring the child back for a fasting lipid profile or to bring the child fasting to the next clinic appointment. The HDL-C is not affected by fasting status. Visceral fat has been associated with metabolic syndrome in youth with subsequent cardiovascular disease developing in adulthood (Bassali, Waller, Gower, Allison, & Davis, 2010; D’Adamo, Santoro, & Caprio, 2011). Waist circumference has been lauded as the best method to measure visceral fat (D’Adamo et al., 2011) and has been referred to as an easy measurement to obtain. According to the CDC (2004), To define the level at which the waist or abdominal circumference is measured, you must first locate and mark a bony landmark, the lateral border of the ilium. Have the study participant (SP) stand and hold the examination gown above the waist. Lower the pants and underclothing of the SP slightly, and standing behind and to the right of the SP, palpate the hip area to locate the right ilium. . . . Draw a horizontal line just above the uppermost lateral border of the right ilium and then Table 1.  Criteria for Metabolic Syndrome in Adults and Adolescents Criterion Adults Adolescents High triglyceride level ≥ 150 mg/dL ≥ 110 mg/dL Low HDL-C level  Males < 40 mg/dL ≤ 40 mg/dL  Females < 50 mg/dL ≤ 40 mg/dL Abdominal obesity  Males > 102 cm ≥ 90th %  Females > 88 cm ≥ 90th % High fasting glucose level ≥ 110 mg/dL ≥ 110 mg/dL High blood pressure ≥ 130/85 mm Hg ≥ 90th % mm Hg Source: Adapted from Cook, Weitzman, Auinger, Nguyen, and Dietz (2003), p. 822. Copyright 2003 by the American Medical Association. Note: HDL-C = high density lipoprotein cholesterol. at UNIV OF KANSAS MEDICAL CENTER on June 9, 2015nas.sagepub.comDownloaded from
  • 4. 4  NASN School Nurse | Month 2015 cross the line to indicate the midaxillary line of the body. Standing on the SP’s right side, place the measuring tape around the trunk in a horizontal plane at the level marked on the right side of the trunk. Hold the zeroend below the measurement value. Use the mirror on the wall to ensure correct horizontal alignment of the measuring tape. (pp. 3-29) Obtaining a waist circumference is not as simple as it would seem on an obese child. In practice, each child needs to be provided some level of modesty, especially as obese youth are likely to be more self-conscious of their size. The size of the abdominal pannus can also create difficulties with measurement, as it makes it difficult to decide where to measure. However, in 2004, waist circumference tables were created using NHANES III data to represent a national sample of African American, European American, and Mexican American youth (Fernandez, Redden, Pietrobelli, & Allison, 2004). An elevated fasting serum glucose • ≥ 110 mg/dL is also one of the criteria for metabolic syndrome in youth (Cook et al., 2003). However, the most recent guidelines by the American Diabetes Association define impaired fasting glucose as a serum glucose drawn after an 8-hour fast from 100 to 125 mg/dL (American Diabetes Association, 2014). Impaired glucose tolerance is defined as a 2-hour glucose result ≥ 140 mg/dL to 199 mg/dL after a 75 g glucose challenge (American Diabetes Association, 2014). The criteria for a diagnosis of type 2 diabetes is a fasting glucose of ≥ 126 mg/ dL (repeated to confirm the diagnosis), a 2-hour glucose response after a 75 g glucose challenge of ≥ 200 mg/dL, or an HbA1c ≥ 6.5%. However, as the oral glucose tolerance test is the “gold standard,” any child with a borderline elevated fasting serum glucose or HbA1c should be scheduled for a 2-hour oral glucose tolerance test to confirm the diagnosis (American Diabetes Association, 2014; Copeland et al., 2013). Hypertension is another criterion used to diagnose metabolic syndrome. However, a child should not be identified as hypertensive by using a single measurement. The definition of hypertension in children is an average systolic blood pressure and/or diastolic blood pressure greater than or equal to the 95th percentile based on gender, age, and height on at least three different occasions (National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents, 2004). Care should be used to select a proper sized cuff for the size of the child’s upper arm. Optimally, a manual mercury sphygmomanometer cuff should be used due to the arm shape of overweight and obese youth. In addition, any child having his or her blood pressure measured should be sitting quietly for 5 minutes, seated with both feet on the floor, and the arm used for the blood pressure measurement should be supported (National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents, 2004). In practice, if an elevated blood pressure is documented, the blood pressure measurement could be repeated after the visit when the child is less likely to be nervous. Providers may request blood pressure measurement at school by the nurse for up to 2 weeks. Once completed, a copy can be faxed to the provider to compare to their office results. If a child is hypertensive, depending upon the experience of the provider, the child could be treated in the primary care office. Otherwise, the hypertensive child should be referred to a pediatric nephrologist. The hypertension tables based on gender, age, and height can be obtained from the National Institutes of Health website ( pocket.pdf). In summary, metabolic syndrome is a cluster of overweight- or obesity-related co-morbidities that have increased in prevalence along with the childhood obesity epidemic. As the majority of youth meeting criteria for metabolic syndrome are overweight or obese, the treatment of choice is to make lifestyle habit changes. One of the easiest changes to make is to avoid the sweetened beverages (soda, sports drinks, flavored milk, sweet tea, and punch). One 12-ounce can of soda a day can add a significant amount of weight over the time span of a year (approximately 17 pounds). Also, increasing exercise by walking can have an impact on weight. The earlier a child is identified and referred, the more likely they will be to succeed at adopting healthier lifestyle habits. Polycystic Ovary Syndrome Polycystic ovary syndrome consists of a set of criteria including hyperandrogenism (clinical or biochemical), ovulatory dysfunction, and polycystic ovaries (Anderson, Solorzano, & McCartney, 2014; Cirik & Dilbaz, 2014). “Polycystic ovary syndrome (PCOS) is the most common endocrinopathy affecting women of reproductive age and is increasingly recognized as a disorder manifesting in the peripubertal and adolescent period” (Hardy & Norman, 2013, p. 751). It was first described in the literature in 1935 by Stein and Leventhal but is now recognized as a disorder that can affect females throughout their lives (Sirmans & Pate, 2013). There are several diagnostic criteria that can be used to diagnose PCOS, which leads to further debate related to identification of who actually has the syndrome. The prevalence of the disorder is dependent upon which criteria are used for diagnosis and has been reported as high as 15% to 20% of women of childbearing age (Sirmans & Pate, 2013). Polycystic ovary syndrome is a condition associated with insulin resistance and metabolic syndrome (Smith, Rosen, & Cedars, 2009). Youth with PCOS are at a higher risk for development of co-morbidities associated with obesity such as impaired glucose metabolism and cardiovascular disease (Legro et al., 2013). Women with PCOS exhibiting central adiposity are at higher risk for development of metabolic syndrome (Cirik & Dilbaz, 2014). All adolescents diagnosed with PCOS should have a BMI at UNIV OF KANSAS MEDICAL CENTER on June 9, 2015nas.sagepub.comDownloaded from
  • 5. Month 2015  |  NASN School Nurse  5 and waist circumference monitored at each visit (Legro et al., 2013). Difficulties associated with diagnosing adolescents with PCOS are that many of the symptoms overlap with normal puberty and can lead to under- or overdiagnosis (Hardy & Norman, 2013). An adolescent presenting with hyperandrogenism should cause suspicion for PCOS (Legro et al., 2013). Symptoms that could be associated with PCOS in adolescents are irregular menstrual cycles, hirsutism (dark thick hair follicles growing on the side of the face, under the chin, on the neck, chest, or back, or around the nipples of the breasts), acne, acanthosis nigricans, and often weight problems (Meriggiola & Zamah, 2013). Typical post-menarche cycles in adolescents can be irregular for several years, which confounds a diagnosis of PCOS in adolescents (Rackow, 2012). The typical number of days between menstrual cycles post-menarche is 28 days with a range from 24 to 35 days (Hardy & Norman, 2013). Days between cycles are measured from the first day of a menstrual cycle to the first day of the next menstrual cycle. Oligomenorrhea is defined as infrequent cycles more than 6 weeks apart. Primary amenorrhea is the absence of menarche by 15 years of age in a female. Secondary amenorrhea is defined as the lack of any menstruation over the preceding 3 months in a post-menarchal female (Paradise, 2014). Diagnosis of PCOS using the Rotterdam Criteria includes exhibiting two of the following criteria in addition to exclusion of other possible disorders (Azziz et al., 2006): •• oligomenorrhea or anovulation •• clinical or biochemical signs of hyperandrogenism •• polycystic ovaries Ultrasound to evaluate ovaries for cysts reveals the best results when done trans-vaginally or trans-rectally, which can be traumatic and inappropriate in a virginal adolescent female (Hardy & Norman, 2013; Williams, Ong, & Dunger, 2013). A trans-abdominal ultrasound on an obese adolescent female can be challenging due to the excess abdominal fat (Williams et al., 2013). Polycystic ovaries have been found in healthy adolescent females without menstrual irregularities, and conversely, adolescent females with menstrual irregularities have not been found to have cystic ovaries on ultrasound (Hardy & Norman, 2013). According to the latest Endocrine Society Guidelines, ultrasound is not recommended to diagnose PCOS if two of the three criteria are already met for diagnosis (Legro et al., 2013). Laboratory evaluation for PCOS in an adolescent (if overweight or obese) includes a basic metabolic panel, HbA1c, lipid profile, and liver function testing, which are the same laboratory tests ordered on an overweight or obese child with possible insulin resistance. Thyroid studies are ordered (thyrotropin stimulating hormone and free thyroxine level [TSH and Free T4]), as hypothyroidism can cause menstrual irregularities. Adrenal hormones are ordered (dehydroepiandrosterone sulfate, androstenedione, and total and free testosterone) to evaluate for adrenal mass and nonclassical congenital adrenal hyperplasia (Smith et al., 2009). Elevated testosterone levels are common in adolescents with PCOS. An elevated 17-hydroxyprogesterone (17-0HP) is specific to nonclassical congenital adrenal hyperplasia and should be ordered. A prolactin level is ordered to evaluate for a prolactinoma. Gonadotropin levels are ordered (luteinizing hormone, follicule stimulating hormone) with an estradiol level to evaluate ovarian function. As with any type of menstrual irregularities in adolescents, a serum pregnancy test should be ordered. If any of these laboratory test results are abnormal, the adolescent should be referred to pediatric endocrinology or adolescent gynecology for further testing and management (Flannery et al., 2013; Rahmanpour, Jamal, Mousavinasab, Esmailzadeh, & Azarkhish, 2012). Treatment of PCOS in adolescents is still controversial. A study was recently conducted to examine treatment regimens for PCOS in adolescents, and the authors reported that treatment was based on specialty (endocrinology or gynecology) clinic attended (Auble, Elder, Gross, & Hillman, 2013). According to the latest Endocrine Society Clinical Practice Guidelines, the initial treatment for adolescents with suspected PCOS with the primary goals to treat acne, hirsutism, or menstrual irregularities or to prevent pregnancy are hormonal contraceptives (Legro et al., 2013). If the adolescent is overweight or obese, lifestyle habit changes are always recommended first to promote weight loss (Legro et al., 2013). Metformin is advised for those with impaired glucose metabolism or metabolic syndrome (Legro et al., 2013). If the adolescent is pre-menarchal with advanced pubertal development (at least Tanner IV), hormone contraceptives are recommended (Legro et al., 2013). However, pregnancy must always be at the forefront of differential diagnosis due to the population of youth and their predisposition for high risk behaviors. Education related to the possibility of pregnancy and PCOS must be reinforced along with safe sex guidelines. Youth with hair growth on the face are frequently ridiculed and laser hair treatment is not always an option due to expense and potential scarring with dark skin color. Antiandrogens can be added to treatment if there is little improvement after 6 months of therapy as outlined above (Sirmans & Pate, 2013). In summary, youth with excess weight are at a higher risk for development of co-morbidities associated with overweight or obesity. Insulin resistance increases in puberty, which places an overweight or obese child at an even higher risk for development of type 2 diabetes or cardiovascular disease in adulthood (Cree-Green et al., 2013; Hannon et al., 2006; Reinehr et al., 2015). The best method of addressing these co-morbidities is to direct efforts toward changing lifestyle habits not only at home but in the community. A recent review of weight management programs reported variability in the success of these programs (Haemer et al., 2014). at UNIV OF KANSAS MEDICAL CENTER on June 9, 2015nas.sagepub.comDownloaded from
  • 6. 6  NASN School Nurse | Month 2015 Recognizing that there is a problem and acting upon it are two separate issues when approaching families of overweight or obese youth. A majority of the time, the parents are also overweight or obese and seldom are willing to change their habits. Frequently, the parent wants to blame a “hormone imbalance” for the child’s rapid weight gain instead of the daily sweet drinks or lack of activity. School nurses are ideally situated to assist in the early identification of youth at risk and try to intervene early by providing education to the child and the family about healthy habits before excess weight becomes a problem, with all of its associated co-morbidities. ■ References American Diabetes Association. (2000). Type 2 diabetes in children and adolescents. Diabetes Care, 23(3), 381-389. American Diabetes Association. (2014). Standards of medical care in diabetes—2014. Diabetes Care, 37(Suppl. 1), S14-S80. doi:10.2337/dc14-S014 Anderson, A. D., Solorzano, C. M., & McCartney, C. R. (2014). Childhood obesity and its impact on the development of adolescent PCOS. Seminars in Reproductive Medicine, 32(3), 202-213. doi:10.1055/s-0034-1371092 Auble, B., Elder, D., Gross, A., & Hillman, J. B. (2013). Differences in the management of adolescents with polycystic ovary syndrome across pediatric specialties. Journal of Pediatric and Adolescent Gynecology, 26(4), 234-238. doi:10.1016/j.jpag.2013.03.007 Azziz, R., Carmina, E., Dewailly, D., Diamanti- Kandarakis, E., Escobar-Morreale, H. F., & Futterweit, W. . . . Androgen Excess Society. (2006). Positions statement: Criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: An Androgen Excess Society guideline. The Journal of Clinical Endocrinology and Metabolism, 91(11), 4237-4245. doi:10.1210/ jc.2006-0178 Bassali, R., Waller, J. L., Gower, B., Allison, J., & Davis, C. L. (2010). Utility of waist circumference percentile for risk evaluation in obese children. International Journal of Pediatric Obesity, 5(1), 97-101. doi:10.3109/17477160903111722 Berenson, G. S. (2001). Bogalusa Heart Study: A long-term community study of a rural biracial (black/white) population. The American Journal of the Medical Sciences, 322(5), 267-274. Centers for Disease Control and Prevention. (2004). National Health and Nutrition Examination Survey: Anthropometry procedures manual. Atlanta, GA: Centers for Disease Control and Prevention. Cirik, D. A., & Dilbaz, B. (2014). What do we know about metabolic syndrome in adolescents with PCOS? Journal of the Turkish German Gynecological Association, 15(1), 49-55. doi:10.5152/jtgga.2014.95776 Cook, S., Weitzman, M., Auinger, P., Nguyen, M., & Dietz, W. H. (2003). Prevalence of a metabolic syndrome phenotype in adolescents: Findings from the third National Health and Nutrition Examination Survey, 1988-1994. Archives of Pediatrics & Adolescent Medicine, 157(8), 821-827. doi:10.1001/ archpedi.157.8.821 Copeland, K. C., Silverstein, J., Moore, K. R., Prazar, G. E., Raymer, T., & Shiffman, R. N., . . . American Academy of Pediatrics. (2013). Management of newly diagnosed type 2 diabetes mellitus (T2DM) in children and adolescents. Pediatrics, 131(2), 364-382. doi:10.1542/peds.2012-3494 Cree-Green, M., Triolo, T. M., & Nadeau, K. J. (2013). Etiology of insulin resistance in youth with type 2 diabetes. Current Diabetes Reports, 13(1), 81-88. doi:10.1007/s11892-012- 0341-0 D’Adamo, E., Santoro, N., & Caprio, S. (2011). Metabolic syndrome in pediatrics: Old concepts revised, new concepts discussed. Pediatric Clinics of North America, 58(5), 1241-1255, xi. doi:10.1016/j.pcl.2011.07.005 Faulconbridge, L. F., & Hayes, M. R. (2011). Regulation of energy balance and body weight by the brain: A distributed system prone to disruption. The Psychiatric Clinics of North America, 34(4), 733-745. doi:10.1016/j. psc.2011.08.008 Fernandez, J. R., Redden, D. T., Pietrobelli, A., & Allison, D. B. (2004). Waist circumference percentiles in nationally representative samples of African-American, European- American, and Mexican-American children and adolescents. The Journal of Pediatrics, 145(4), 439-444. doi:10.1016/j. jpeds.2004.06.044 Flannery, C. A., Rackow, B., Cong, X., Duran, E., Selen, D. J., & Burgert, T. S. (2013). Polycystic ovary syndrome in adolescence: Impaired glucose tolerance occurs across the spectrum of BMI. Pediatric Diabetes, 14(1), 42-49. doi:10.1111/j.1399-5448.2012.00902.x Gallagher, E. J., LeRoith, D., & Karnieli, E. (2011). The metabolic syndrome—from insulin resistance to obesity and diabetes. The Medical Clinics of North America, 95(5), 855- 873. doi:10.1016/j.mcna.2011.06.001 Giannini, C., Weiss, R., Cali, A., Bonadonna, R., Santoro, N., Pierpont, B.,  . . . Caprio, S. (2012). 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