Leptin levels in children with central precocious puberty

Several studies have suggested that sufficient serum leptin levels may be involved in the initiation of puberty. To assess further the relationship between leptin and the onset of puberty in humans, we measured the serum leptin concentration in children with central precocious puberty (CPP). We studied 65 children with either idiopathic (IPP; n = 50 girls and 3 boys) or neurogenic central precocious puberty (NPP; n = 5 girls and 7 boys). The serum leptin levels in these patients were compared with normative data from healthy children and adolescents using SD scores that adjust for body mass index (BMI) and Tanner stage. The mean SD scores of IPP and NPP girls were +0.4 +/- 0.1 and +1.0 +/- 0.5, respectively, compared with that of age-matched prepubertal girls and +0.7 +/- 0.2 and +1.6 +/- 0.6 compared with that of girls matched for pubertal stage. The CPP girls with lower BMIs contributed larger SD scores, such that the leptin SD score was negatively correlated with BMI. A similar, modest increase in leptin levels in the CPP girls was evident when additional normative data were considered. The mean leptin SD scores of IPP and NPP boys were -0.9 +/- 0.5 and +0.7 +/- 0.3, respectively, compared with that of normal boys at Tanner stage 3-4. Serum leptin levels in the boys with CPP were not different from those in healthy boys in any of the normative studies. These data should be interpreted cautiously, but they suggest that girls with CPP have modestly elevated serum leptin concentrations compared with those in healthy children and adolescents. In addition, the negative correlation between the leptin SD score and BMI suggests that sufficient leptin levels may be associated with initiation of puberty in girls.     

Influence of spontaneous calcium intake and physical exercise on the vertebral and femoral bone mineral density of children and adolescents

Peak bone mass is determined mainly by genetic-ethnic factors, but environmental factors such as calcium intake and physical activity during childhood and adolescence could play a role. We have measured the bone mineral density (BMD) of 151 healthy children and adolescents, ages 7-15.3 years. Density was measured by dual X-ray absorptiometry (DXA) at two sites (lumbar verterbrae L1-L4 and the upper femur), and the data were analyzed in terms of the height, weight, sexual maturation, spontaneous calcium intake, and physical activity. Of the children, 57-71% had calcium intakes below 1000 mg/day. BMD increased with pubertal maturation from 0.68 +/- 0.08 to 0.92 +/- 0.09 g/cm2 (vertebral bone density, VBD) and from 0.87 +/- 0.10 to 1.03 +/- 0.09 g/cm2 (femoral bone density, FBD) between Tanner stage 1 and 5. Multiple regression analysis showed that body weight and Tanner stage were main determinants of bone density when expressed as g/cm2. The weekly duration of sports activity also influenced both the vertebral (p < 0.001) and femoral (p = 0.01) sites, especially in girls and during puberty. Dietary calcium appeared to be another independent determinant of BMD, especially before puberty, at the vertebral (p = 0.02) site. Most important, dietary calcium was found to be the main determinant of vertebral mineral density, when expressed as z score, in both sexes. Moreover, 93% of the 28 children with low vertebral z score values (below -1) and 84% of the 31 children with low femoral z score values (below -1) had dietary calcium intakes below 1000 mg/day.     

Serum concentrations of type I and III procollagen propeptides in healthy children and girls with central precocious puberty during treatment with gonadotropin-releasing hormone analog and cyproterone acetate

Serum levels of type I and III procollagen propeptides (s-PICP and s-PIIINP) were measured in 466 healthy school children and in 23 girls with central precocious puberty (CPP) during GnRH analog and cyproterone acetate therapy, using two commercially available RIAs. In normal children, s-PICP and s-PIIINP changed significantly with age and pubertal development stages. For s-PIIINP, a peak was seen at 12 yr for girls and 13 yr for boys; no peak could be discerned for s-PICP. The prepubertal (Tanner stage 1) s-PICP value (mean +/- SD) for girls was 374 +/- 132 micrograms/L, the midpubertal value (stage 3) was 442 +/- 135 micrograms/L, and the postpubertal value (stage 5) was 203 +/- 103 micrograms/L. The mean s-PIIINP levels for girls were 9.1 +/- 2.4, 15.0 +/- 4.3, and 6.8 +/- 3.1 micrograms/L, respectively. For boys, levels were 362 +/- 119, 544 +/- 138, and 359 +/- 256 micrograms/L for s-PICP and 8.5 +/- 2.2, 14.5 +/- 5.0, and 8.6 +/- 3.8 micrograms/L for s-PIIINP (P < 0.001 for both propeptides in both boys and girls). There was, however, a large variation in normal values for both propeptides within the age groups and pubertal stages. There was a significant correlation of s-PICP and s-PIIINP levels to height velocity in girls (r = 0.35; P < 0.001 and r = 0.33; P < 0.001, respectively), while in boys, only s-PIIINP showed significant correlation to height velocity (r = 0.40; P < 0.001). In untreated girls with CPP, serum levels of s-PIIINP were elevated [PIIINP SD score (SDS), 2.13]. Levels of s-PICP were normal (PICP SDS, 0.39). Levels of both propeptides decreased within 2 months after initiation of therapy and remained below initial values (P < 0.01). The decrease in s-PIIINP after 2 months of therapy showed a significant correlation with the fall in height velocity SDS for chronological age after 6 months of therapy (r = 0.64; P < 0.01). We conclude that s-PIIINP and, to a lesser degree, s-PICP reflect growth in normal children, but due to the large variation, both propeptides seem unsuitable as markers for screening of growth disorders in children.     

Development's tortoise and hare: Pubertal timing, pubertal tempo, and depressive symptoms in boys and girls.

Although the sequence of pubertal maturation remains consistent across most individuals, the timing and tempo of development fluctuate widely. While past research has largely focused on the sequelae of pubertal timing, a faster tempo of maturation might also present special challenges to children for acclimating to new biological and social milestones. Using latent growth curve modeling, the present study investigated how pubertal tempo and pubertal timing predicted depressive symptoms over a 4-year period in a sample of children recruited from New York City area public schools. Rate of intraindividual change in parent-reported Tanner stages was used as an index of pubertal tempo, and more advanced Tanner development at an earlier chronological age was used as an index of pubertal timing. For girls (N = 138, M = 8.86 years old at Time 1), pubertal timing emerged as the most salient factor, and the tempo at which girls progressed through puberty was not significant. In boys (N = 128, M = 9.61 years old at Time 1), both timing and tempo of development were significant; notably, however, the effects of pubertal tempo were stronger than those of timing. These findings highlight the need to consider multiple sources of individual variability in pubertal development and suggest different pubertal challenges for boys and girls. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A highly polymorphic microsatellite within intron 5 of the porcine 54/56 kDa vacuolar H(+)-ATPase subunit gene (V-ATPase)

OBJECTIVE: To assess the validity of a short calcium food frequency questionnaire (FFQ) for use in young children. DESIGN: Calcium intake from an estimated 4 d diet record (4DDR) was compared with the calcium intake from a 35 item FFQ specifically designed to assess habitual calcium intake and previously validated for adult women. SUBJECTS: Forty-one girls and 26 boys aged 3-6 y recruited by advertisement for studies of nutrition and bone health. RESULTS: Mean (s.d.) calcium intakes were 798 mg (271) and 942 mg (419) for the 4DDR and FFQ respectively, (r = 0.52). Mean difference (s.d. of difference) in calcium intake between the two methods was 144 mg (355), showing that the FFQ may estimate calcium intakes 565 mg below to 854 mg above diet record values. 84% of subjects when classified by the 4DDR fell into the same or adjacent quartiles when classified by the FFQ. Only two subjects were classified in extreme quartiles for the two methods. The FFQ correctly identified 68% of children with recorded intakes less than 800 mg. CONCLUSIONS: The short calcium FFQ tended to overestimate actual calcium intakes in young children, and would not be appropriate for determining calcium intake of individuals. However, the FFQ demonstrated good ability to classify subjects into extremes of calcium intake. Moreover, the predictive value of the FFQ in identifying children with intakes below the current recommended intake of 800 mg was reasonably high (79%).     

Tumor-related arthrodesis. Reconstruction of the shoulder contour using a free TRAM (Transverse Rectus Abdominis Musculocutaneous) flap]

We evaluated growth hormone binding protein (GHBP) activity in a group of obese children (12 boys and 12 girls, age 3.1-14.7 years, BMI 21.1-33.3, 11 prepubertal and 13 early pubertal) and in 26 age-matched normal weight children (14 boys and 12 girls, age 2.1-16.0 years, BMI 14.2-21.4, 18 prepubertal and 8 early pubertal). All children were of normal stature. GHBP activity was significantly higher in the obese (39.1 +/- 1.1%) than in the control children (28.3 +/- 1.0%, p < 0.0001). Mean serum GHBP was not different between boys and girls or between prepubertal and pubertal subjects. A positive correlation was found between BMI and GHBP levels only in the normal weight children (r = 0.425, p < 0.05). Baseline insulin concentrations in the obese children were 97.6 +/- 7.9 pmol/l (normal values, 45.0 +/- 18.6 pmol/l), and the mean insulin AUC following OGTT in the obese was 811.3 +/- 160.7 pmol/l (normal values, 373.1 +/- 150.1 pmol/l). Serum GHBP activity in the obese was not correlated with baseline serum insulin concentrations or with the insulin AUC following OGTT. In conclusion, we found that obese children have elevated GHBP activity, and speculate that this phenomenon may serve to compensate for their reduced GH secretion and accelerated GH clearance.     

Serum zinc in highly trained adolescent gymnasts

Serum zinc was measured in 20 adolescent gymnasts (9 boys, 11 girls, age 12-15 yr) explored for detecting possible adverse effects of intense training on pubertal maturation and growth. They had low serum zinc (0.599 +/- 0.026 mg/L) when compared to matched control sedentary children (n = 118 mean 0.81 +/- 0.014 p < 0.001). Girls had lower zinc than boys (0.557 +/- 0.023 vs 0.651 +/- 0.044 p < 0.001). Zinc was correlated to isometric adductor strength (r = 0.468 p < 0.05). Children with serum zinc < 0.6 mg/L had lower insulin-like growth factor binding protein 3 than others (2.326 +/- 0.264 vs 2.699 +/- 0.12 p < 0.01). Thus, zinc is lowered in trained adolescent gymnasts and even lower in females. This reduction could play some role in abnormalities of puberty, growth, or muscular performance.     

Comprehensive analysis of risk factors for acquisition of Pseudomonas aeruginosa in young children with cystic fibrosis

Racial differences in insulin secretion and insulin sensitivity in healthy children were studied by administering a 2-hour hyperglycemic clamp (225 mg/dL) to 14 black and 16 white healthy adolescents (Tanner II-V), and 12 black and 11 white prepubertal children, matched for age, body mass index, and Tanner I pubertal development. In prepubertal children, fasting and first-phase insulin concentrations were higher in blacks compared with whites (14.7+/-1.3 vs 10.4+/-1.2, P=0.02, and 76.9+/-6.8 vs 52.1+/-6.4 microu/mL, P=0.016). There were no differences in second-phase insulin levels and insulin sensitivity index. In pubertal adolescents, first-phase and second-phase insulin concentrations were higher in blacks compared with whites (first-phase: 157.3+/-18.3 vs 77.0+/-8.7 microu/mL, P=0.0003; second-phase: 175.0+/-24.3 vs 108.7+/-8.8 microu/mL, P=0.012). Insulin sensitivity index was 35% lower in black adolescents compared with whites (P=0.02). These findings indicate that significant differences in insulin secretion and sensitivity are detectable early in childhood in healthy African-American vs American whites. However, genetic (race) vs environmental factors (physical activity/fitness, energy balance) should be carefully scrutinized as potential factors responsible for such differences.     

Zinc metabolism and requirement in Chinese preschool children consuming different diets

Zinc metabolism of children differs due to diet and this can affect zinc requirement. We used the balance method to study zinc metabolism in 11 Chinese preschool children (six males and five females, 5.5-6.5 y old with a mean age of 6 y) of normal zinc status as judged by comprehensive criteria before and after they were fed a balanced diet. Zinc intakes and excretions via feces, urine, whole body surface and hair were determined in each subject. After all subjects consumed a balanced diet for 3 wk, losses of zinc in feces and urine increased from 3.77 +/- 0.62 mg/d to 5.28 +/- 0.92 mg/d (P < 0.05) and 0.19 +/- 0.05 mg/d to 0.23 +/- 0.05 mg/d (P < 0.05), respectively, as dietary zinc intakes increased from 5.38 +/- 0.71 mg/d to 7.12 +/- 0.64 mg/d (P < 0.05). Whole body surface zinc loss did not change (0.25 +/- 0.07 mg/d vs 0.27 +/- 0.09 mg/d (P = 0.57). Hair zinc loss was 5.26 +/- 2.49 microgram/d. Post-treatment, zinc excretions via feces, urine and whole body surface positively correlated with dietary zinc intakes (0.68-0.88, P < 0.05). Zinc retention did not change (1.17 +/- 0.78 mg/d vs 1.35 +/- 0.52 mg/d, P = 0.53) with balanced diet treatment. After treatment zinc metabolism in these children was positive and stable. The absorbed zinc, 1.84 +/- 0.47 mg/d, was considered their absolute zinc requirement. Assuming that zinc availability is 20%, the zinc requirement in the daily diet of Chinese preschool children should be 9.23 +/- 2.35 mg/d (6.88-11.58 mg/d).     

Effects of luteinizing hormone-releasing hormone analog-induced pubertal delay in growth hormone (GH)-deficient children treated with GH: preliminary results

To study the effect of delaying epiphyseal fusion on the growth of GH-deficient children, we studied 14 pubertal, treatment naive, GH-deficient patients (6 girls and 8 boys) in a prospective, randomized, placebo-controlled trial. Chronological age was 14.5 +/- 0.5 yr, and bone age was 11.6 +/- 0.3 yr (mean +/- SEM) at the beginning of the study. Patients were assigned randomly to receive GH and LH-releasing hormone (LHRH) analog (n = 8) or GH and placebo (n = 6) during 3 yr, with planned continuation of GH treatment until epiphyseal fusion. Patients were measured with a stadiometer and had serum LHRH tests, serum testosterone (boys), serum estradiol (girls), and bone age performed every 6 months. Patients treated with GH and LHRH analog showed a clear suppression of their pituitary-gonadal axis and a marked delay in bone age progression. We observed a greater gain in height prediction in these patients than in the patients treated with GH and placebo after 3 yr of treatment (mean +/- SEM, 14.0 +/- 1.6 vs. 8.0 +/- 2.4 cm; P < 0.05). These preliminary findings suggest that delaying epiphyseal fusion with LHRH analog in pubertal GH-deficient children treated with GH increases height prediction and may increase final height compared to treatment with GH alone.     

Iron status, menarche, and calcium supplementation in adolescent girls

The effects of growth, menstrual status, and calcium supplementation on iron status were studied over 4 y in 354 girls in pubertal stage 2 who were premenarcheal at baseline (x+/-SD age: 10.8+/-0.8 y). Girls were randomly assigned to placebo or treatment with 1000 mg Ca/d as calcium citrate malate. Anthropometric characteristics, bone mass, and nutritional status were measured biannually; ferritin was measured annually; and red blood cell indexes were determined at 4 y. The simultaneous effects of iron intake and menstrual status on serum ferritin, after change in lean body mass (LBM) was controlled for, were evaluated in subjects in the upper and lower quartiles of cumulative iron intake. The average maximal accumulation of LBM (386 g/mo; 95% CI: 372, 399) occurred 0.5 y before the onset of menarche. Change in LBM was a significant predictor of serum ferritin (P < 0.0001), with a negative influence on iron status (t ratio=-4.12). The 2 fitted mathematical models representing ferritin concentrations of subjects in the upper and lower quartiles of cumulative iron intake were significantly different (P < 0.018). The regression line of the ferritin concentration in menstruating girls with high iron intakes had a less negative slope than the line fit to serum ferritin concentrations in girls with low iron intakes (NS). Serum ferritin concentrations at 0, 1, 2, 3, and 4 y were not significantly different between groups. In addition, there was no significant difference between groups in any of the red blood cell indexes. In summary, growth spurt and menstrual status had adverse effects on iron stores in adolescent girls with low iron intakes (<9 mg/d), whereas long-term supplementation with calcium (total intake: approximately 1500 mg/d) did not affect iron status.     

Alterations in growth and body composition during puberty: III. Influence of maturation, gender, body composition, fat distribution, aerobic fitness, and energy expenditure on nocturnal growth hormone release

We examined the relationships among gender, sexual maturation, four-compartment model estimates of body composition, body fat distribution (magnetic resonance imaging for abdominal visceral fat and anthropometrics), aerobic fitness, basal and total energy expenditure, and overnight GH release in an ultrasensitive chemiluminescence assay in healthy prepubertal and pubertal boys (n = 18 and 11, respectively) and girls (n = 12 and 18, respectively). Blood samples were withdrawn every 10 min from 1800-0600 h to determine the area under the serum GH-time curve (AUC), sum of the GH peak heights (sigma GH peak heights), and the mean nadir GH concentration. GH release was greater in the pubertal than prepubertal subjects due to an increase in sigma GH peak heights (43.8 +/- 3.6 vs. 24.1 +/- 3.5 ng.mL-1, P = 0.0002) and mean nadir (1.7 +/- 0.2 vs. 0.7 +/- 0.2 ng.mL-1, P = 0.0002), but not peak number (4.3 +/- 0.2 vs. 4.5 +/- 0.2). The girls had a greater sigma GH peak heights (39.0 +/- 3.5 vs. 28.8 +/- 3.6 ng.mL-1, P = 0.05) and mean nadir concentration (1.4 +/- 0.2 vs. 0.9 +/- 0.2 ng.mL-1, P = 0.05) than the boys. Significant inverse relationships existed between sigma GH peak heights (r = -0.35, P = 0.06) or mean nadir (r = -0.39, P = 0.04) and four-compartment percent body fat for all boys but not for all girls or when combining all subjects. For all girls, significant inverse relationships existed between sigma GH peak heights (r = -0.39, P = 0.03) or mean nadir (r = -0.37, P = 0.04) and waist/hip ratio. Similar inverse relationships in all boys or all subjects were not significant. Forward stepwise regression analysis determined that bone age (i.e. maturation, primary factor) and gender were the significant predictors of AUC, sigma GH peak heights, and mean nadir. The influence of maturation reflects rising sex steroid concentrations, and the gender differences appear to be because of differences in estradiol concentrations rather than to body composition or body fat distribution.     

Evidence suggesting an additional control mechanism regulating episodic secretion of luteinizing hormone and follicle stimulating hormone in pre-pubertal children and post-menopausal women

The possible differential regulation of pulsatile follicle stimulating hormone (FSH) and luteinizing hormone (LH) secretion in pre-pubertal children and in post-menopausal women was investigated. Children were studied for 4 h and post-menopausal women for 6 h; blood samples were taken every 10 min. Post-menopausal women were studied before and 21 days after administration of a single i.m. dose of gonadotrophin-releasing hormone (GnRH) analogue. Eight post-menopausal women and 18 children (nine boys and nine girls) were enrolled. The children were divided into two groups: A, at Tanner stages 0-1 (four boys and three girls); B, at Tanner stage 2-3 (five boys and six girls). Plasma LH and FSH concentrations were determined using an immunofluorimetric assay. Time series were analysed and the specific concordance (SC) index was computed to determine the degree of concordance between episodes of LH and FSH secretion. While children of group A had LH concentrations below the minimal detectable dose of 0.1 IU/l, group B showed measurable LH plasma concentrations (1.4 +/- 0.3 IU/l, mean +/- SEM). Plasma FSH concentrations were detectable in both groups. Group A showed FSH plasma concentrations significantly lower than those of group B (0.75 +/- 0.2 and 1.95 +/- 0.4 IU/l respectively; P < 0.05), but FSH pulse frequency was higher in group A (P < 0.05). Children of group B showed significant concomitance of LH and FSH secretory events at time 0 (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

The human mast cell line HMC-1 binds and responds to C3a but not C3a(desArg)

OBJECTIVE: To evaluate the breakfast intake of calcium and milk products and to determine whether these correlate with total intake of both calcium and milk products. METHODS: Food taken at breakfast and throughout the day was recorded using a 7 consecutive day food record in 200 schoolchildren aged between 9 and 13 years. RESULTS: 65.3% of boys and 80.5% of girls showed intakes of calcium which were lower than recommended. Milk products were the foods most frequently included in breakfast (95.5% of subjects included them in this meal). A relationship was seen between energy provided by breakfast and the quantities of milk products (r = 0.5735) and calcium (r = 0.6908) taken at this meal. A relationship was also seen between energy provided by breakfast and daily intake of milk products (r = 0.4633) and calcium (r = 0.4954). The percentage of intakes of calcium lower than those recommended decreased when breakfast provided > or = 20% of total energy intake, and when the consumption of milk products at breakfast was greater than the 50th percentile (200 ml). Subjects with breakfast milk product intakes > or = 200 ml showed higher intakes of the same over the rest of the day (233.3 +/-140.4 g) than did those who took lesser quantities of these foods at breakfast (161.5 +/- 100.6 g). Further, those who took > or = 25% of the recommended intake of calcium at breakfast showed greater intakes of the same over the rest of the day (600.4 +/- 213.8 mg compared to 510.8 +/- 200.7 mg in subjects with lower calcium intakes). CONCLUSIONS: The intake of milk products (r = 0.7587) and calcium (r = 0.7223) at breakfast correlates with the consumption of these foods in the whole diet. However, the total daily intake of milk products and calcium does not depend solely on breakfast intake. Subjects with the greatest intakes at breakfast also showed greater intakes over the rest of the day (r = 0.3953 for milk products and r = 0.4122 for calcium).     

Zinc balance in adolescent females consuming a low- or high-calcium diet

There is increasing evidence that calcium intake up to the threshold amount (1480 mg/d) increases bone mass during growth. However, there is concern that such a high calcium intake may interfere with the utilization of other nutrients such as zinc, which is also important for skeletal development. The purpose of our study was to investigate the effect of long-term calcium supplementation on zinc utilization in 26 adolescent females (mean +/- SD age 11.3 +/- 0.5 y) during a 14-d period. Each day subjects consumed a metabolic diet containing 722 mg Ca and 6.3 mg Zn. Participants were randomly assigned to receive either a placebo or a calcium supplement containing 1000 mg supplemental Ca/d as calcium citrate malate. Supplementation began 15 wk before the balance period to allow for adaptation to the greater calcium intake. Mean (+/-SD) zinc balance (0.8 +/- 0.8 compared with 0.3 +/- 1.1 mg/d, P = 0.23), fecal zinc (4.3 +/- 0.6 compared with 4.7 +/- 1.4 mg/d, P = 0.27), urinary zinc (0.4 +/- 0.2 compared with 0.5 +/- 0.1 mg/d, P = 0.55), and net zinc absorption (21% compared with 15%, P = 0.33) were not significantly different between the high- and low-calcium groups. Our results suggest that increasing the recommended dietary allowance of calcium to 1500 mg/d as recommended by the National Institutes of Health consensus panel will not have adverse effects on zinc utilization in adolescent females.     

Sensitive immunoassay and in vitro bioassay demonstrate constant bioactive/immunoreactive ratio of luteinizing hormone in healthy boys during the pubertal maturation

The quality of serum LH was assessed during pubertal maturation in boys by measuring immunoreactive (I) LH by a time-resolved immunofluorometric assay (IFMA, Delfia), and bioactive (B) LH by a sensitized in vitro bioassay. Seven samples were collected at 3-mo intervals from 14 healthy boys (median starting age 11.8 y) during pubertal maturation from Tanner stage I-III or II-IV (n = 7 for each). The mouse Leydig cell in vitro bioassay was sensitized 10-fold, to 0.05-0.1 IU/L, by including 1.5 mumol/L of forskolin in the incubation medium. The I- and B-LH levels showed good linear correlation throughout the concentration range analyzed. Mean I-LH increased between the pubertal stages I-IV from 0.42 to 2.24 IU/L and that of B-LH from 1.35 to 5.04 IU/L. No concomitant change occurred in the B-LH/I-LH (B/I) ratio, which was 2.84 +/- 0.54 in stage I and 2.58 +/- 0.48 in stage IV (mean +/- SEM, n = 7). Although the B/I ratios of LH varied from 0.59 to 5.85 in the samples analyzed, the intraindividual variation was small (mean coefficient of variance, 22%). In conclusion, IFMA and sensitized in vitro bioassay showed in healthy boys a similar 4-5-fold increase in the mean LH concentration during pubertal maturation, with no concomitant change in the B/I ratio. The sensitized in vitro bioassay of LH is useful for analysis of the low peripubertal LH levels. The good correlation between the I-LH and B-LH levels, and the lack of change in LH B/I ratio, indicate that IFMA correctly estimates the LH levels upon evaluation of pubertal maturation.     

Serum leptin levels in normal children: relationship to age, gender, body mass index, pituitary-gonadal hormones, and pubertal stage

It is commonly accepted that at least in girls puberty starts when a minimum level of body mass or a certain amount of body fat are present. However the precise signal by which adipose stores inform the hypothalamus of the degree of energetic reserves is unknown. Leptin is a hormone produced by the adipocytes to regulate food intake and energy expenditure at the hypothalamic level. To understand whether leptin is the adipose tissue signal that allows puberty, 789 normal children of both sexes, age 5-15 yr, were transversally studied. Leptin levels, as well as gonadal and gonadotropins, levels, were analyzed in addition to the determination of auxological parameters. In an age-related analysis, leptin levels in girls rose from 5-15 yr (from 4.3 +/- 0.4 to 8.5 +/- 0.9 micrograms/L) in parallel with body weight. Boys always had lower leptin levels than girls (3.3 +/- 0.3 micrograms/L at 5 yr), but they rose in parallel with weight until 10 yr (5.3 +/- 0.7 micrograms/L), when a striking decrease was observed until 15 yr (3.0 +/- 0.3 micrograms/L). In girls, leptin was the first hormone to rise followed by FSH and later by LH and estradiol. A similar pattern occurred in boys, despite the fact that leptin dropped after 10 yr when testosterone rises. Divided into three pubertal stages, i.e. P1 = prepuberty, P2 = early puberty, and P3 = overt puberty, in girls the four hormones rose progressively from P1 to P3, but from P2 to P3 the present increment was greater for LH and estradiol. In boys, leptin decreased from P1 to P3, whereas FSH, LH, and testosterone rose. The age-related changes were not caused by adiposity variations, because data did not change when subtracting values of children over 97% of standard deviation score of body mass index. In conclusion: 1) leptin appears to increase in both boys and girls before the appearance of other reproductive hormones related to puberty; 2) leptin levels in boys are always lower than in girls, although they increase with age until the age 10 yr; 3) leptin in boys declines about the time testosterone increases. Leptin may well be a permissive factor for the initiation of pubertal events.     

Absorption of macronutrients and nitrogen balance in children with dysentery fed an amylase-treated energy-dense porridge

The aim of this study was to determine the absorption of macronutrients and energy from an energy-dense diet liquefied with amylase from germinated wheat (ARF) in children suffering from acute dysentery. Thirty male children aged 6-35 months presenting with acute dysentery were randomly assigned to receive either an ARF-treated porridge or a standard porridge liquefied with water to make its consistency similar to the ARF porridge. After 24-h stabilization a 72-h metabolic balance was performed. Sixteen children received an ARF-treated porridge and 14 received a standard porridge liquefied with water. The mean +/- SD coefficients of absorption (%) of carbohydrate, fat, protein and energy (ARF porridge vs regular porridge) were 81.4 +/- 11 vs 86.9 +/- 7, 86.1 +/- 10 vs 82.8 +/- 15, 57.3 +/- 12 vs 48.4 +/- 24 and 81.4 +/- 9 vs 83.1 +/- 8, respectively. The stool loss of carbohydrate, protein, fat and energy was similar in the two groups. The net absorption of energy was substantially greater in the ARF-fed than regular porridge-fed children (by 28%, p = 0.01). The nitrogen balance was 6.9 +/- 3.4 mg kg(-1) d(-1) in the ARF porridge group and 1.1 +/- 6.7 mg kg(-1) d(-1) in the regular porridge group (p = 0.01). These results show that, despite being hyperosmolar, an amylase-treated liquefied energy-dense porridge is absorbed as well as a regular porridge by malnourished children with severe dysentery. Consequently, its use substantially increased the absorption of a net amount of macronutrients and resulted in a better nitrogen balance. These results further support this innovative approach of feeding sick children in developing countries.     

Dietary protein restriction and selective preference for a protein-containing diet in the golden hamster (Mesocricetus auratus)

The corrected midparental height method was introduced by Tanner in 1970 (Tanner method) and is commonly used to estimate target height in children to evaluate the effectiveness of growth-promoting therapies. It has not been established if the equation used to compute target height should be the same for children with short, normal, or tall parents. In this study, we examined the predicted target height values by parental heights in a large population-based study (n = 2402). A simple linear function of midparental height (x) was proposed to estimate target height (y): y = 45.99 + 0.78x (boys), y = 37.85+0.75x (girls), with a 95% predicted interval of about +/-10 cm. The prediction model was similar for boys and girls in SD scores (SDS), and was not affected by assortative mating or difference in parental heights. The model may underestimate the potential stature by about 2 cm for children with midparental height below -2 SDS, or 163 cm. In comparison, the Tanner method may lead to a 6-cm error in underestimating target height for these children. The function would be a better choice than the Tanner method for estimating target height in the clinical evaluation of growth promotion treatments because it is common that short children also have short parents. Children with very short parents will usually be much taller than their parents in adult stature, and we believe that a different function should be developed. The results support the proposed nondominant, non-sex-linked, polygenic inheritance in stature. The estimated heritability values were 0.75-0.78 in cm or 0.55-0.60 in SDS.