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Biomedical subjects

W Kiess

Publications and source records attributed to W Kiess.

At least 109 records · Page 6Linked to original sources
PubMed1999

Lipoprotein(a) levels in formerly small-for-gestational-age children.

Lipoprotein(a) (Lp(a)) is an independent and inherited risk factor for coronary artery disease. Concentrations of Lp(a) have been widely described in adolescents, but little is known about its concentration in children born small for gestational age (SGA). To assess the influence of intrauterine growth on Lp(a) levels we examined 50 children born SGA and 21 children born adequate for gestational age (AGA). Lp(a) blood levels (mean +/- SD) of the SGA children differed significantly (p < 0.05) from AGA children (22.3 +/- 22.1 vs. 10.9 +/- 7.6 mg/dl). 14 out of 50 adolescents of the SGA group but 1 out of 21 of the AGA group had elevated Lp(a) (>30 mg/dl) concentrations (p < 0.05). These children also had higher triglyceride (1.0 +/- 0.6 mmol/l vs. 0.74 +/- 0.38 mmol/l) levels (p < 0.05) compared to children with Lp(a) levels <30 mg/dl. Adolescents with Lp(a) levels >30 mg/dl showed a significant inverse relation between Lp(a) levels and gestational age (r = -0.68, p < 0. 005). We hypothesize that impairment of fetal growth might influence serum Lp(a) levels in later life.

Adolescent↗
PubMed1999

A role for leptin in sexual maturation and puberty?

Leptin, the ob gene product, is involved in the regulation of body weight in rodents, primates and humans. It provides a molecular basis for the lipostatic theory of the regulation of energy balance. White adipose tissue and placenta are the main sites of leptin synthesis. There is also evidence of ob gene expression in brown fat. Leptin seems to play a key role in the control of body fat stores by coordinated regulation of feeding behaviour, metabolic rate, autonomic nervous system regulation and body energy balance. Apart from the function of leptin in the central nervous system on the regulation of energy balance, it may well be one of the hormonal factors that signal to the brain the body's readiness for sexual maturation and reproduction. During late pregnancy and at birth when maternal fat stores have been developed, leptin levels are high. During these developmental stages leptin could be a messenger molecule signalling the adequacy of the fat stores for reproduction and maintenance of pregnancy. At later stages of gestation leptin could signal the expansion of fat stores in order to prepare the expectant mother for the energy requirements of full-term gestation, labour and lactation. Leptin serum concentrations change during pubertal development in rodents, primates and humans. In girls, leptin serum concentrations increase dramatically as pubertal development proceeds. The pubertal rise in leptin levels parallels the increase in body fat mass. In contrast, leptin levels increase shortly before and during the early stages of puberty in boys and decline thereafter. Testosterone has been found to suppress leptin synthesis by adipocytes both in vivo and in vitro. The decline of leptin levels in late puberty in boys accompanies increased androgen production during that time and most likely reflects suppression of leptin by testosterone and a decrease in fat mass and relative increase in muscle mass during late puberty in males. This overview focuses on those topics of leptin research which are of particular interest in reproductive and adolescent medicine.

Animals↗
PubMed1999

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.

Androstenedione↗
PubMed1998

Good growth despite very low levels of insulin-like growth factors.

UNLABELLED: A 12.5-year-old girl presented with short stature. Insulin-like growth factor 1(IGF-I) and insulin- like growth factor binding protein (IGFBP-3) were below the 0.1 percentile. Growth hormone provocation tests disclosed normal responses to L-arginine and insulin-induced hypoglycaemia. A huge benign mesenteric cyst was discovered by abdominal ultrasound and completely removed. Subsequently, the girl showed a marked catch-up growth; however, IGF-I and IGFBP-3 remained below the 0.1 percentile. CONCLUSION: These observations imply that growth may take place even with very low levels of insulin-like growth factors. The interpretation of low IGF-I and IGFBP-3 levels in short children still requires good clinical judgement and basic knowledge of their biological action.

Body Height↗
PubMed1998

Practical aspects of managing preschool children with type 1 diabetes.

Day-to-day variations in diet and physical exercise, large variations in the glucose response to small changes in insulin doses, and high insulin sensitivity are characteristic of preschool children with diabetes. Hence, difficulties in achieving adequate metabolic control and stable glycaemia in preschool children are common. In addition, hypoglycaemic episodes tend to be frequent and severe in this age group. Problems identifying and treating hypoglycaemia present an additional challenge for the diabetes team and for the family caring for the young child with diabetes. Specific glucose targets are provided for this age group: premeal levels of 6-12 mmoll(-1)(110-220 mg dl(-1)) with bedtime levels above 8 mmoll(-1)(140 mg dl(-1)). It is important to note that children who suffer severe hypoglycaemic events at a young age show evidence of subtle cognitive deficits when tested during adolescence. The question of whether or not the years before pubertal onset contribute less towards the development of diabetes-related microvascular complications than do the years starting with the onset of puberty remains controversial. Twice-daily or multiple insulin injections, dietary adjustments and considerations, home blood-glucose monitoring, family education, support groups and 24-h hotline information facilities can help to achieve good metabolic control without severe hypoglycaemia in the preschool child. In general, good metabolic control without severe hypoglycaemia can be achieved using frequent counselling and a caring team approach.

Aging↗
PubMed1998

Catch-up growth after childhood-onset substitution in primary hypothyroidism: is it a guide towards optimal growth hormone treatment in idiopathic growth hormone deficiency?

Catch-up growth was analyzed in 20 prepubertal children with primary hypothyroidism (PH) starting treatment at an age of 4.4 (1.2-10.1) years and a height (HT) SD score (HT SDS) of -3.1 (+/-0.8). All patients were followed for at least 3 prepubertal years. HT velocity was 12.3 +/- 2.3, 9.0 +/- 1.8 and 7.5 +/- 2.2 cm/year, and change in HT SDS was 1.60 +/- 0.56, 0.57 +/- 0.33 and 0.28 +/- 0.38 during the 1st, 2nd and 3rd year, respectively. The 11 children followed to adult height reached a HT SDS of -0.11 +/- 1.1, all within their target HT range. HT gain (DeltaHT SDS) during the 1st year was correlated with the degree of catch-up growth (r2 = 0.78, p < 0.001). While catch-up growth in childhood-onset PH is complete, this is not the case in GH deficiency (GHD). Based on the auxological characteristics of the patients with PH, HT velocities during the first 2 years were predicted applying prediction models devised for prepubertal children with idiopathic GHD. The modalities of GH treatment observed in the models were used to calculate predicted HT velocities of the PH patients. Observed HT velocities in PH were higher than predicted HT velocities during the 1st (10.67 +/- 1.37 cm/year, p < 0.01) and 2nd (8.35 +/- 0.86 cm/year, p = 0.128) year. The data show that catch-up potential in idiopathic GHD of childhood onset is reduced compared to PH. Since early catch-up as well as total HT recovery in children with GHD are often not reached by present treatment modalities, catch-up growth in PH may serve as a model towards optimizing GH treatment. The data suggest that initial GH doses of 1.0 IU/kg/week, rather than the presently recommended 0. 6 IU/kg/week, need to be given in GHD in order to achieve the degree of early catch-up observed in PH and to consequently improve the final outcome.

Body Height↗
PubMed1998

Longitudinal analysis of maternal serum leptin levels during pregnancy, at birth and up to six weeks after birth: relation to body mass index, skinfolds, sex steroids and umbilical cord blood leptin levels.

Leptin is an important regulator of body fat mass and energy expenditure during adult life. The mechanisms by which maternal and fetal weight are regulated during pregnancy are poorly understood. In order to gain more insight into a potential role of leptin during gestation, a prospective, longitudinal study was carried out to measure leptin concentrations in maternal serum of 29 healthy women during pregnancy up to 6 weeks after birth and also in umbilical cord blood of their newborns. Leptin concentrations were measured using a specific RIA. In addition, estradiol, testosterone, and sex hormone binding globulin were determined using commercially available RIAs. The mothers' skinfolds were determined at four sites using a Holtain caliper. Leptin levels increased continuously during pregnancy and reached 25.8 +/- 14.7 ng/ml at 38-40 weeks. At birth, leptin concentrations were 23.5 +/- 15.4 ng/ml. Three days after delivery a significant decrease of leptin levels to 10.6 +/- 6.0 ng/ml was observed. Six weeks after birth the leptin concentration in maternal serum was 13.8 +/- 8.6 ng/ml. At birth, maternal serum levels were significantly higher than levels in cord blood and did not correlate with leptin levels in cord blood or neonatal weight. Furthermore, leptin levels did not correlate with maternal sex steroids and sex hormone binding globulin levels. At 6-8 weeks of pregnancy, maternal leptin serum levels correlated significantly with BMI (r = 0.81). The correlation coefficients (leptin vs. BMI) dropped with increasing gestational age and at birth only a poor correlation persisted (r = 0.50). Six weeks after birth there was again a high correlation between leptin levels in maternal serum and BMI (r = 0.76). Subscapular skinfold thickness was correlated to leptin concentrations in maternal serum during the whole period of the investigation. In conclusion, maternal leptin levels continuously increased from 6-8 weeks up to 38-40 weeks of pregnancy. Maternal leptin levels decreased dramatically after birth. Six weeks after delivery, leptin levels were comparable to the values measured at the beginning of pregnancy. We hypothesize that leptin might play an important role during pregnancy and fetal development.

Adipose Tissue↗
PubMed1998

Improvements and new potentials in pharmacological therapy of diabetes mellitus in children and adolescents.

Subcutaneous insulin substitution is not physiological. Despite the many attempts using intensified insulin regimens to render current insulin substitution protocols more physiological, a nondiabetic circulating insulin profile cannot be simulated in patients with type 1 diabetes. Despite many efforts, the pharmacological treatment of type 1 diabetes consists of an unphysiological attempt to substitute only one of the hormones which are lost after beta-cell destruction, namely insulin. It is therefore mandatory to search for additional means to achieve physiological regulation of glucose homeostasis and overall metabolic status. Peptides which are being developed as additional new therapeutic compounds for type 1 diabetes include, for example, IGF-I, leptin, C-peptide and amylin. In addition, the application of insulin analogues has already been introduced into clinical practice. However, so far none of these pharmaceutical compounds has been shown to offer real clinical benefits and substantially improve metabolic control in patients with type 1 diabetes. The results of long-term clinical trials using the peptide compounds listed above for the treatment of type 1 diabetes are still not available.

Adolescent↗
PubMed1998

Development of a highly sensitive nonisotopic immunoassay for the determination of salivary 17-hydroxyprogesterone: reference ranges throughout childhood and adolescence.

A sensitive nonisotopic immunoassay for the determination of 17-hydroxyprogesterone (17-OHP) levels in saliva was developed. The new time-resolved fluorometric immunoassay employs a specific polyclonal anti-17-OHP antiserum immobilized onto microtiter plates, a 17-OHP-biotin conjugate as a tracer, and streptavidin-europium a as secondary probe. The lower detection limit of the assay is 23.6 pmol/L (mean -3 s of a 22-fold zero determination) corresponding to 0.39 pg/well. The coefficients of intraassay variation are 8.8, 5.3, and 8.3% at the respective concentrations of 90.9, 454.5, and 1363.5 pmol/L. The coefficients of interassay variation are 8.8, 5.3, and 8.3% at the respective concentrations. Saliva was collected in commercially available devices. Reference ranges were established using 394 saliva samples from 132 healthy children, adolescents, and adults. Morning, midday, and evening levels of 17-OHP levels in saliva varied significantly in all age groups with morning levels being higher than midday and evening levels. Saliva samples (n = 57) were also obtained from 18 children with congenital adrenal hyperplasia (CAH). Salivary 17-OHP levels in the limited number of CAH patients studied ranged from 121 to 106,050 pmol/L. In conclusion 1) a new, sensitive nonisotopic immunoassay for measurement of 17-OHP in saliva has been developed; 2) reference ranges for healthy children, adolescents, and adults have been established; 3) there is a circadian pattern of 17-OHP levels in saliva at all ages; and 4) measurement of 17-OHP in saliva should be further evaluated over a longer period of time as a potentially reliable and powerful technique to monitor metabolic control in patients with CAH. As 17-OHP levels in saliva are stable for > 10 wk at 4 degrees C, the technique is ideally suited for outpatient sampling.

17-alpha-Hydroxyprogesterone↗
PubMed1998

Hormonal control of programmed cell death/apoptosis.

Apoptosis or programmed cell death is a physiological form of cell death that occurs in embryonic development and during involution of organs. It is characterized by distinct biochemical and morphological changes such as DNA fragmentation, plasma membrane blebbing and cell volume shrinkage. Many hormones, cytokines and growth factors are known to act as general and/or tissue-specific survival factors preventing the onset of apoptosis. In addition, many hormones and growth factors are also capable of inducing or facilitating programmed cell death under physiological or pathological conditions, or both. Steroid hormones are potent regulators of apoptosis in steroid-dependent cell types and tissues such as the mammary gland, the prostate, the ovary and the testis. Growth factors such as epidermal growth factor, nerve growth factor, platelet-derived growth factor (PDGF) and insulin-like growth factor-I act as survival factors and inhibit apoptosis in a number of cell types such as haematopoietic cells, preovulatory follicles, the mammary gland, phaeochromocytoma cells and neurones. Conversely, apoptosis modulates the functioning and the functional integrity of many endocrine glands and of many cells that are capable of synthesizing and secreting hormones. In addition, exaggeration of the primarily natural process of apoptosis has a key role in the pathogenesis of diseases involving endocrine tissues. Most importantly, in autoimmune diseases such as autoimmune thyroid disease and type 1 diabetes mellitus, new data suggest that the immune system itself may not carry the final act of organ injury: rather, the target cells (i.e. thyrocytes and beta cells of the islets) commit suicide through apoptosis. The understanding of how hormones influence programmed cell death and, conversely, of how apoptosis affects endocrine glands, is central to further design strategies to prevent and treat diseases that affect endocrine tissues. This short review summarizes the available evidence showing where and how hormones control apoptosis and where and how programmed cell death exerts modulating effects upon hormonally active tissues.

Animals↗
PubMed1998

Serum leptin levels in children and adolescents with insulin-dependent diabetes mellitus in relation to metabolic control and body mass index.

The ob protein, termed leptin, is produced by adipocytes and is thought to act as an afferent satiety signal regulating weight through suppressing appetite and stimulating energy expenditure in humans and/or rodents. Insulin has been found to be a potent stimulator of leptin expression in rodents. It is unclear at present whether this insulin action is a direct or an indirect effect. To investigate whether leptin concentrations in children and adolescents with type 1 diabetes (IDDM) were related to metabolic status, body weight, body mass index and insulin treatment, we have measured leptin concentrations in serum from 13 newly diagnosed IDDM patients before the beginning of insulin treatment (8 girls, 5 boys, aged 4.7-17.5 years) and in 134 patients with IDDM during treatment (64 girls, 70 boys, aged 2.6-20.1 years) using a specific radioimmunoassay. The data from patients with diabetes were compared with normative data that were derived from a large cohort of healthy children and adolescents. Serum from children with newly diagnosed diabetes had significantly lower levels of leptin (mean 1.28+/-1.60 ng/ml, range 0.14-6.13 ng/ml) compared with healthy children (n=710) (mean 2.2 ng/ml, range 0.26-14.4ng/ml) and compared with insulin-treated children and adolescents (mean 5.18+/-5.48 ng/ml, range 0.26-29.77 ng/ml) (P<0.0001) even after adjustment for gender and body mass index (BMI). Serum leptin levels in patients with IDDM were significantly correlated with BMI (r=0.42, P<0.0001). Multiple regression analysis showed that age and BMI were significantly correlated with leptin levels, while duration of diabetes, mean HbA1c levels, insulin dose and plasma glucose, triglyceride and cholesterol levels were not. Females had higher serum leptin concentrations than males even when adjusted for BMI (P<0.0001). Surprisingly and most importantly, leptin levels in insulin-treated young adult (Tanner stage 5) patients were significantly higher than values found in the healthy nondiabetic reference population when adjusted for sex, Tanner stage and BMI. These findings suggest that leptin levels in IDDM patients show a similar dependency on adipose tissue and age as in healthy, normal children. The data provide evidence that insulin may be of importance as a regulator of serum leptin levels in vivo not only in rodents but also in humans. It is hypothesized that the elevated BMI-adjusted leptin levels in adolescents with IDDM could indicate either that these patients may be oversubstituted by the intensified insulin therapy that they are receiving or that their body composition and body fat content may differ from that of healthy adolescents in the sense that they have a relative increase in fat mass.

Adolescent↗