leptin and Down-Syndrome

Children with Down syndrome (DS) are more likely to be overweight or obese than the general population of youth without DS.. To review the prevalence of overweight and obesity and their determinants in youth with DS. The health consequences and the effectiveness of interventions were also examined.. A search using MEDLINE, Embase, Web of Science, Scopus, CINAHL, PsycINFO, SPORTDiscus, LILACS, and COCHRANE was conducted. From a total of 4280 studies, we included 45 original research articles published between 1988 and 2015.. The combined prevalence of overweight and obesity varied between studies from 23% to 70%. Youth with DS had higher rates of overweight and obesity than youths without DS. Likely determinants of obesity included increased leptin, decreased resting energy expenditure, comorbidities, unfavorable diet, and low physical activity levels. Obesity was positively associated with obstructive sleep apnea, dyslipidemia, hyperinsulinemia, and gait disorder. Interventions for obesity prevention and control were primarily based on exercise-based programs, and were insufficient to achieve weight or fat loss.. Population-based research is needed to identify risk factors and support multi-factorial strategies for reducing overweight and obesity in children and adolescents with DS.

Topics: Adolescent; Child; Diet; Down Syndrome; Dyslipidemias; Energy Metabolism; Exercise; Exercise Therapy; Humans; Hyperinsulinism; Leptin; Obesity; Overweight; Prevalence; Risk Factors; Sleep Apnea, Obstructive

It is widely accepted that muscle strength plays a key role on functional tasks of daily living and employability in individuals with Down syndrome (DS). Recent studies have also reported resistance training may improve chronic inflammation in other clinical situations. This is the first study conducted to determine the effect of resistance circuit training on low-grade systemic inflammation in adults with DS.. A total of 40 young male adults with DS were recruited for the trial through different community support groups for people with intellectual disabilities and their families. They had medical approval for physical activity participation. Twenty-four were randomly assigned to perform resistance circuit training with 6 stations, 3 days per week for 12 weeks. Exercise intensity was based on function of the 8RM assessments. The control group included 16 age-, sex-, and BMI-matched adults with Down syndrome. Plasma levels of leptin, adiponectin, and TNF-a were assessed by commercial ELISA kits. C-reactive protein (CRP) was assessed by nephelometry. Body composition was also determined, measuring fat-free mass percentage and waist circumference (WC). This protocol was approved by our Institutional Ethics Committee.. Plasma levels of leptin, TNF-a, and IL-6 were significantly decreased after the completion of the training program, as were fat-free mass and WC. No sports-related injuries or withdrawals from the program were reported during the entire study period. No changes were observed in the control group.. Resistance circuit training improved low-grade systemic inflammation in male sedentary adults with DS.

Topics: Adiponectin; Adult; Body Composition; Down Syndrome; Enzyme-Linked Immunosorbent Assay; Humans; Inflammation; Leptin; Male; Nephelometry and Turbidimetry; Resistance Training; Tumor Necrosis Factor-alpha

Recent studies have reported that obese young people with Down syndrome suffer from low-grade systemic inflammation. Whereas this condition may be improved in the general population by regular exercise, the problem has received no attention in the case of people with intellectual disability. Therefore, the authors' aim was to assess the influence of aerobic training on plasma adipokines in obese women with Down syndrome. Twenty obese young women with Down syndrome volunteered for this study, 11 of whom were randomly assigned to a 10-wk aerobic-training program. They attended 3 sessions/wk, which consisted of warm-up exercises followed by the main activity on a treadmill (30-40 min) at a work intensity of 55-65% of peak heart rate and ended with a cooling-down period. The control group included 9 women with Down syndrome matched for age, sex, and body-mass index. Fat-mass percentage and distribution were measured, and plasma adipokine levels (leptin and adiponectin) were assessed. In addition, each participant performed a maximal graded continuous treadmill exercise test. These parameters were assessed pre- and postintervention. Aerobic training produced a significant increase in participants' maximal oxygen uptake (20.2 ± 5.8 vs.23.7 ± 6.3 ml · kg-1 · min-1; p < .001), and plasma leptin levels were significantly reduced in the intervention group (54.2 ± 6.7 vs.45.7 ± 6.1 ng/ml; p = .026). Further significant correlations between plasma leptin and indices of obesity were found. In contrast, no significant changes were found in adiponectin levels (p > .05). None of the tested parameters changed in the control group. In conclusion, a 10-week training program reduced leptin levels in obese young women with Down syndrome.

Topics: Adiponectin; Adolescent; Adult; Body Composition; Body Height; Body Mass Index; Body Weight; Down Syndrome; Exercise; Exercise Test; Female; Humans; Inflammation; Leptin; Obesity; Waist-Hip Ratio; Young Adult

The aim of the present study was to analyse whether hormonal responses could explain an exercise limitation in Down's syndrome (DS). Fourteen young men with DS (mean age 22.5 +/- 0.7 years) and 15 controls (CONT, mean age 22.5 +/- 0.3 years) participated in the study. During a treadmill submaximal incremental test, blood samples were collected for determination of hormonal and metabolic variables. Compared to CONT, DS individuals showed lower VO(2max) (P < 0.05), and lower duration of submaximal incremental exercise (P < 0.001). At rest, DS individuals showed greater catecholamines, insulin and leptin values (P < 0.05), but lower testosteronemia and cortisolemia (P < 0.05), compared to CONT. During submaximal incremental tests, catecholamines and cortisol were not increased, whereas the insulin concentration of DS individuals was significantly higher (P < 0.01) compared to CONT. Glycaemia increased significantly at the end of submaximal incremental test for CONT but not for DS individuals (P < 0.01). Maximal fat oxidation was lower (P < 0.01), whereas non-esterified fatty acids concentrations rose significantly during submaximal exercise in DS individuals. These results indicate an altered hormonal response to exercise in DS individuals. This endocrine profile at rest and during exercise may limit endurance performance in DS individuals.

Topics: Adult; Body Composition; Body Height; Catecholamines; Down Syndrome; Exercise; Exercise Test; Fatty Acids, Nonesterified; Hormones; Humans; Hydrocortisone; Leptin; Male; Physical Endurance

Recent data indicates that adults with Down syndrome (DS) are at increased risk for cardiovascular disease (CVD) that significantly contributes to their morbidity and mortality. Although identification of cardiometabolic risk factors during childhood is desirable to design preventive interventions, the data on such risk factors in children with DS is scarce. The aim of this study was to study the cardiometabolic risk factors such as insulin resistance (IR), leptin and adiponectin concentrations, lipid abnormalities and leptin resistance in non-obese children with DS.. This cross-sectional case control study included karyotype confirmed trisomy-21 DS children aged 2-12 years and their matched healthy controls. After detailed anthropometry, weight, height and body mass index (BMI) standard deviation scores (SDSs) were calculated with reference data. Laboratory evaluation included determination of fasting lipid parameters, insulin, glucose, leptin and adiponectin concentrations. The homeostasis model assessment method (HOMA-IR) was used to assess IR and the ratio of leptin to BMI was used as an index of leptin resistance.. Seventy-seven children (39 with DS and 38 controls) comprised the study cohort. The anthropometric parameters were similar in the two groups. Children with DS showed significantly higher mean leptin concentrations (2.098±1.68 ng/mL vs. 1.44±0.52 ng/mL, p-value: 0.00) and higher indices of leptin resistance (0.127±0.085 vs. 0.09±0.03, p-value: 0.001) as compared to controls. Fasting adiponectin concentrations were lower (20.64±19.87 ng/mL vs. 32.58±34.25 ng/mL, p-value: 0.21) and fasting glucose higher (89.25±8.12 mg/dL vs. 85.71±5.52 mg/dL, p-value: 0.06) in the DS group as compared to the controls but the differences did not reach statistical significance. The concentrations of insulin, various lipid parameters and calculated HOMA-IR values were similar in the two groups. In the DS group, five children were identified to have high (>75th centile) leptin levels and four as impaired fasting glucose as compared to none in the controls.. Alterations of several cardiometabolic risk factors, in particular, leptin concentrations and leptin resistance are present in children with DS. The presence of hyperleptinemia without hyperinsulinemia suggests a probable inherent genetic basis for increased leptin resistance in patients with DS. There is a need for larger studies to further understand increased leptin resistance in DS that may contribute to increased CVD related morbidity and mortality in these patients.

Topics: Adiponectin; Blood Glucose; Body Mass Index; Cardiovascular Diseases; Case-Control Studies; Child; Child, Preschool; Cross-Sectional Studies; Down Syndrome; Female; Humans; Insulin Resistance; Leptin; Male; Risk Factors

Molecular pathogenesis of Down syndrome (DS) is still incompletely understood. Epigenetic mechanisms, including miRNAs gene expression regulation, belong to potential influencing factors. The aims of this study were to compare miRNAs expressions in placentas with normal and trisomic karyotype and to associate differentially expressed miRNAs with concrete biological pathways.. A total of 80 CVS samples - 41 with trisomy 21 and 39 with normal karyotype - were included in our study. Results obtained in the pilot study using real-time PCR technology and TaqMan Human miRNA Array Cards were subsequently validated on different samples using individual TaqMan miRNA Assays.. Seven miRNAs were verified as upregulated in DS placentas (miR-99a, miR-542-5p, miR-10b, miR-125b, miR-615, let-7c and miR-654); three of these miRNAs are located on chromosome 21 (miR-99a, miR-125b and let-7c). Many essential biological processes, transcriptional regulation or apoptosis, were identified as being potentially influenced by altered miRNA levels. Moreover, miRNAs overexpressed in DS placenta apparently regulate genes involved in placenta development (GJA1, CDH11, EGF, ERVW-1, ERVFRD-1, LEP or INHA).. These findings suggest the possible participation of miRNAs in Down syndrome impaired placentation and connected pregnancy pathologies. © 2016 John Wiley & Sons, Ltd.

Topics: Adult; Cadherins; Case-Control Studies; Chorionic Villi Sampling; Connexin 43; Down Syndrome; Epidermal Growth Factor; Epigenesis, Genetic; Female; Gene Expression Regulation, Developmental; Gene Products, env; Humans; Inhibins; Leptin; MicroRNAs; Pilot Projects; Placenta; Placentation; Pregnancy; Pregnancy Proteins; Real-Time Polymerase Chain Reaction; Transcriptome; Up-Regulation

Our purpose was to analyse if catecholamine responses to exercise would be different in Down syndrome (DS) with or without chronotropic incompetence.. Twenty five men with DS (mean age 22.2 ± 3.2) and twenty six controls (CONT, mean age 22.5 ± 1.4) participated in the study, and are divided into 3 groups: CONT, DS with chronotropic incompetence (DS+) and DS without chronotropic incompetence (DS-). During two treadmill incremental tests, blood samples were collected for the determination of hormonal and metabolic variables.. Ten out of 25 DS had chronotropic incompetence whereas no CONT. At rest, compared to CONT, despite similar physical activity, DS with chronotropic incompetence had significantly higher subcutaneous fat mass (p<0.001), lower epinephrine concentration (p<0.01), and higher leptin (p<0.01) and insulin concentrations (p<0.05). At peak exercise, all DS had lower heart rate, oxygen uptake and blood lactate concentrations than controls (p<0.001). During a 'Submaximal incremental test', DS with chronotropic incompetence had lower HR and lactate values (p<0.001) compared to CONT and DS without chronotropic incompetence (p<0.01). They also had blunted epinephrine and impaired norepinephrine responses to exercise compared to DS without chronotropic incompetence and CONT (p<0.01 and p<0.05 respectively).. Our results indicate that catecholamine adaptations to exercise are not adequate in DS+ and are associated with exercise intolerance. Thus, this endocrine profile at rest and during exercise may limit endurance performance of DS.

Topics: Cardiovascular Diseases; Down Syndrome; Epinephrine; Exercise; Exercise Test; Heart Rate; Humans; Insulin; Lactic Acid; Leptin; Male; Norepinephrine; Oxygen Consumption; Subcutaneous Fat; Young Adult

The objective of this study was to find a possible correlation between Down syndrome and amniotic fluid leptin. We compared 2nd trimester amniotic fluid leptin levels of fetuses with normal karyotype and with trisomy 21. We retrospectively found 15 fetuses with Down syndrome and we randomly selected 48 fetuses with normal karyotype as controls from our perinatology record database, in order to analyse their 2nd trimester amniotic fluid leptin levels. Amniotic fluid leptin levels were analysed by enzyme-linked immunosorbent assay (ELISA). The results were evaluated by Mann-Whitney U test. It was found that amniotic fluid leptin levels did not show any significant difference between amniotic fluids of fetuses with normal karyotype and those with trisomy 21 (p = 0.061). Median level of leptin was 10.06 ng/ml (range 2.10-36.69) for trisomy 21 fetuses and 14.53 ng/ml (range 2.30-67.33) for normal fetuses. In conclusion, leptin levels were not found to change in the amniotic fluids of fetuses with trisomy 21. This excludes a possible involvement of leptin in pathogenic processes associated with trisomy 21 during the fetal period and its potential employment as a diagnostic tool.

Topics: Adult; Amniotic Fluid; Biomarkers; Down Syndrome; Female; Fetal Diseases; Humans; Leptin; Pregnancy; Retrospective Studies

To investigate a possible role of leptin contributing to the pathophysiology of Down's syndrome by assessing amniotic fluid leptin levels in the 2nd trimester of normal pregnancy and pregnancy complicated by Down's syndrome.. We retrospectively assessed leptin levels of 2nd trimester amniotic fluid from 15 pregnancies diagnosed with Down's syndrome and 15 matched unaffected singleton pregnancies (controls). All amniotic fluid samples were obtained from women undergoing genetic amniocentesis at 16-20 weeks of gestation. Leptin levels were measured by enzyme-linked immunosorbent assay.. Amniotic fluid leptin levels were significantly decreased in the Down's syndrome group (3.26 +/- 2.36 ng/ml) compared to the controls (8.26 +/- 9.11 ng/ml, p < 0.05).. This study showed significantly decreased leptin levels in the 2nd trimester amniotic fluid of fetuses with Down's syndrome. This result suggests a possible role of leptin in the pathophysiology of Down's syndrome during the fetal period.

Topics: Adult; Amniocentesis; Amniotic Fluid; Down Syndrome; Female; Humans; Leptin; Pregnancy; Pregnancy Trimester, Second; Sensitivity and Specificity

To compare levels of leptin and other obesity-related hormones in prepubertal children with Down syndrome (DS), a population at high obesity risk, and those in unaffected siblings to better understand the pathophysiology of obesity in children with DS.. This was a cross-sectional study of 35 children with DS and 33 control siblings, ages 4 to 10 years, with a fasting blood sample and anthropometric measurements to estimate body composition. Generalized estimating equations were used to account for the lack of independence between siblings.. In addition to having higher body mass index and percent body fat, children with DS had higher leptin levels than unaffected siblings, even after adjustment for age, sex, race, and ethnicity (difference, 5.8 ng/mL; 95% CI, 2.4-9.3; P = .001) and further adjustment for percent body fat (difference, 2.7 ng/mL; 95% CI, 0.08-5.40, P = .04). Leptin and percent body fat were positively associated in both groups (P < .0001), but with a significantly greater positive association in the DS group, suggesting a significant effect modification (P < .0001).. This group of children with DS had increased leptin levels for percent body fat than their unaffected siblings. This difference may contribute to the increased risk for obesity in children with DS.

Topics: Biomarkers; Body Fat Distribution; Body Mass Index; Child; Child, Preschool; Cross-Sectional Studies; Down Syndrome; Female; Follow-Up Studies; Humans; Incidence; Leptin; Male; Obesity; Probability; Prospective Studies; Reference Values; Risk Assessment; Siblings

Leptin is a key regulator of satiety; and the serum concentration is considered to reflect nutritional status. Expressed predominantly by the adipocytes, leptin is also expressed in placenta, which is a major source of both leptin and the leptin receptor in pregnancy serum. As a placenta protein, leptin serum concentrations may be perturbed in Down syndrome (DS) pregnancies as seen for pregnancy-associated plasma protein-A (PAPP-A) and human chorionic gonadotrophin-beta (hCGbeta). We examined whether leptin is a maternal serum marker for foetal DS in the first trimester.. Serum samples from 44 pregnant women with a DS foetus, and 135 control pregnant women in week 8 to 14 had the leptin concentration determined by immunoassay and the concentrations were converted into multiples of the median (MoM) of controls based on log-regression analysis. The distributions of log10 MoM leptin was compared in DS and control pregnancies.. Serum leptin increased significantly with gestational age in controls (p = 0.02). The mean log10 MoM in controls was - 0.0486, with a median empirical MoM of 0.89, and - 0.0618, with a median empirical MoM of 0.80, in DS pregnancies. This difference was not significant. The log10 MoM leptin values in DS pregnancies did not change with gestational age (p = 0.32).. Leptin is not a first-trimester marker for foetal DS.

Topics: Biomarkers; Down Syndrome; Female; Humans; Leptin; Linear Models; Pregnancy; Pregnancy Trimester, First; Prenatal Diagnosis

Alterations in energy balance and feeding behavior and the subsequent high frequency of obesity are hallmarks of 2 chromosomal diseases: the Prader-Willi syndrome (PWS) and the Down syndrome (DS). Leptin, an important regulator of food intake and energy homeostasis, circulates in 2 forms: a free, therefore active, fraction and a fraction bound to the soluble leptin receptor, whose bioavailability consequently participates in the regulation of leptin action. To investigate the possible role of the free-bound leptin balance in the pathogenesis of obesity in PWS and DS, we enrolled 7 obese women with DS, 5 obese women with PWS, 7 obese women, and 7 normal-weight healthy control women. Basal hormonal concentrations, total and free leptin levels, and leptin receptors levels were measured in plasma samples obtained from the 4 groups. No significant differences were observed in the hormonal milieu. Women with DS exhibited lower total leptin concentrations (P<.01), comparable leptin receptor level and, therefore, lower free leptin values (P<.01) when compared with obese controls, then resembling the profile peculiar to normal-weight control women. At variance, subjects with PWS did not differ from obese controls regarding both leptin and leptin receptor levels. Our data suggest that, whereas subjects with PWS have a leptin assessment corresponding to their degree of obesity, subjects with DS may have a defect in the secretion of leptin that could at least partially account for this form of syndromal obesity.

Topics: Adult; Down Syndrome; Female; Hormones; Humans; Leptin; Obesity; Prader-Willi Syndrome; Radioimmunoassay; Receptors, Cell Surface; Receptors, Leptin

Although trisomy 21 (T21) is the most frequent genetic abnormality and some maternal serum markers for this fetoplacental aneuploidy are of placental origin, little is known of its impact on placental development. We therefore studied the influence of T21 on trophoblast behaviour. Using cultured cells from 46 human T21 pregnancies, we confirmed the defective morphological and functional differentiation of the villous cytotrophoblast in this setting; indeed, villous cytotrophoblast cells aggregate normally but fuse inefficiently to form the syncytiotrophoblast. This is in part related to the abnormal oxidative status of the T21 cytotrophoblast, characterized by a gene dosage-related increase in SOD-1 (copper-zinc superoxide dismutase) expression and activity. This was associated with a significant (P < 0.01) increase in catalase activity but no significant change in glutathione peroxidase activity. On the basis of these in vitro findings and studies of large panels of maternal serum, we propose a pathophysiological explanation for trisomy 21 maternal serum markers of placental origin.

Topics: Adult; Biomarkers; Catalase; Cell Aggregation; Cell Fusion; Cells, Cultured; Chorionic Gonadotropin, beta Subunit, Human; Chorionic Villi; Down Syndrome; Female; Glutathione Peroxidase; Humans; Leptin; Pregnancy; Superoxide Dismutase; Superoxide Dismutase-1; Trophoblasts

To evaluate plasma total, free (FL) and protein-bound (BL) leptin in children with Down's syndrome (DS) and different degrees of adiposity and its relationship with thyroid stimulating hormone (TSH), free thyroxine (FT(4)), and free triiodothyronine (FT(3)).. A total of 24 prepubertal clinically euthyroid DS children.. Plasma leptin, TSH, FT(4), and FT(3) concentrations were determined by immunometric/radioimmunologic assays. FL and BL were evaluated by fast protein liquid chromatography.. In DS children, leptin circulates in two fractions, corresponding to BL and FL. The amount of BL and FL is negatively and positively correlated to body mass index (BMI), respectively. Plasma leptin concentrations correlate with BMI, but not with TSH, FT(4), and FT(3).. In prepubertal DS children, leptin circulates as both BL and FL, correlates with adiposity and its concentration appears independent of thyroid function.

Topics: Adipose Tissue; Adolescent; Body Mass Index; Child; Child, Preschool; Down Syndrome; Female; Humans; Leptin; Male; Thyroid Gland; Thyrotropin; Thyroxine; Triiodothyronine

To assess the correlation of fetal and maternal plasma leptin concentrations during the second half of uncomplicated, euploid pregnancies and to compare these values with those obtained from pregnancies with Down syndrome.. Paired maternal venous and fetal umbilical blood samples were obtained during cordocentesis in 36 uncomplicated, euploid pregnancies and nine pregnancies with Down syndrome fetuses. Concentrations of leptin were measured by sensitive radioimmunoassay.. Among pregnancies with euploid fetuses, there was significant correlation between both fetal and maternal leptin levels and gestational age (r = 0.464, p = 0.005 and r = 0.629, p < 0.001, respectively). Fetal plasma leptin concentrations also correlated with maternal levels (r = 0.485, p = 0.003), but fetal levels were significantly lower than maternal values (mean 2.12 +/- 0.44 ng/ml vs. 17.79 +/- 5.48 ng/ml, respectively; p < 0.001). Down syndrome fetuses had significantly lower fetal plasma leptin levels than gestational age-matched control euploid fetuses (0.72 + 0.54 ng/ml vs. 2.12 + 0.44 ng/ml; p < 0.002). However, there was no difference in maternal leptin concentrations between euploid and Down syndrome pregnancies.. In euploid pregnancies, fetal leptin levels were significantly lower than the corresponding maternal values but increased across gestation. Down syndrome was associated with significantly lower fetal leptin levels.

Topics: Cordocentesis; Down Syndrome; Female; Fetal Blood; Gestational Age; Humans; Leptin; Pregnancy; Radioimmunoassay

Recent studies suggest that leptin, the product of the obese gene, is produced by the placenta during pregnancy. The present study addressed the question whether second trimester maternal serum leptin could be altered by fetal Down syndrome or Edwards syndrome. Maternal serum leptin concentrations were measured in 18 pregnancies complicated with Down syndrome, six pregnancies complicated with Edwards syndrome and 183 uncomplicated pregnancies during the second trimester of pregnancy. The present results demonstrate that leptin concentrations in uncomplicated pregnancies slightly decrease from the 16th week of pregnancy, reaching a minimum of 18.8 ng/ml around the 20th week, and then rapidly increase to 28.2 ng/ml by the 24th week. Leptin correlation with maternal body weight decreases from r=0.695 at 16-17 week of gestation to r=0.544 at >22 weeks of gestation. There was no significant difference between the mean MoMs of Down syndrome- (0.926) or Edwards syndrome- (0.960) affected pregnancies and normal pregnancies (1.002). A weak correlation (r=0.18, p<0.02) was observed between corrected leptin MoMs and human chorionic gonadotrophin (hCG) MoMs in normal pregnancies. It is assumed that around the 20th week of pregnancy placental leptin production is activated or at least is accelerated and it is added to the amount of leptin produced by maternal adipose tissue. Fetal Down syndrome or Edwards syndrome does not seem to alter maternal leptin concentration and therefore leptin cannot be used as a marker for these chromosomal abnormalities in the early second trimester of pregnancy.

Topics: Adult; Body Weight; Chorionic Gonadotropin; Chromosome Aberrations; Down Syndrome; Female; Humans; Leptin; Pregnancy; Pregnancy Trimester, Second

We have evaluated serum leptin concentrations in two forms of genetic obesity. The subjects examined were eight women with Down syndrome and eight women with Prader-Willi syndrome. All patients were in the reproductive age range and were obese (body mass index > or = 27 kg/m2). Plasma leptin values, analyzed as a function of body mass index showed a statistically significant correlation in both Prader-Willi (r = 0.985; p < 0.001) and Down syndrome patients (r = 0.943; p < 0.001). Obese Down syndrome women exhibited significantly lower leptin values (10.8 +/- 1.1) as compared to patients with Prader-Willi syndrome (31 +/- 2.6; p < 0.01). The linear correlation between leptin and insulin in the two groups of patients was not statistically significant. The data suggested that obesity in Prader-Willi subjects could be caused by failure of leptin to reach its target in the brain, as a consequence of defects in the receptor or in postreceptor processing, whereas data on obese patients with Down syndrome could be due to a different pathogenetic origin.

Topics: Adult; Androstenedione; Body Mass Index; Dehydroepiandrosterone; Down Syndrome; Estradiol; Female; Follicle Stimulating Hormone; Humans; Insulin; Insulin-Like Growth Factor I; Leptin; Luteinizing Hormone; Obesity; Prader-Willi Syndrome; Progesterone; Prolactin; Proteins; Radioimmunoassay; Testosterone