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The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 8 3790-3794
Copyright © 2004 by The Endocrine Society

Adiponectin before and after Weight Loss in Obese Children

T. Reinehr, C. Roth, T. Menke and W. Andler

Vestische Kinder- und Jugendklinik Datteln, University of Witten-Herdecke (T.R., T.M., W.A.), 45711 Datteln, Germany; and Department of Pediatrics, University of Bonn (C.R.), 53113 Bonn, Germany

Address all correspondence and requests for reprints to: Dr. Thomas Reinehr, Vestische Kinder- und Jugendklinik, University of Witten-Herdecke, Dr. F. Steiner Strasse 5, 45711 Datteln, Germany. E-mail: t.reinehr{at}kinderklinik-datteln.de.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Adiponectin is decreased in obesity and seems to be involved in insulin resistance. The influences of age, gender, puberty, and weight loss on adiponectin have not been studied in obese children. We measured body fat mass based on skinfold thickness, age, pubertal stage, gender, adiponectin, and insulin resistance (homeostasis model assessment) in 42 obese children. We analyzed adiponectin and homeostasis model assessment 1 yr later in these obese children and separated them into two groups according to degree of weight loss (decrease in SD score for body mass index, ≥0.5 vs. <0.5). Adiponectin was negatively correlated to percentage body fat (r = –0.44; P = 0.002), insulin resistance (r = –0.33; P = 0.016), and age (r = –0.41; P = 0.003). Adiponectin levels were significantly (P = 0.017) higher in pubertal girls compared with boys, but there was no significant difference in prepubertal children in respect to gender (P = 0.833). Adiponectin was significantly (P < 0.001) lower in pubertal compared with prepubertal children. The significant weight loss in 16 children was associated with a significant increase in adiponectin (P = 0.010) and a decrease in insulin resistance (P = 0.013), whereas there were no changes in the 26 children without significant weight loss. Adiponectin levels in obese children were negatively correlated to age, body fat, and insulin resistance and were decreased in puberty. Significant weight loss led to an increase in adiponectin levels and an improvement of insulin resistance.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
ADIPOSE TISSUE SERVES not only as an energy storage organ, but also as an endocrine organ by releasing factors into the circulation that have distant sites of action (1, 2). The secretory products of adipose tissue, collectively referred to as adipocytokines, include adiponectin and other factors such as leptin or TNF-{alpha} (3). Hypoadiponectinemia may contribute to insulin resistance and accelerated atherogenesis associated with obesity (3, 4).

In adults and children, the plasma adiponectin concentration negatively correlates with the degree of body fat (3, 5, 6, 7). In adults, adiponectin negatively correlates to insulin resistance (3). Weight reduction is accompanied by an increase in plasma adiponectin concentrations (8, 9, 10, 11, 12). In contrast, fasting plasma insulin as a parameter of insulin resistance was not associated with adiponectin concentrations in children (6), whereas studies of adiponectin levels in weight loss of obese children are still lacking. The correlation among age, gender, puberty, and adiponectin has not been examined in childhood. Therefore, we studied plasma adiponectin levels in obese children in relation to these factors and measured adiponectin before and after significant weight loss.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
We examined 42 obese children who attended the Obeldicks intervention program (13, 14). Children with endocrine disorders, premature adrenarche, or syndromal obesity were excluded from the study. Obesity was defined according to the body mass index (BMI) 97th percentile using population-specific data (15).

The pubertal developmental stage was determined according to Marshall and Tanner and categorized into two groups (prepubertal, boys with pubic hair and gonadal stage I and girls with pubic hair stage and breast stage I; pubertal, boys with pubic hair and gonadal stage ≥II and girls with pubic hair stage and breast stage ≥II).

Fasting adiponectin, insulin, and blood glucose were measured before and after the 1-yr Obeldicks intervention program. Blood sampling was performed at 0800 h. Plasma adiponectin was determined by ELISA (Human Adiponectin ELISA Kit, Linco Research, Inc., St. Charles, MO; intraassay coefficient of variation, 1.0–7.4%; interassay coefficient of variation, 2.4–8.4%; sensitivity, 0.5 ng/ml). Insulin was measured by microparticle enzyme assay (Abbott, Chicago, IL). Blood glucose was determined by a colorimetric test (Vitros GLU-Analyseplättchen, Ortho-Clinical Diagnostics, Rochester, NY). Intra- and interassay coefficients of variation were 5% or less in both methods. Homeostasis model assessment (HOMA) was used to detect the degree of insulin resistance (16). The resistance can be assessed from the fasting glucose and insulin concentrations by the formula: resistance (HOMA) = [insulin (mU/liter) x glucose (mmol/liter)]/22.5.

Height and weight were measured before and after the 1-yr Obeldicks intervention program. The weight status was recorded as BMI and the BMI SD score (SDS-BMI) using the LMS method (17), in which the M and S curves correspond to the median and coefficient of variation body mass index for German children at each age and gender, whereas the L curve allows for the substantial age-dependent skewness in the distribution of BMI (15). The assumption underlying the LMS method is that after Box-Cox power transformation, the data at each age are normally distributed (17).

Furthermore, the percentage of body fat was calculated based on a skinfold thickness equation using the following formulas (18): boys: body fat % = 0.783 x (skinfold thickness subscapularis + triceps in mm) + 1.6; girls: body fat % = 0.546 x (skinfold thickness subscapularis + triceps in mm) + 9.7. The triceps and subscapularis skinfold thicknesses were measured in duplicate and averaged. One investigator performed all anthropometrical measurements using a caliper.

The reduction in weight was achieved through the Obeldicks intervention program for obese children (13, 14). This 1-yr out-patient training is based on a program of physical exercise, nutrition education (high carbohydrate and fat-reduced diet), and behavior therapy, including individual psychological care of the child and his or her family.

The children were divided into two groups according to their changes in SDS-BMI over a 1-yr period. The following classification was used because in a reduction of less than 0.5 SDS-BMI, no improvement in insulin resistance and cardiovascular risk factors could be measured in obese children (19): group I (significant weight loss), decrease in SDS-BMI of 0.5 or more; and group II (no significant weight loss), decrease in SDS-BMI of less than 0.5.

Statistical analysis was performed by the Winstat software package. Adiponectin levels were correlated to the percentage of body fat and the degree of overweight (SDS-BMI) by Spearman’s rank test. Adiponectin was correlated to age and insulin resistance (HOMA) using partial correlation adjusted to percentage of body fat. Adiponectin levels were compared between prepubertal and pubertal children by the nonparametric Mann-Whitney U test. Furthermore, adiponectin levels were compared between boys and girls in prepubertal and pubertal children by the nonparametric Mann-Whitney U test. The changes in adiponectin and insulin resistance (HOMA) were analyzed in children with and without significant weight loss over the period of 1 yr by nonparametric Wilcoxon test. Qualitative items (pubertal stage and gender) were tested by {chi}2 test, and quantitative items (age and SDS-BMI) were tested by nonparametric Mann-Whitney U test at baseline. A value of P < 0.05 was considered as significant. Values are expressed as the median and range. Informed consent was obtained from all subjects.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
The age, stage of puberty, gender, degree of overweight (weight, BMI, SDS-BMI), percentage of body fat, and the adiponectin, insulin, blood glucose, and insulin resistance levels of the 42 studied children are shown in Table 1Go.


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  		TABLE 1. Age, stage of puberty, gender, degree of overweight (weight, BMI, SDS-BMI), percentage of body fat, adiponectin, insulin, glucose levels, and insulin resistance index in the 42 children studied

 
Adiponectin plasma concentrations were significantly negatively correlated to percentage of body fat (r = –0.44; P = 0.002; Fig. 1Go), insulin resistance (r = –0.33; P = 0.016; Fig. 2Go), and age (r = –0.41; P = 0.003; Fig. 3Go), whereas there was no significant correlation to SDS-BMI (r = –0.17; P = 0.142).



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  		FIG. 1. Relationship between plasma adiponectin levels and percentage of body fat (r = –0.44; P = 0.002).

 


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  		FIG. 2. Relationship between plasma adiponectin levels and insulin resistance (HOMA; r = –0.33; P = 0.016).

 


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  		FIG. 3. Relationship between plasma adiponectin levels and age (r = –0.41; P = 0.003).

 
The adiponectin plasma levels were significantly (P < 0.001) lower in the 21 pubertal children (median adiponectin, 9.2; range, 4.9–15.6 µg/ml) compared with the 21 prepubertal children (median adiponectin, 14.5; range, 6.0–22.2 µg/ml; Fig. 4Go), whereas there were no significant differences in SDS-BMI, percentage of body fat, or gender between prepubertal and pubertal children. The insulin resistance index (HOMA) was significantly (P = 0.002) increased in the 21 pubertal children (median HOMA, 4.3; range, 1.6–17.9) compared with the 21 prepubertal children (median HOMA, 2.5; range, 0.6–5.2).



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  		FIG. 4. Plasma adiponectin levels in 21 pubertal and 21 prepubertal obese children (data as median, interquartile range, and range).

 
The 14 pubertal girls (median adiponectin, 11.6; range, 4.9–15.6 µg/ml) demonstrated significantly (P = 0.017) higher adiponectin levels than the seven pubertal boys (median adiponectin, 7.4; range, 5.5–7.9 µg/ml). There were no significant differences in SDS-BMI, percentage of body fat, or age in these two groups.

Adiponectin levels did not differ significantly (P = 0.833) between the 10 prepubertal girls (median adiponectin, 15.2; range, 6.0–22.2 µg/ml) and the 11 prepubertal boys (median adiponectin, 13.3; range, 12.1–18.3 µg/ml). There were no significant differences in SDS-BMI, percentage of body fat, or age in these two groups.

The significant weight loss (decrease in SDS-BMI, ≥0.5) in 16 obese children led to a significant increase in adiponectin levels (P = 0.010) and a significant decrease in insulin resistance (HOMA; P = 0.013), whereas there were no significant changes in the 26 obese children without significant weight loss (decrease in SDS-BMI, <0.5) over the 1-yr period (Table 2Go). There were no significant differences in gender, SDS-BMI, or percentage of body fat in these two groups, although the children losing weight were significantly (P < 0.01) younger and more often prepubertal.


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  		TABLE 2. Changes in weight, BMI, SDS-BMI, skinfold thickness (ST), percentage of body fat, adiponectin, insulin, glucose levels, and insulin resistance index over a 1-yr period in obese children with significant weight loss (decrease in SDS-BMI, ≥0.5) and obese children without significant weight loss (decrease in SDS-BMI, <0.5)

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
This is the first study in obese children concerning the relation of adiponectin to age, gender, puberty, degree of body fat, and changes in adiponectin during weight reduction. In agreement with reports in adults (3, 5) and normal weight children (6, 7), our study showed that adiponectin correlates negatively to percentage of body fat. There was no significant relation between adiponectin and SDS-BMI, pointing to skinfold thickness measurement as a better tool to describe the degree of body fat mass than SDS-BMI.

In adults, the mean adiponectin level was 3.7 µg/ml in a group of obese patients (20, 21), whereas in nonobese subjects these values reached a mean of 8.9 µg/ml. In our study of obese children, the mean adiponectin level was 12.2 µg/ml, similar to the study by Nemet et al. (7), which demonstrated a mean adiponectin level of 10.8 µg/ml in 30 healthy children. Therefore, adiponectin levels appear to be higher in children than in adults. According to this, adiponectin correlated negatively to age. Adiponectin levels decreased most substantially during puberty. In adults, adiponectin concentrations seem to be gender dependent, being higher in women than men (8, 21, 22, 23). Sex hormones may influence adiponectin levels, because adiponectin concentrations were higher in prepubertal compared with pubertal children. Furthermore, adiponectin levels demonstrated no gender differences in prepubertal children of our sample, in contrast to the gender effect found in pubertal children.

In contrast to the study of children by Stefan et al. (6), insulin resistance was negatively correlated with adiponectin levels in our study. This is in accordance with many reports in adults (8, 9, 10, 11, 12). In the study of Stefan et al. (6), insulin and not insulin resistance index was measured. Despite the small sample, this may explain the missing association to adiponectin, because the insulin resistance index (HOMA) is a better measurement of insulin resistance than insulin (16, 24). There seems to be a logarithmic connection between insulin resistance and adiponectin. Furthermore, insulin resistance increased in puberty (25), a time when adiponectin levels decreased in obese children.

The metabolic pathways leading from hypoadiponectinemia to insulin resistance are not yet completely understood. Animal studies have demonstrated that adiponectin reduces hyperglycemia (3, 26, 27). The glucose-lowering effects of adiponectin are thought to be mediated via direct muscle and hepatic actions, such as increased lipid oxidation, direct improvement of insulin signaling at the receptor/postreceptor level, inhibition of gluconeogenesis, and inhibition of TNF-{alpha} signaling in adipose tissue (3, 10, 21).

Adiponectin is the first known adipocytokine that is down-regulated in obesity. The mechanism of this negative regulation remains unclear, because adiponectin is secreted exclusively by fat cells (3, 21). Adiponectin expression decreased when visceral adipose tissue was isolated and cultured in vitro (3, 28). This effect was reduced by decreasing the amount of tissue cultured per dish. In addition, the effect was prevented by inhibitors of transcription and translation. Probably, the increasing mass of white adipose tissue in obesity reduces adiponectin protein synthesis by a feedback inhibition (21, 29). Furthermore, adiponectin secretion in vitro is lower in visceral vs. sc adipocytes in children (30), pointing to an influence of body fat distribution. Because adiponectin is stimulated by insulin and inhibited by TNF-{alpha}, insulin resistance and enhanced TNF-{alpha} expression may contribute to hypoadiponectinemia (3). Glucocorticoids are also reported to inhibit adiponectin gene expression and secretion (10, 21, 28, 31), suggesting that decreased adiponectin production could play a role in glucocorticoid-induced insulin resistance.

This is the first study in childhood demonstrating the increase in adiponectin levels due to a significant weight loss over a 1-yr period. This change cannot be explained by other factors, because there were no significant changes in a control group without significant weight loss. The group of children with weight loss were younger and more often prepubertal than the control group. Because increasing age and puberty were associated with a decrease in adiponectin concentrations in our study, the long time period of 1 yr during which many of these children may enter puberty cannot explain an increase in adiponectin levels. In adults, weight reduction in obese individuals is also accompanied by an increase in plasma adiponectin concentrations (8, 9, 10, 11, 12). These data suggest the existence of the above-discussed negative feedback mechanism between adipose mass and the production of adiponectin in humans. In our study, insulin resistance decreased in the group of obese children with significant weight loss and increasing adiponectin levels, supporting the relationship between hypoadiponectinemia and insulin resistance.

In summary, adiponectin levels in obese children were negatively correlated to age, body fat, and insulin resistance and were decreased in puberty. Adiponectin concentrations were independent of gender in prepubertal, in contrast to pubertal, children. Significant weight loss was associated with an increase in adiponectin levels and an improvement of insulin resistance. This points to a connection between adiponectin and body fat in relation to insulin resistance.


   Footnotes
 
Abbreviations: BMI, Body mass index; HOMA, homeostasis model assessment; SDS, SD score.

Received November 6, 2003.

Accepted April 14, 2004.


   References
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 Introduction
 Subjects and Methods
 Results
 Discussion
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