Changes in leptin, insulin and body composition in obese children during a weight reduction program

BACKGROUND: Girls have higher leptin concentrations than boys at all stages of biological development and this is also seen in the state of obesity. Little is known about whether gender and biological development of obese children influence changes in leptin associated with a short-term weight reduction program. OBJECTIVE: To study whether leptin concentration, body composition and insulin levels in obese children were influenced by a 3-week intervention program including diet and sports. STUDY DESIGN: Sixty-two obese children (32 boys and 30 girls) were examined before and after the intervention program. Body composition was measured by bioelectrical impedance and BMI-SDS was calculated. Serum leptin and serum insulin were determined by RIA. RESULTS: Girls had higher leptin levels than boys, before and after the weight reduction program. Body mass, fat mass (FM), leptin and insulin were decreased after the intervention in both sexes. We found a greater change in serum leptin in girls but the change in FM was of greater magnitude in boys. However, percentage changes in leptin were not significantly different between the sexes. Before the intervention, leptin concentrations were correlated with %FM, FM and moderately with BMI-SDS in all children. Only in pubertal boys did correlation of leptin with %FM increase after the intervention (from r=0.57 to r=0.75, p<0.01). Changes in leptin were found to be associated with initial leptin values in boys (r=0.95, p<0.01) and in girls (r=0.93, p<0.01), independent of Tanner stages. CONCLUSION: Serum leptin levels were positively correlated with adiposity in obese children and a diet and sports intervention program decreased serum leptin, insulin and body fat in all children. Changes in leptin were best described by the initial leptin concentration. The increase in correlation of leptin with %FM in obese pubertal boys after the intervention could have its underlying mechanism in an increased sensitivity to leptin and anabolic hormones.     

No evidence for leptin as an independent associate of blood pressure in childhood and juvenile obesity

We studied whether leptin is an independent associate of blood pressure in obese children and adolescence. 102 obese children (48 girls, age: 11.6 +/- 2.22 yr; body mass index [BMI]: 27.45 +/- 4.4; blood pressure: 122.5 +/- 11.1/64.7 +/- 10.6 mm Hg and 54 boys, age: 11.5 +/- 2.4 yr; BMI: 27.6 +/- 4.4; blood pressure: 122.5 +/- 13.2/60.9 +/- 8.1 mm Hg [mean +/- SD]) were investigated. Serum leptin and insulin were measured by RIA; glucose was determined enzymatically. Fat mass (FM) was calculated by bioelectrical impedance. Leptin was higher in girls than in boys (p=0.018) but no significant gender differences were found with respect to indices of adiposity and systolic blood pressure (SBP). Children were divided into three groups, according to pubertal stage (Group 1: prepubertal, 32 boys/13 girls; Group 2: pubertal, 17 boys/25 girls; Group 3: late/postpubertal, 5 boys/10 girls). SBP and DBP correlated with body weight in the whole group (r=0.49, p<0.0001, and r=0.27, p=0.004). In Group 1, BMI showed the highest correlation to SBP; in Group 3 no indices of adiposity were related to SBP. In no case was leptin significantly associated with SBP after adjustment for adiposity. In Group 2, glucose was significantly associated with SBP after adjustment for body weight. In Group 3, however, no correlations were found between SBP, DBP and metabolic characteristics, perhaps due to small sample size. Stepwise multiple regression revealed that body weight and glucose contributed to the variation in SBP in the whole group (R2=0.31, p<0.0001). Insulin accounted for almost 8% of the variation in DBP (R2=0.08, p=0.0034). Body weight contributed significantly to SBP in boys (R2=0.39, p<0.0001) and girls (R2=0.24, p< 0.001). The results imply that body weight contributes independently to the variation in blood pressure. Glucose and insulin contribute to mean blood pressure to some extent, but our data do not support the assumption that leptin per se serves as an independent predictor of blood pressure in obese children and adolescents.     

Serum leptin levels during childhood and adolescence: relationship with age, sex, adiposity and puberty

We studied serum leptin levels in 189 healthy children to evaluate related factors during childhood and adolescence. Leptin correlated with body mass index (BMI), triceps skinfold thickness (p<0.001) and body weight (p<0.01). Obese children and girls had higher leptin levels than non-obese children and boys, respectively (p<0.001). In girls, leptin correlated positively with age, skinfold thickness and BMI (p<0.001). In boys, leptin correlated negatively with age (p<0.001) and positively with skinfold thickness (p<0.05). Prepubertal boys had higher leptin levels than prepubertal girls and pubertal boys (p<0.05). Pubertal girls had higher leptin levels than prepubertal girls and pubertal boys (p<0.001). Leptin levels in girls were higher at Tanner stages 4 and 5 than at stage 1 (p<0.001). In conclusion, serum leptin levels are related with adiposity, have obviously age-related gender differences during childhood and adolescence, and may be involved in the maturation of reproductive capacity.     

Body mass index in Bengali adolescents

We describe a mixed longitudinal analysis of body mass index (BMI) in a group of Bengali adolescents (age 11-17 years) from a middle income family background and compare this against existing national and international data. Healthy school children, comprising of 416 boys and 343 girls were consented for annual repeat measurements of weight, height and pubertal staging between the years 1998 and 2001. The LMS method was used to construct smoothed BMI mean and standard deviation (SD) curves. Bengali adolescents have lower BMI than affluent Indian children and are -1 to -2 SD below US children. BMI increases in adolescence (boys: r = 0.49, p < 0.001, girls: r = 0.54, P < 0.001) with age but SMR does not have an independent effect on BMI.     

Serum leptin levels in patients with progressive central precocious puberty.

Leptin is a metabolic signal that may be involved in signaling adequacy of energy metabolism for the onset of reproductive function. The aim of this study was to investigate the relationship between leptin serum levels and pubertal development in girls with progressive central precocious puberty (CPP). We investigated longitudinally 14 girls with CPP before and during treatment with depot leuprorelin acetate. Mean (+/-SEM) chronological age and bone age at start of therapy were 6.0+/-0.6 y and 9.5+/-0.7 y, respectively. Leptin was determined by RIA. Girls with CPP showed no significant difference in leptin levels at pretreatment and after 1 and 2 y of treatment compared with healthy girls of the same body mass index (BMI). Mean leptin SD score adjusted for BMI was 0.31+/-0.4, 0.24+/-0.2, and 0.49+/-0.3, respectively (not significant). In a stepwise regression analysis model with BMI, bone age, chronological age, basal and stimulated LH, estradiol, dehydroepiandrosterone, androstenedione, and clinical pubertal signs, BMI was the only parameter that showed a significant correlation with leptin (p = 0.006). In conclusion, these data suggest that serum leptin levels are not significantly elevated at the onset of CPP compared with normal girls. Treatment with depot gonadotropin releasing hormone agonist seems to have no influence on leptin concentrations. As in normal girls, serum leptin levels in girls with CPP are mainly determined by BMI. Thus, we have no evidence that alterations of leptin are related to premature onset of puberty.     

Pubertal changes in serum leptin levels in adolescents with type 1 diabetes mellitus: a controlled longitudinal study

The mechanism of the pubertal delay seen in some adolescents with type 1 diabetes mellitus is not entirely clear. Since leptin has been implicated as a neuroendocrine modulator of puberty, we measured serum leptin levels longitudinally in 24 post-'honeymoon' patients with diabetes mellitus (M/F = 15/9) with a mean (+/- SD) age of 10.5 +/- 0.9 years and 26 controls (M/F = 15/11) with a mean age of 10.0 +/- 1.1 years. Physical examinations; serum leptin, IGF-I, IGFBP-3 and IGFBP-1 levels; and bone age X-rays were performed annually for up to 48 months. Glycosylated hemoglobin (HbA1c) was measured 2-4 times a year in patients with diabetes mellitus. Serum leptin levels strongly correlated with the body mass index z-scores (BMI-Z) in both controls (r = 0.666, p <0.00001) and diabetic patients (r = 0.577, p <0.00001). Girls had increased serum leptin levels for a given BMI compared to boys (p <0.005). There were no significant differences in serum leptin levels of patients with diabetes mellitus compared to controls, nor were differences seen when the groups were stratified by age, Tanner stage, or gender. There were also no significant correlations between serum leptin levels and degree of metabolic control (i.e. HbA1c) or insulin dose standardized for body weight. Although there was no significant diabetes-related or metabolic control-related delay in bone age z-score or pubertal development, there was a significant negative correlation between HbA1c and growth velocity z-score, indicating that children with poor diabetes control had modest but significant slowing of growth. It is concluded that neither pubertal development nor serum leptin levels are significantly altered in adolescents with diabetes mellitus managed with standard therapy. The potential role of leptin in initiation of pubertal development is not easily demonstrable in observational studies.     

Sex‐specific association between leptin receptor polymorphisms and leptin levels and BMI in healthy adolescents*

Aim: To examine the relationship of three common polymorphisms in the leptin receptor (LEPR) gene, implicated in the regulation of body weight, with leptin levels and obesity‐related phenotypes in a population‐based sample of healthy pubertal children in Spain. Methods: The study included 806 boys and girls aged 12–16 whose anthropometrical data and body composition were recorded. Serum leptin levels were determined by ELISA. The LEPR Q223R, K109R and K656N polymorphisms were determined by TaqMan® allelic discrimination assays. Results: When analysing the Q223R polymorphism, we observed that female carriers of the RR genotype had significantly higher plasma leptin levels (18.2 vs. 15.1 ng/mL p = 0.016) and significantly higher mean BMI values (22.5 vs. 21.3 Kg/m² p = 0.032) than QR carriers. Furthermore, the frequency of the RR genotype in overweight‐obese girls was significantly higher than that found in normal‐weight girls. No significant differences were observed in boys. Neither boys nor girls showed significant differences when comparing leptin levels, anthropometric variables or body composition by K109R or K656N genotype. Conclusion: The fact, that the Q223R polymorphism in the LEPR gene is significantly associated with leptin levels and BMI only in girls, suggests a sex‐specific influence of this polymorphism on these variables.     

Leptin is closely related to body fat in prepubertal children aged 8-11 years

BACKGROUND: In adults and obese children, serum leptin concentrations are closely related to body fat. AIM: To investigate whether such a relationship between leptin concentrations and body fat is also evident in children with a relatively normal body composition. METHODS: The study was a cross-sectional population study in 170 Caucasian children (91 boys and 79 girls), with a mean age of 9.9+/-0.6 y (range 8.5-10.9 y) and a mean BMI of 17.4+/-2.6 (range 12.8-28.1). Serum leptin was measured and compared to total body fat as determined by dual-energy X-ray absorptiometry. RESULTS: In the whole population, serum leptin concentrations were highly correlated with total body fat (r=0.83, p<0.001). A stepwise forward multi-regression analysis revealed that the inclusion of other anthropometrical data did not add any significance to the model. Leptin concentrations were significantly higher in girls (5.2 ng/ml) than in boys (3.2 mg/ml; p=0.003). Gender differences still prevailed (p=0.007) after adjusting for number of kilograms of fat tissue. CONCLUSION: This study shows that, already at the young age of 9-11 y, an adult-like pattern of regulation of leptin exists. This indicates similar risk factor dependency of leptin across all age groups.     

经济不发达地区3～9岁儿童血清瘦素水平的变化

目的：了解经济不发达地区3～9岁儿童在营养状况相对较差时血清瘦素的水平及与相关生长发育指标的关系。方法：根据年龄和性别将研究对象分为<6岁女孩组(F36组)、<6岁男孩组(M36)、≥6岁女孩组(F69组)和≥6岁男孩组(M69组)共4组,调查其年龄、体重、身高并计算体重指数(BMI)、体脂百分量(BF%),使用双抗体夹心ELISA法检测瘦素浓度,比较各组间瘦素浓度的差异,同时在各组分析瘦素与各指标间的相关性。结果：①瘦素浓度在同性别比较中,差异无显著性(P>0.05),在同年龄比较中,女孩明显高于男孩(P<0.05);②无论是男孩还是女孩,在3～6岁儿童瘦素与BMI和BF无明显相关(P>0.05),而在6～9岁儿童瘦素浓度与BMI和BF显著相关(P<0.05)。结论：在经济不发达地区3～9岁儿童中瘦素存在性别差异,6～9岁儿童中瘦素与BMI和BF密切相关。     

Inappropriate leptin secretion in thalassemia: a potential cofactor of pubertal timing derangement

The objective of the present study was to gain a better understanding of the role played by scarce leptin production in the deranged sexual development observed in patients with thalassemia. We studied 101 patients at different stages of puberty. Patients of both sexes were divided into three groups according to Tanner stages: T1-2 (20 males and 12 females), T3-4 (9 males and 4 females) and T5 (48 males and 8 females). Serum levels of leptin, ferritin, testosterone and estradiol were assessed. Leptin levels were adjusted for body mass index (BMI) using reference ranges stratified on the basis of gender and pubertal development. Deviations from the mean reference values were evaluated by calculating the standard deviation scores. Mean leptin standard deviation scores were significantly lower than expected in pubertal stage T1-2 and T3-4 in males and T3-4 and T5 in females. The peak leptin level was delayed in boys (13 years). In girls, parallelism between leptin and BMI was present until age 7-10 years; thereafter, although BMI constantly increased, leptin levels fell dramatically. Mean ferritin levels were significantly higher in pubertal stage T1-2 among males and in T5 among females. These findings show that in thalassemia adipose tissue is unable to assure adequate leptin production just when the highest leptin secretion is required and suggest that this inappropriate leptin secretion may be a cofactor of the derangement in pubertal timing observed in patients with thalassemia.     

Leptin levels in boys with pubertal gynecomastia

BACKGROUND: It has been reported that there is a relationship between circulating leptin and sex steroid hormones and leptin is able to stimulate estrogen secretion by increasing aromatase activity in adipose stromal cells and breast tissue. Leptin receptors have been also shown in mammary epithelial cells and it has been suggested that leptin is involved in the control of the proliferation of both normal and malignant breast cells. AIM: To investigate circulating leptin levels in boys with pubertal gynecomastia. METHODS: Twenty boys with pubertal gynecomastia who were in early puberty and had no obesity, and 20 healthy individuals matched for age, pubertal stage and body mass index (BMI) with the study group, were enrolled in the study. Body weight, height and left midarm circumference (MAC) and left arm triceps skinfold thickness (TSF) were measured and BMI was calculated. A fasting blood sample was collected and routine hormonal parameters including prolactin, beta-human chorionic gonadotropin (betaHCG), total and free testosterone, estradiol, luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin, androstenedione (AS) and dehydroepiandrosterone sulfate (DHEAS) levels were studied. Serum leptin levels were analyzed using radioimmunoassay. RESULTS: The mean ages of the study and control group were not different (13.9 +/- 0.89 and 14.2 +/- 0.66, respectively). No significant difference was found for BMI, MAC and TSF values between the two groups. There was no significant difference for hormonal parameters including FSH, LH, total and free testosterone, estradiol, AS, DHEAS and estradiol/total testosterone ratio between boys with pubertal gynecomastia and the controls. Serum leptin levels were found significantly higher in the study group compared with the healthy controls (5.58 +/- 0.81 and 2.39 +/- 0.29 ng/ml, respectively; p <0.001). No correlation could be determined between serum leptin levels and hormonal parameters. CONCLUSION: The presence of higher leptin levels in boys with pubertal gynecomastia indicates that leptin may be involved in the pathogenesis of pubertal gynecomastia. The role of circulating leptin in pubertal gynecomastia is probably related to increase in estrogen and/or estrogen/ androgen ratio by the stimulating effect of leptin on aromatase enzyme activity in both adipose and breast tissues, or a direct growth stimulating effect of leptin on mammary epithelial cells, or increase in sensitivity of breast epithelial cells to estrogen with inducing functional activation of estrogen receptors by leptin in breast tissue.     

No relationship between leptin and cortisol in obese children and adolescents

Recent findings have shown that leptin downregulates the steroid producing system in the adrenal. We studied the interactions of leptin, insulin and cortisol in obese children and adolescents at different stages of maturation. In 44 boys (age 11+/-3.1 yr, body mass index [BMI] 29+/-5.3 [mean +/- SD]) and 35 girls (age 11.4+/-2.6 yr, BMI 29+/-4.3), blood levels of leptin, insulin, cortisol, and glucose were determined. Fat mass (FM) was calculated by bioelectrical impedance. No significant differences were found between boys and girls with respect to humoral and anthropometric characteristics. When children were divided according to maturation stage (prepubertal, pubertal, and late/postpubertal) insulin was higher in the more mature groups (p<0.01) and leptin was higher in the pubertal group (p=0.03). In the prepubertal and pubertal groups, the expected positive relationship between adiposity and leptin was found although the magnitude of this association decreased with maturity. In none of the groups studied was cortisol significantly correlated to leptin. Insulin (p=0.03) and glucose (p=0.01) were positively associated with cortisol in the prepubertal group after adjustment for adiposity. However, in the pubertal group an inverse correlation was found between insulin and cortisol (p=0.03), and between insulin and glucose after control for adiposity. In the late/ postpubertal group, no significant correlations were found between estimates of adiposity and humoral parameters even after adjustment for gender. Stepwise multiple regression failed to detect a significant influence of cortisol to explain the variation in leptin, and vice versa. BMI contributed to the variation in leptin (adj. R2 =0.275, p<0.0001), and glucose added 5% to the variation in cortisol (p=0.03). The results do not confirm the inverse association between leptin and cortisol found in adults. Although BMI reflects levels of leptin, it is likely that several other factors in conjunction with fatness modulate the relationship with leptin. Whether leptin per se exerts an influence on the hypothalamic-adrenal-adipo axis remains to be investigated in longitudinal studies.     

Possible effect of leptin on renal magnesium excretion in adolescent patients with type 1 diabetes

BACKGROUND: Hypomagnesaemia and hyperleptinemia are common in patients with diabetes. Moreover, it has been demonstrated that leptin stimulates diuresis and natriuresis. The aim of this study was to evaluate the relationship between serum leptin, serum magnesium (Mg) and urinary Mg/urinary creatinine levels in patients with type 1 diabetes. METHODS: Serum leptin and Mg and urinary Mg/urinary creatinine levels were measured in 67 patients with diabetes (33 girls and 34 boys). The age, diabetes duration, anthropometric and metabolic parameters of the subjects were matched between girls and boys. The relation of serum leptin levels to serum and urinary Mg/urinary creatinine levels was assessed. RESULTS: Serum leptin levels of girls with diabetes were higher than those of the boys (14 +/- 5.3 microg/L vs 5.8 +/- 1.5 microg/L, P < 0.001, respectively). The differences for serum Mg and for urinary Mg/urinary creatinine levels were not significant between girls and boys with diabetes. Leptin levels were correlated with urinary Mg/urinary creatinine levels in both girls and boys (r = 0.39, P = 0.02 and r = 0.37, P = 0.03, respectively). In a multivariate regression model, leptin emerged as independent correlates for mean urinary Mg/urinary creatinine in both girls and boys with the total variance explained being 14%, and 15%, respectively. CONCLUSION: The data suggest that serum leptin might be related to increased urinary Mg loss in patients with type I diabetes.     

Pubertal progression and serum lipid profile in obese children

BACKGROUND: During puberty, sex hormones are associated with decrease in serum lipids in healthy individuals. AIM: To investigate the relationships between pubertal development, serum lipid profile and atherogenic indices in obese children and adolescents. METHODS: Body mass index (BMI), blood pressure, and serum lipids of 340 obese children (182 girls, 158 boys) aged 3.6-17.8 years were measured. Atherogenic index, total cholesterol (TC)/high-density lipoprotein-cholesterol (HDL-C) and low-density lipoprotein-cholesterol (LDL-C)/HDL-C were calculated as indices of atherogenic risk. RESULTS: Weight (F = 62.078; p < 0.001), BMI (F = 21.083; p < 0.001), systolic blood pressure (SBP) (F = 11.956; p < 0.001) and diastolic blood pressure (DBP) (F = 3.947, p = 0.005) differed significantly between pubertal stages and increased with advance in stages in males. HDL-C (F = 4.586; p = 0.004) differed significantly between pubertal stages and decreased with advancing stages in males. Weight (F = 66.915; p <0.001), BMI (F = 23.101; p <0.001), SBP (F = 10.873; p <0.001), DBP (F = 2.839; p = 0.040) and LDL-C (F = 3.072; p = 0.029) differed significantly between pubertal stages and increased with advancing stages in girls. Triglyceride, TC, LDL-C and SBP were statistically significant determinants for HDL-C according to multivariate linear regression analysis. SBP was significantly affected by chronological age, BMI, glucose, TC and HDL-C according to stepwise linear regression analysis. CONCLUSION: The increasing rate of obesity is associated with an increase in cardiovascular risk factors in parallel with advance in pubertal stages, particularly in boys.     

The role of diabetes duration, pubertal development and metabolic control in growth in children with type 1 diabetes mellitus

OBJECTIVE: To investigate whether pubertal development, duration of type 1 diabetes mellitus (DM1), or metabolic control play some role in the anomalies in growth observed in diabetic children. PATIENTS: We conducted a prospective evaluation of 83 patients (37 female, 46 male) who were followed from the onset of DM1 at the prepubertal stage until they reached final height. All patients were treated with a conventional regimen of insulin. METHODS: Height SDS, weight SDS, BMI SDS, duration of DM1 in years, and values of HbA1c were the study variables. RESULTS: In prepubertal (P1) girls (data for the initial vs the intermediate evaluations): weight SDS was -0.14 +/- 0.19 vs 0.11 +/- 0.20, p = ns; BMI SDS -0.25 +/- 0.15 vs 0.01 +/- 0.13, p = ns. In postpubertal (P3) girls, weight SDS was 0.49 +/- 0.2 vs 1.2 +/- 0.32, p <0.01; BMI SDS 0.09 +/- 0.16 vs 1.03 +/- 0.24, p <0.01, whereas in P1 boys, height SDS was 0.16 +/- 0.30 vs -0.20 +/- 0.27, p <0.05; and in P3 boys: 0.09 +/- 0.21 vs -0.28 +/- 0.26, p <0.05. Thus pubertal development influenced changes observed in girls with DM1, but did not do so in boys. The anomalies described in children with DM1 were observed from the third year of DM1 duration in both girls and boys. We did not observe any correlation between HbA1c values with height SDS, weight SDS or BMI SDS. CONCLUSIONS: The anomalies in growth observed in girls with DM1 are related to pubertal development, but this is not the case in boys. Alterations in children with DM1 were found from the third year of DM1 duration. Furthermore, the present data also indicate that the degree of metabolic control observed in our patients treated with modern but conventional regimen did not play a major role in the anomalies observed.     

Relationships of IGF-I and andrrogens to skeletal maturation in obese children and adolescents

IGF-I and androgens are postulated to accelerate skeletal maturation in obese children. METHODS: We studied weight status (BMI-SDS), height-SDS, IGF-I, cortisol, DHEA-S, and testosterone in 356 obese children (aged 4-15 years; 54% females) and correlated them to differences between bone age and chronological age (deltaBA-CA). Direct multivariate linear regression analyses were conducted for the dependent variable deltaBA-CA, including BMI, age, gender, pubertal stage, IGF-I-SDS, cortisol, DHEA-S, and testosterone as independent variables separately in prepubertal and pubertal girls, and prepubertal and pubertal boys. RESULTS: Height-SDS (r = 0.52), IGF-I (r = 0.33), and IGF-I-SDS (r = 0.36) were significantly (p < 0.001) correlated to deltaBA-CA. In multiple regression analyses, BMI and IGF-I-SDS were significantly positively (p < 0.001) correlated to deltaBA-CA independently of gender and pubertal stage. Testosterone was significantly positively correlated to detaBA-CA only in prepubertal girls (p = 0.035). CONCLUSIONS: Since IGF-I concentrations were positively associated to deltaBA-CA independently of pubertal stage and gender, we put forward the hypothesis that this hormone may contribute to acceleration of skeletal maturation in obese children.     

Are C‐reactive protein and homocysteine cardiovascular risk factors in obese children and adolescents?

Background: Several prospective epidemiological studies have demonstrated that high-sensitivity C-reactive protein (hsCRP) and plasma homocysteine (hcy) are predictors of future coronary events among healthy men and women. The aim of the present study was therefore to investigate a possible relationship between hsCRP, hcy levels and body mass index (BMI), relative weight (RW), serum leptin levels, and cardiovascular risk factors in obese children and adolescents.
Methods: The study involved 28 obese children and adolescents (13 girls, 15 boys; BMI>95‰ for age and sex), 4.5–15 years of age (mean 10.7 ± 0.6 years), who attended hospital for a basic obesity check-up. The association between hsCRP, hcy levels and BMI, RW, serum leptin levels, and cardiovascular risk factors such as blood pressure (BP), lipid profile, serum fasting insulin levels, and insulin resistance indexes, was investigated.
Results: Serum hsCRP level was positively correlated with BMI ( r = 0.512, P  < 0.01), RW ( r = 0.438, P  < 0.05), systolic and diastolic BP ( r = 0.498, P  < 0.01), serum leptin levels ( r = 0.457, P  < 0.05), but not with serum lipid, glucose, fasting insulin, plasma hcy levels or insulin resistance indexes. For hcy level, in contrast, no correlation was found with BMI, RW, systolic and diastolic BP, serum lipid levels, leptin, hsCRP, glucose, fasting insulin levels, or insulin resistance indexes.
Conclusions: hsCRP is correlated with BMI, RW, BP and leptin, which are risk factors for coronary heart disease, which supports the relationship between obesity, inflammation and atherosclerosis. hsCRP in childhood obesity might be a useful index to predict possible atherosclerotic events.     

Long‐term effects of rapid weight gain in children,adolescents and young adults with appropriate birth weight for gestational age: the kiel obesity prevention study

Aim: This study investigates the effect of rapid weight gain in term children, adolescents and young adults born appropriate for gestational age. Methods: In all, 173 girls and 178 boys aged 6.1–19.9 (12.5 ± 3.1)years participated. Rapid weight gain (group 1) was defined as a change in weight‐SDS (standard deviation score) from birth till two years >0.67, ‘no change’ as ≥?0.67 and ≤0.67 (group 2) vs ‘slow weight gain’ as 90th age‐/sex‐specific BMI‐percentile was defined as overweight. Parental BMI, socio‐economic status and lifestyle were assessed as confounders. Results: A total of 22.8% gained weight rapidly, and 15.7% was overweight. Group 1 compared with group 2 and 3 subjects was taller, heavier and had a higher prevalence of overweight (girls/boys: 26.2%/28.9% vs 11.6%/19.0% vs 2.8%/5.0%; p < 0.01/p < 0.05). Concomitantly, a higher WC, %FM and FFM were observed. Rapid weight gain was positively associated with REE (adjusted for FFM) in boys (r = 0.26; p < 0.01), but not with cardio‐metabolic risk factors. Conclusion: Rapid weight gain was related to increases in height, weight, a higher prevalence of overweight and central fat distribution. In addition, rapid weight gain was related to a higher REE in boys, but not to cardio‐metabolic risk factors.     

Time course and determinants of leptin decline during weight loss in obese boys and girls.

OBJECTIVE: To investigate whether changes in leptin concentrations during weight loss can be explained by gender, puberty, baseline adiposity and changes in adiposity, body composition, rate of weight loss, physical activity and insulin concentrations. DESIGN: A longitudinal study with 9 repeated measures during a 12-week weight loss programme. SUBJECTS: Fifty-three boys and 62 girls (7.9-15.2 years) with body mass index (BMI) standard deviation scores (SDS) of median 2.78 and 2.70, respectively. MEASUREMENTS: Height, weight, fat mass percentage assessed by bioimpedance, Tanner stages, testicular size, physical activity scores, blood leptin (ng/ml) and insulin concentrations (pmol/l) were measured at baseline, and except for Tanner stage and testicular size, repeated regularly during the programme. RESULTS: The weight loss was accompanied by a steep decline in leptin concentrations during the first 10-11 days, followed by a less steep decline until day 82. Leptin declined to 39% in boys and 51% in girls of the level that was expected given the relationship at baseline between leptin and BMI SDS, and the BMI SDS changes during weight loss. The biphasic leptin decline was independent of gender, puberty, baseline adiposity or concomitant changes in BMI SDS, fat mass percentage, rate of weight loss, physical activity scores or insulin concentrations. CONCLUSION: The biphasic leptin decline, which exceeded the level expected, was independent of puberty, baseline adiposity and changes in adiposity, body composition, rate of weight loss, physical activity scores and insulin concentrations. The dissociation of the leptin-weight relationship during weight loss may contribute to the general leptin variability in obese subjects.     

Diurnal rhythm in serum leptin

AIM: To assess 24-hour serum leptin levels in children. SUBJECTS AND METHODS: Five girls and two boys aged 10.4-13.6 (mean 12.2) years with pubertal stages I to III were studied. All children were healthy. A fasting blood sample was drawn at 08.00 hours, and thereafter samples were obtained every 2 hours throughout 24 hours until 08.00 hours the next morning. Serum leptin was measured by a specific radioimmunoassay. RESULTS: A statistically significant circadian variation was found in mean leptin profile expressed as a percentage of overall day mean (F-ratio =10.4; P<0.001) with trough and peak levels (+/- SEM) at 10.00 (6.55+/-1.52 mg/l) and 24.00 hours (10.99+/-2.34 mg/l), respectively. CONCLUSIONS: In normal children serum leptin levels exhibit a nocturnal increase and a decrease during the morning. The nocturnal rise may represent a time lagged stimulating effect of insulin. The diurnal rhythm needs to be considered when serum leptin is assessed in clinical studies.