Abstract
Context: Changes in appetite-regulating peptides may impact food intake during puberty and facilitate the pubertal growth spurt. Peptide YY (PYY) is an anorexigenic hormone that is high in anorexia nervosa and low in obesity, inhibits GnRH secretion, and is suppressed by GH administration. The relationship between PYY and GH has not been examined across puberty.
Objectives: We hypothesized that PYY would be inversely associated with GH in adolescents and would be lowest when GH is highest.
Design and Setting: We conducted a cross-sectional study at a Clinical Research Center.
Subjects: We studied 87 children, 46 boys and 41 girls ages 9–17 yr at Tanner stages 1–5 of puberty (10th–90th percentiles for body mass index).
Outcome Measures: We measured fasting PYY and nadir GH levels after administration of an oral glucose load. Leptin levels were also measured.
Results: Fasting PYY was lowest and nadir GH highest in boys in Tanner stages 3–4 (P = 0.02) and in girls in Tanner stages 2–3 (P = 0.02). Leptin levels were highest in early pubertal boys and late pubertal girls. For the group as a whole and within genders, even after controlling for body mass index, log nadir GH correlated inversely with log PYY (P = 0.003, 0.07, and 0.02). PYY levels did not correlate with leptin levels.
Conclusions: During mid-puberty, at a time when GH levels are the highest, PYY is at a nadir, and these low PYY levels may facilitate pubertal progression and growth.
Data demonstrate that PYY levels change across puberty and are lowest when GH levels are the highest.
Puberty is characterized by many important physiological changes, which include gender-specific alterations in body composition and the pubertal growth spurt. These changes occur in conjunction with rising levels of GH. In addition, an increase in body mass index (BMI) and body fat precedes peak pubertal height velocity (1), and in animal models, body weight and food intake are important determinants of pubertal onset (2). Similarly, in humans, decreased food intake and associated low BMI are associated with failure to start or progress through puberty (3). Therefore, the impressive appetite of pubertal children may well be an adaptive mechanism that enables sufficient food intake and facilitates consequent increases in BMI and body fat necessary for pubertal onset, progression, and growth. Whereas many studies have examined changes in appetite-regulating hormones such as leptin (4) and more recently in ghrelin (5) through the stages of puberty, gut-derived hormones that negatively regulate food intake, such as peptide YY (PYY), have not been studied in a pubertal population.
PYY is an anorexigenic peptide produced in the colon that induces satiety and is secreted after food intake in proportion to caloric intake (6,7). Importantly, PYY levels are inversely related to BMI and body fat mass and are elevated in conditions of chronic starvation such as anorexia nervosa (8), a condition of decreased food intake associated with very low BMI and body fat where the body reverts to a prepubertal state as regards gonadal function. Consistent with this, central PYY injection inhibits LH secretion in male rats in vivo (9). In addition, PYY levels are decreased in obesity (6). Importantly, an animal study demonstrated that GH administration causes a marked decrease in PYY levels (10). These data raise the possibility that during puberty, an increase in GH concentrations should be associated with a decrease in PYY, thus facilitating food intake to ensure growth and pubertal maturation.
We therefore hypothesized that PYY levels would be inversely associated with GH concentrations in healthy adolescent boys and girls, and that levels would be lowest when GH concentrations and growth are the highest, therefore in early to mid puberty in girls and mid to late puberty in boys.
Subjects and Methods
Subject selection
We analyzed data from 87 children and adolescents 9–17 yr old to determine pubertal changes in PYY in relation to GH secretion, as well as predictors of PYY. GH dynamics for these subjects, as assessed by the oral glucose tolerance test, but not PYY levels, have been previously reported (11). BMIs for all subjects were between the 10th-90th percentiles for age. We analyzed data for 46 boys and 41 girls across the five Tanner stages (six boys and seven girls in Tanner stage 1, 12 boys and seven girls in Tanner stage 2, six boys and seven girls in Tanner stage 3, seven boys and five girls in Tanner stage 4, and 15 boys and 15 girls in Tanner stage 5). We used breast staging for girls and genital staging for boys to determine pubertal stage. Subjects were excluded if they had disorders that may affect glucose and GH metabolism such as thyroid dysfunction, hypercortisolism, diabetes mellitus, or renal failure, or if they were taking medications known to affect glucose and GH metabolism within 3 months of the study such as estrogen, GH, or thyroid supplements. Subjects were recruited from pediatric practices at Massachusetts General Hospital (MGH), MGH-affiliated health care centers, and community practices using mass mailing, fliers, and posters. The study was approved by the Institutional Review Board of MGH, and informed consent and assent were obtained from all parents and subjects.
Experimental protocol
After obtaining consent from the parents and assent from the subjects, a history and physical examination were performed along with height and weight measurements to determine eligibility. The physical examination included Tanner staging, which was performed by two pediatric endocrinologists trained for consistency in this measure. Eligible girls and boys were subsequently studied at a single outpatient visit to the Clinical Research Center. Postmenarchal girls were examined during the follicular phase of their menstrual cycles (d 1–10) to minimize cycle stage-specific fluctuations in GH (12). Fasting blood was drawn for glucose, insulin, and PYY, and nadir GH levels after an oral glucose load were used as an indicator of GH secretory status.
Suppression of GH after an oral glucose load is used as an indicator of GH status in conditions of GH excess, and we have previously demonstrated in adolescent girls (healthy and low weight) spanning the pubertal spectrum (n = 39) that GH nadir after an oral glucose load correlates very strongly with measures of GH secretion obtained from frequent sampling (13). Thus, subjects with higher GH secretion and concentration as assessed by frequent sampling had a higher nadir level during the OGTT. Additionally, we have previously demonstrated that highest GH levels occur in Tanner stages 2 and 3 in girls and in Tanner stages 4 and 5 in boys after an oral glucose load (11), consistent with data reported by other investigators using frequent sampling for GH (14,15). Thus, the nadir of GH after oral glucose administration appears to be a good indicator of states of GH excess, and because puberty is a time when maximal GH secretion occurs, we deemed this to be a good method for assessing GH secretory status in our subjects, without subjecting them to frequent blood sampling.
A solution of glucose (2.35 g/kg up to a maximum of 100 g) was administered orally over a maximum of 10 min after a 10- to 12-h fasting period. This dose per kilogram calculation was based on similar dose calculations for glucose tolerance tests for diabetes (where the dose per kilogram is 1.75 g/kg up to a maximum dose of 75 g), and the maximum dose of 100 g was based on dosing to assess GH suppression in adults (16,17). Of note, both a 75-g and a 100-g glucose load have been used to assess GH suppression after oral glucose administration; however, in this study, we chose the 100-g glucose load based on current practice in our unit at the time of the study. Blood samples were drawn at baseline and then 30, 60, 90, and 120 min after the glucose load for GH, glucose, and insulin. A bone age reading was used to supplement Tanner stage assessment as an indicator of pubertal maturity. Bone age was estimated from left hand and wrist x-rays using the standards of Greulich and Pyle (18) by a single pediatric endocrinologist trained for consistency in this measure.
Biochemical assays
Glucose was measured by the MGH laboratory using previously established methods (19). Insulin was measured by RIA (Linco Diagnostics, Inc., St. Charles, MO; intraassay coefficient of variation, 2.2–7.7%; detection limit, 2 μIU/ml). GH was measured using an immunoradiometric assay (Immulite 2000 Analyzer; Diagnostic Products Corp., Los Angeles, CA; detection limit, 0.01 ng/ml; intraassay coefficient of variation, 5.7%). Levels of GH may be converted to SI units (micrograms per liter) by multiplying by 1. Cluster analysis was used to determine area under curve (AUC) for GH and insulin as previously described (20). Total PYY was measured using ELISA (Millipore, Billerica, MA; intraassay coefficient of variation, 0.9–5.8%; sensitivity, 1.4 pg/ml). Leptin levels were measured by ELISA (Millipore, St. Charles, MO) with a lower limit of detection of 0.5 ng/ml and intraassay coefficient of variation ranging from 2.6–4.6%. Samples were stored at −80 C until analysis, and all samples were run in duplicate.
Statistical methods
Data are described as means ± sd. Version 5.01 of the JMP program (SAS Institute, Cary, NC) was used for statistical analysis. A Student t test was used to calculate differences between means when two groups were being compared. For data that did not have a normal distribution [PYY, GH nadir, GH AUC, insulin AUC, and homeostasis model of assessment for insulin resistance (HOMA-IR)], log or reciprocal transformations were used to approximate normality. The latter was necessary to approximate a normal distribution for PYY levels in boys. For three group comparisons, ANOVA was used to determine differences between groups followed by a Tukey-Kramer test to control for multiple comparisons. Correlational analysis (using Spearman's correlation) was used to determine predictors of PYY. We also performed multivariate analysis to control for BMI and pubertal stage in determining associations between PYY and covariates.
Girls were first compared with the boys. PYY levels were then compared within the two genders for different pubertal stages. Grouping by pubertal stage was based on expected timing of maximum growth and peak GH levels. In girls, maximum growth typically occurs at Tanner stages 2 to 3 (mean age, 11.5 yr), whereas in boys this occurs at Tanner stages 3 to 4 (mean age, 13.5 yr) (21). Whereas girls begin their growth spurt early in Tanner stage 2, growth velocity remains almost prepubertal until early Tanner stage 3 in boys. In addition, studies indicate that GH (as assessed by frequent sampling) peaks at Tanner stage 3 in girls (15), whereas highest GH levels have been reported in boys at Tanner stage 4 or a testicular volume of 10–15 ml in some studies (15,22) and between Tanner stages 3–5 in other studies (14). Our previous study using an oral glucose load indicated that nadir GH was highest in Tanner 2–3 girls and Tanner 3–4 boys (mean testicular volume, 12.2 ml) compared with the other two groups (11). Based on the timing of maximum growth and available data regarding GH secretion in puberty, girls were thus grouped as follows: prepubertal (Tanner 1), early-mid pubertal (Tanner 2–3), and mid-late pubertal (Tanner 4–5). Boys were grouped as follows: prepubertal and very early pubertal (Tanner 1–2), mid-late pubertal (Tanner 3–4), and late pubertal (Tanner 5).
Results
Gender-based comparisons
Boys and girls did not differ for baseline measures or PYY (Table 1). Insulin AUC and leptin were higher in girls than in boys.
Table 1.
PYY levels and baseline characteristics for all subjects
| Girls | Boys | P value | |
|---|---|---|---|
| n | 41 | 46 | |
| Chronological age (yr) | 13.2 ± 2.2 | 13.6 ± 2.3 | NS |
| Bone age (yr) | 13.1 ± 2.7 | 13.7 ± 2.8 | NS |
| Weight (kg) | 46.9 ± 12.6 | 50.3 ± 13.2 | NS |
| Height (cm) | 154.5 ± 11.4 | 160.0 ± 14.9 | 0.06 |
| BMI (kg/m2) | 19.3 ± 3.0 | 19.3 ± 2.3 | NS |
| BMI-SDS | 0.04 ± 0.77 | 0.06 ± 0.65 | NS |
| Tanner stage | 3.4 ± 1.5 | 3.2 ± 1.6 | NS |
| Nadir GH (ng/ml) | 0.24 ± 0.23 | 0.17 ± 0.15 | NSa |
| GH AUC (ng/ml · 120 min) | 152.4 ± 179.6 | 101.5 ± 131.3 | NSa |
| Insulin AUC (μIU/ml · 120 min) | 8622 ± 4988 | 6692 ± 4068 | 0.04a |
| HOMA-IR | 1.03 ± 0.51 | 1.00 ± 0.47 | NSa |
| PYY (pg/ml) | 95.6 ± 98.9 | 92.8 ± 64.9 | NSa |
| Leptin (ng/ml) | 9.4 ± 6.5 | 3.7 ± 3.3 | <0.0001 |
Values are expressed as means ± sd.
Comparisons performed with transformed values to approximate a normal distribution.
PYY levels in girls
Table 2 and Fig. 1 show our data across pubertal stages for girls after they were divided into three groups as described above (see Statistical methods). As expected per study design, the groups differed significantly for age, bone age, height, and Tanner stage. Weight and BMI were higher in mid-late pubertal (Tanner 4–5) compared with prepubertal (Tanner 1) girls, and in mid to late-pubertal (Tanner 4–5) girls compared with early to mid-pubertal (Tanner 2–3) girls. PYY values differed between the groups and were lower in Tanner 2–3 girls compared with Tanner 1 girls after controlling for multiple comparisons. Early to mid-pubertal (Tanner 2–3) girls had higher nadir GH levels than prepubertal (Tanner 1) girls, whereas insulin levels did not differ between the groups. HOMA-IR, however, trended higher in girls in Tanner stages 4–5 compared with Tanner 1 girls. Leptin levels were highest in late pubertal (Tanner 4–5) girls. Even after excluding overweight girls (BMI between the 85th and 90th percentiles; n = 4), our results remained comparable for all variables.
Table 2.
PYY levels and other characteristics in girls
| Tanner 1 | Tanner 2 and 3 | Tanner 4 and 5 | P value | |
|---|---|---|---|---|
| n | 7 | 14 | 20 | |
| Chronological age (yr) | 10.4 ± 0.7 | 12.2 ± 1.2a,b | 14.9 ± 1.4a | <0.0001 |
| Bone age (yr) | 9.8 ± 0.9 | 11.5 ± 1.8a,b | 15.4 ± 1.3a | <0.0001 |
| Weight (kg) | 33.2 ± 3.2 | 40.3 ± 5.1b | 56.3 ± 10.9a | <0.0001 |
| Height (cm) | 139.7 ± 5.8 | 150.6 ± 8.6a,b | 162.4 ± 7.4a | <0.0001 |
| BMI (kg/m2) | 17.0 ± 1.8 | 17.7 ± 1.3b | 21.3 ± 3.0a | <0.0001 |
| BMI-SDS | −0.13 ± 0.81 | −0.22 ± 0.61 | 0.28 ± 0.81 | NS |
| Tanner stage | 1.0 ± 0.0 | 2.5 ± 0.5a,b | 4.8 ± 0.6a | <0.0001 |
| Nadir GH (ng/ml) | 0.10 ± 0.05 | 0.37 ± 0.31a | 0.19 ± 0.15 | 0.02c |
| GH AUC (ng/ml · 120 min) | 82.5 ± 86.5 | 235.9 ± 235.0 | 114.9 ± 135.2 | NSc |
| Insulin AUC (μIU/ml · 120 min) | 9640 ± 7331 | 8156 ± 5399 | 8592 ± 3863 | NSc |
| HOMA-IR | 1.38 ± 1.19 | 1.50 ± 0.78 | 2.21 ± 1.18a | 0.03c |
| PYY (pg/ml) | 185.9 ± 218.8 | 66.8 ± 10.2a | 83.6 ± 34.8 | 0.02c |
| Leptin (ng/ml) | 8.2 ± 5.8 | 5.9 ± 3.4b | 12.9 ± 7.3 | 0.01 |
Values are expressed as means ± sd. NS, Not significant.
P < 0.05 compared with Tanner 1.
P < 0.05 compared with Tanner 4 and 5.
Comparisons performed with transformed values to approximate a normal distribution.
Figure 1.
A, Fasting PYY levels in prepubertal girls (Tanner 1), early-mid pubertal girls (Tanner 2 and 3), and late pubertal girls (Tanner 4 and 5). B, Fasting PYY levels in prepubertal and early pubertal boys (Tanner 1 and 2), mid-late pubertal boys (Tanner 3 and 4), and late pubertal boys (Tanner 5). PYY levels were lowest in Tanner 2–3 girls and Tanner 4–5 boys. *, P < 0.05 for transformed data to approximate a normal distribution.
PYY levels in boys
Table 3 and Fig. 1 show our data across pubertal stages for boys after they were divided into three groups as described in Statistical Methods. Age, bone age, Tanner stage, weight, and height increased significantly across the three groups. BMI was significantly higher in late pubertal (Tanner 5) boys compared with pre- to early pubertal (Tanner 1–2) boys and mid-late pubertal (Tanner 3–4) boys. PYY levels were lowest in mid-late pubertal (Tanner 3–4) boys, and these boys differed significantly from late pubertal (Tanner 5) boys for PYY after controlling for multiple comparisons. Nadir GH and GH AUC after the oral glucose load were highest in the mid-late pubertal group, whereas insulin levels did not differ across the groups. However, after controlling for BMI sd score (BMI-SDS) in a multivariate model, boys in Tanner stages 3–4 had significantly higher insulin AUC, whereas boys in Tanner stages 1–2 had significantly lower insulin AUC than Tanner 5 boys. Leptin levels were highest at Tanner stage 2 and were overall lower for boys at Tanner stages 3–4 compared with boys at Tanner stages 1–2. After excluding the one overweight boy (BMI between the 85th and 90th percentiles), our results remained comparable for all variables.
Table 3.
PYY levels and other characteristics in boys
| Tanner 1 and 2 | Tanner 3 and 4 | Tanner 5 | P value | |
|---|---|---|---|---|
| n | 18 | 13 | 15 | |
| Chronological age (yr) | 11.4 ± 1.3 | 13.8 ± 0.9a,b | 16.0 ± 1.4a | <0.0001 |
| Bone age (yr) | 11.2 ± 1.1 | 13.8 ± 1.0a,b | 17.0 ± 1.5a | <0.0001 |
| Weight (kg) | 38.7 ± 6.0 | 50.3 ± 9.0a,b | 64.3 ± 7.7a | <0.0001 |
| Height (cm) | 145.7 ± 8.1 | 164.3 ± 10.4a,b | 173.5 ± 8.2a | <0.0001 |
| BMI (kg/m2) | 18.1 ± 1.7 | 18.5 ± 1.7b | 21.4 ± 2.1a | <0.0001 |
| BMI-SDS | 0.21 ± 0.59 | −0.30 ± 0.67 | 0.21 ± 0.62 | 0.05 |
| Tanner stage | 1.4 ± 0.6 | 3.4 ± 0.8a,b | 5.0 ± 0.0a | <0.0001 |
| Testicular volume | 3.6 ± 1.1 | 12.2 ± 3.4a,b | 20.1 ± 3.8a | <0.0001 |
| Nadir GH (ng/ml) | 0.13 ± 0.09 | 0.26 ± 0.20a,b | 0.14 ± 0.14 | 0.01c |
| GH AUC (ng/ml · 120 min) | 51.2 ± 54.9 | 186.7 ± 163.0a,b | 99.0 ± 148.4 | 0.007c |
| Insulin AUC (μIU/ml · 120 min) | 5326 ± 2085 | 8527 ± 5040 | 7032 ± 4818 | 0.09c |
| HOMA-IR | 1.06 ± 0.59 | 0.89 ± 0.36 | 1.09 ± 0.50 | NSc |
| PYY (pg/ml) | 96.0 ± 75.5 | 69.6 ± 28.1b | 113.3 ± 72.8 | 0.02c |
| Leptin (ng/ml) | 5.5 ± 4.3 | 2.2 ± 1.6a | 3.1 ± 2.2 | 0.02 |
Values are expressed as means ± sd. NS, Not significant.
P < 0.05 compared with Tanner 1 and 2.
P < 0.05 compared with Tanner 5.
Comparisons performed with transformed values to approximate a normal distribution.
Associations of PYY with covariates
Overall, for the group as a whole, there was a negative association of PYY levels with nadir GH (r = −0.33; P = 0.003) (Fig. 2) and GH AUC (−0.29; P = 0.01). Similarly, in girls, PYY was inversely associated with GH nadir (−0.31; P = 0.05) and GH AUC (r = −0.35; P = 0.03). In male subjects, PYY again correlated inversely with nadir GH (r = −0.36; P = 0.02), although these associations were weaker with GH AUC (r = −0.25; P, not significant). We tested for BMI-SDS as a possible confounder or effect modifier of the association between PYY and GH using multivariate analysis and found that BMI-SDS did not influence the correlation of PYY with nadir GH (Table 4). After controlling for BMI-SDS, P values for the association between PYY and nadir GH were 0.003, 0.07, and 0.02 for the group as a whole, within girls, and within boys, respectively. After exclusion of an outlier, the P value in girls was 0.02. No associations were observed between PYY and insulin or leptin levels. As expected, leptin levels correlated positively with BMI-SDS for the group as a whole (r = 0.53; P < 0.0001) and within boys (r = 0.65; P < 0.0001) and girls (r = 0.66; P < 0.0001). Additionally, we noted inverse associations between leptin and GH nadir for the group as a whole (r = −0.34; P = 0.003), as well as within boys (r = −0.39; P = 0.01) and girls (r = −0.47; P = 0.005).
Figure 2.
Associations of fasting PYY values with GH nadir values after an oral glucose load for the group as a whole. PYY correlated inversely with nadir GH levels (r = −0.31; P = 0.005) after log transformation.
Table 4.
Multivariate analysis showing associations of PYY with GH nadir after controlling for BMI-SDS
| Log PYY | Parameter estimate | F ratio | P | r2 |
|---|---|---|---|---|
| All subjects | ||||
| Intercept | 1.736 | |||
| Log GH nadir | −0.213 | 9.55 | 0.003 | 0.11 |
| BMI-SDS | −0.039 | 1.28 | 0.26 | |
| All girls | ||||
| Intercept | 1.769 | |||
| Log GH nadir | −0.075 | 3.47 | 0.07a | 0.10 |
| BMI-SDS | −0.057 | 1.69 | 0.20 | |
| All boys | ||||
| Intercept | 1.684 | |||
| Log GH nadir | −0.266 | 5.78 | 0.02 | 0.15 |
| BMI-SDS | −0.009 | 0.02 | 0.88 |
P value for association of log nadir GH with log PYY after controlling for BMI-SDS was 0.02 after exclusion of an outlier.
Discussion
Our data indicate that during midpuberty PYY levels in both boys and girls are lowest at a time when GH levels are the highest. These data are consistent with our hypothesis that PYY levels would be the lowest at the time of maximum growth.
The role of the appetite-regulating peptides such as leptin, ghrelin, and PYY in the induction of puberty and pubertal progression is a subject of great interest, and whereas much attention has been given to the importance of leptin in puberty induction and progression, the impact of other hormones such as ghrelin and PYY on puberty is not known. PYY is a novel anorexigenic hormone secreted by the distal gut, which acts through the Y2 receptor of neuropeptide Y to induce satiety after meals (6). Administration of PYY to obese adults causes a decrease in food intake, suggesting that a decrease in PYY levels should be associated with increased food intake. Importantly, PYY has been demonstrated in animal models to inhibit GnRH and gonadotropin secretion (9), which would indicate that a decrease in PYY levels might facilitate pubertal progression. During periods of rapid growth, increased food intake becomes necessary, and the voracious appetite of adolescents is likely an adaptive mechanism to facilitate the pubertal growth spurt. We speculate that low PYY levels during early to mid puberty in girls and mid to late puberty in boys may facilitate energy intake when the pubertal growth spurt is at its maximum. The mechanism that leads to lower PYY levels at this time is not known. However, in animal models, administration of GH leads to a suppression of PYY levels (10), and GH concentrations peak at the time of the pubertal growth spurt. Hence, one may also speculate that an increase in GH levels in puberty causes a suppression of PYY levels, thereby facilitating increased energy intake and the pubertal growth spurt. Consistent with this, we observed an inverse association between log PYY and log nadir GH concentrations for the group as a whole and within the two genders, consistent with animal data. These associations remained significant even after controlling for BMI.
Other appetite-regulating peptides that impact gonadotropin secretion and may therefore affect pubertal progression are ghrelin and leptin. The anorexigenic hormone leptin increases in both genders at the onset of puberty (4). However, after pubertal onset, a gender-specific dichotomy occurs whereby leptin continues to increase in girls while levels decrease in boys (4). In this study, leptin levels were highest in late pubertal girls and early pubertal boys, and as expected, leptin levels decreased in the mid-late pubertal boys. This decrease in leptin in boys suggests that it may not be essential for pubertal progression, although decreased levels may contribute to increased food intake and facilitate growth. Leptin levels did correlate inversely with nadir GH levels in both boys and girls. Ghrelin, an orexigenic hormone, suppresses gonadotropin secretion in animals and humans (23,24). We did not measure ghrelin levels in this study; however, other investigators have reported a decrease in ghrelin across puberty in boys (5), which may facilitate pubertal progression; however, a decrease in ghrelin across puberty suggests a decreased stimulus for food intake despite the associated pubertal growth spurt.
In contrast, one may speculate that the decrease in PYY levels around mid-puberty in both genders may stimulate food intake at a time when an adequate intake of calories is essential for an optimal growth spurt and may also facilitate pubertal progression. The subsequent increase in PYY may signal a decreased requirement for food intake as the pubertal growth spurt slows down. It will be important for future studies to examine the appetite-regulating peptides in the context of caloric intake through the different pubertal stages and in relation to gonadotropin pulsatility patterns.
Limitations of this study include its cross-sectional and associative nature, relatively small sample size, and lack of growth data. However, the strength of the data and consistency across genders suggest that the role of PYY in puberty merits further exploration. This is the first study to examine levels of PYY across the different pubertal stages in girls and boys, and we demonstrate that this anorexigenic peptide reaches its nadir in mid-puberty at the time when the pubertal growth spurt is at its maximum and GH levels are at their peak.
Footnotes
This work was supported by National Institutes of Health Grants 1 UL1 RR025758-01, R01 DK 062249, and 1 R01 HD060827-01A1.
Disclosure Summary: The authors have no conflict of interest to declare.
First Published Online April 7, 2010
Abbreviations: AUC, Area under the curve; BMI, body mass index; BMI-SDS, BMI sd score; HOMA-IR, homeostasis model of assessment for insulin resistance; PYY, peptide YY.
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