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Neuropeptide Y (NPY) and peptide YY (PYY) are involved in metabolic regulation. The purpose of the study was to assess the serum levels of NPY and PYY in adolescents with anorexia nervosa (AN) or obesity (OB), as well as in a healthy control group (CG). The effects of potential confounders on their concentrations were also analysed. Eighty-nine adolescents were included in this study (AN = 30, OB = 30, and CG = 29). Anthropometric measurements and psychometric assessment of depressive symptoms, eating behaviours, body attitudes, and fasting serum levels of NPY and PYY were analysed. The AN group presented severe depressive symptoms, while the OB group held different attitudes towards the body. The levels of NPY were lower in the AN and OB groups as compared with the CG. The PYY levels were higher in the OB group than in the AN group and the CG. The severity of eating disorder symptoms predicted fasting serum concentrations of NPY. Lower levels of NPY in AN, as well as in OB suggests the need to look for a common link in the mechanism of this effect. Higher level of PYY in OB may be important in explaining complex etiopathogenesis of the disease. The psychopathological symptoms may have an influence on the neurohormones regulating metabolism.

BACKGROUND Youth with type 1 diabetes (T1D) (16-18 y.o.) present worst disease control of all age groups and need structured interventions. Those should be based on unbiased, national-scale outcomes, which have not yet been successfully assessed in Poland. OBJECTIVE To evaluate the glycemic control in young patients with T1D in Poland. METHOD All pediatric diabetes care centers and the nine largest centers for adults with T1D were invited to this cross-sectional study, conducted in March 2018. Eligibility was defined as age ≤ 30 years and diabetes duration ≥1 year. Blinded samples of capillary blood and clinical questionnaires were sent to coordinating center, where HbA1c was measured by high-pressure liquid chromatography. RESULTS Nine adult and 25/28 pediatric centers participated, providing data for 1255 patients (50.8% males), mean age 12.3 years (95%CI:12.1-12.6) for children and 23.2 years (22.9-23.6) for adults; mean diabetes duration 7.1 years (6.8-7.3). This covered ~8% of pediatric population and 2% of 18-30-years-olds with T1D. Mean HbA1c was comparable between children and adults (57 mmol/mol [7.4%], 95%CI:56-57 mmol/mol [7.3-7.4%] vs. 57 mmol/mol [7.4%], 95%CI:56-60 mmol/mol [7.3-7.6%], p = 0.1870). Overall, 45.2% of patients achieved ISPAD target (

The aim of the study was to investigate factors related to the occurrence of nighttime hypoglycemia after a football tournament in children with type 1 diabetes mellitus. The multicenter study (GoalDiab study) included 189 children and adolescents with type 1 diabetes mellitus, from 11 diabetes care centers in Poland. Hypoglycemia was defined according to the International Hypoglycemia Study Group Statement. We analyzed the data of 95 participants with completed protocols with regards to nighttime hypoglycemia (82% male), aged 11.6 (9.8–14.2) years, diabetes duration 5.0 (2.0–8.0) years. There were 47 episodes of nighttime Level 1 hypoglycemia (≤3.9 mmol/L). Occurrence of clinically important Level 2 hypoglycemia (

Type 1 diabetes (T1D) is an autoimmune disorder caused by the T-cell mediated destruction of the insulin-producing pancreatic beta cells. T1D is a consequence of complex processes, influenced by genetic, epigenetic and environmental factors. MicroRNAs (miRNAs) are small non-coding RNAs that target multiple mRNAs and regulate gene expression. The implication of miRNAs in T1D pathogenesis, as potential modulators of immune response genes, remains poorly defined. The aim of this study was to investigate the expression profile of miRNAs in new onset T1D and the impact of deregulated miRNAs on target genes.Total RNA from peripheral blood mononuclear cells of newly diagnosed T1D pediatric patients and age-matched controls was screened for disease-associated miRNAs by a microarray analysis, with subsequent validation by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). miRNA targets were identified by luciferase reporter assays.The microarray analysis revealed 91 deregulated miRNAs (P 0.05) in T1D group compared to non-diabetic controls. Within this group we observed one upregulated and seven downregulated miRNAs with fold change2.0. qRT-PCR validation revealed overexpression of miR-487a-3p which has not been previously reported in the context of T1D. Luciferase reporter assays indicated CTLA4 and FOXO3 genes as miR-487a-3p targets.Our study suggests that miR-487a-3p might repress CTLA4 and FOXO3 by binding to their 3'UTRs and contribute to the development of T1D.

Aims To assess the prevalence of ZnT8-ab and its correlation to other autoimmune markers and diabetic ketoacidosis occurrence in children and adults with T1DM onset. Methods The study included 367 patients (218 children; 149 adults) at the T1DM onset. Selected diabetes-related autoantibodies such as GAD-ab, IA2-ab, ZnT8-ab were tested before the initiation of insulin therapy. Diabetic ketoacidosis was defined as glucose concentration > 13.9 mmol/l, pH

Prader-Willi Syndrome is a genetic condition caused by an abnormality of chromosome 15, mostly resulting from a deletion.The prevalence of syndrome in Europe has been reported between 1 in 8,000 to 1 in 45,000 births. Characteristic features of the syndrome include hypotonia, short stature, psychomotor development delay, hypogonadism and progressive, life-threatening obesity. Treatment of Prader-Willi Syndrome consists of intensive rehabilitation, psychologicalcare, speech therapy and also, if patient is fulfilling appropriate criteria, growth hormone treatment. An extremely important element of therapy is also properly planned and implemented nutritional management. Adequate diet prevents the malnutrition in the first stage of life and the development of excessive weight in subsequent years. The aim of this article is to provide practical and accurate guidance on nutritional management and diet therapy for physicians and nutritionists who work with children, adolescents and adults with Prader-Willi Syndrome.Zespół Pradera-Williego to choroba uwarunkowana genetycznie, spowodowana nieprawidłowością w obrębie chromosomu 15, najczęściej wynikająca z delecji w chromosomie ojca. Zespół ujawnia się na terenie Europy z różną częstotliwością od 1:8000 do 1:45000 urodzeń. Charakterystyczne cechy zespołu to hipotonia w pierwszym okresie życia, niskorosłość, opóźnienie w rozwoju psychoruchowym, hipogonadyzm i postępująca, zagrażająca życiu otyłość. Leczenie zespołu Pradera-Williego składa się z intensywnej rehabilitacji od pierwszych dni życia, opieki logopedy i psychologa, a także, po spełnieniu odpowiednich kryteriów, leczenia hormonem wzrostu. Niezmiernie istotnym elementem terapii jest również odpowiednio zaplanowane i wdrożone postępowanie dietetyczne. Ma ono na celu niedopuszczenie do rozwoju niedożywienia w pierwszym okresie życia, a następnie zapobieganie rozwojowi nadmiernej masy ciała w latach kolejnych. Artykuł porusza zagadnienia postępowania dietetycznego oraz terapii żywieniowej na każdym etapie życia pacjentów z zespołem Pradera-Williego, z uwzględnieniem stanów niedożywienia, prawidłowej wagi oraz nadmiernej masy ciała u tych pacjentów.

Purpose Leptin and adiponectin are adipokines presenting a wide range of impacts, including glycemic balance regulations. Insulin is one of the main regulators of adipose tissue function. In type 1 diabetes mellitus (T1DM) endogenous insulin secretion is replaced by the exogenous supply, which is not regulated naturally. The aim of the study was to establish serum leptin and adiponectin levels, and their relations to body fat mass and disease course in children with T1DM. Material/methods The study included 75 children with T1DM and the control group of 20 healthy coevals. All children had estimated serum leptin and adiponectin concentrations, lipid profile, and bioelectrical impedance analysis. Results Serum leptin concentrations in children with T1DM were not significantly different from the control group ( p = 0.067, mean values ± SD: 3.11 ± 2.98 vs. 5.29 ± 5.06 μg/l, respectively), and related positively to body fat mass in both groups. Adiponectin serum concentrations were significantly higher in children with T1DM than in the control group ( p vs. 12.10 ± 5.53 μg/ml, respectively), and were not related to the body fat content in the study group. Both, leptin and adiponectin, showed no relation to any of the analyzed parameters of the disease course. Conclusions Differences observed between children with T1DM and their healthy coevals, when similar in terms of age, body weight, and body fat mass, seem not to depend directly on the disease duration, its metabolic control or insulin supply.

Purpose: To assess glycemic control and safety of children and adolescents with type 1 diabetes participating in a 2-day football tournament. Methods: In total, 189 children with type 1 diabetes from 11 diabetes care centers, in Poland, participated in a football tournament in 3 age categories: 7–9 (21.2%), 10–13 (42.9%), and 14–17 (36%) years. Participants were qualified and organized in 23 football teams, played 4 to 6 matches of 30 minutes, and were supervised by a medical team. Data on insulin dose and glycemia were downloaded from personal pumps, glucose meters, continuous glucose monitoring, and flash glucose monitoring systems. Results: The median level of blood glucose before the matches was 6.78 (4.89–9.39) mmol/L, and after the matches, it was 7.39 (5.5–9.87) mmol/L (P = .001). There were no episodes of severe hypoglycemia or ketoacidosis. The number of episodes of low glucose value (blood glucose ≤3.9 mmol/L) was higher during the tournament versus 30 days before: 1.2 (0–1.5) versus 0.7 (0.3–1.1) event/person/day, P P Conclusions: Large football tournaments can be organized safely for children with type 1 diabetes. For the majority of children, moderate mixed aerobic–anaerobic effort did not adversely affect glycemic results and metabolic safety.

IFIH1 (Interferon Induced with Helicase C domain 1) gene encodes a sensor of double-stranded RNA, which initiates antiviral activity. Recent studies have indicated the association of rare and common IFIH1 variants with type 1 diabetes mellitus (T1D). The aim of this study was to investigate whether polymorphisms in the IFIH1 locus are a risk factor for T1D in Caucasian patients from Poland.We genotyped 514 T1D patients and 713 healthy control individuals for rs3747517, rs1990760, rs2111485 and rs13422767 variants. Cumulative genetic risk score (CGRS) was calculated using unweighted and weighted approaches. We also examined the expression of IFIH1 gene in a cohort of 90 T1D patients.All studied polymorphisms showed significant association with type 1 diabetes. The risk alleles G of rs3747517, rs2111485, rs13422767 and A of rs1990760 were observed more frequently in T1D group with P values and allelic odds ratio OR (95%CI)0.0001, 1.742 (1.428-2.126); 0.001, 1.336 (1.125-1.588);0.0001, 1.799 (1.416-2.285); 0.0005, 1.359 (1.144-1.616), respectively. The risk for type 1 diabetes increased with the growing number of the risk alleles. OR (95%CI) for carriers of ≥ 6 risk alleles reached 2.387 (1.552-3.670) for unweighted CGRS and 3.132 (1.928-5.089) for weighted CGRS. Furthermore, IFIH1 gene expression levels in unstimulated peripheral blood mononuclear cells of T1D patients were significantly higher compared to healthy individuals (mean ± SEM mRNA copy number 163.8 ± 15.7 vs. 117.8 ± 7.2; P = 0.046).This study confirms the association of the IFIH1 locus with susceptibility to T1D in the Polish population. The cumulative effect of rs3747517, rs1990760, rs2111485 and rs13422767 variants on type 1 diabetes risk was observed.

Summary Objective Since metabolic syndrome shares several clinical features with hypercortisolism, it was hypothesised that genes altering individual glucocorticoid (GC) sensitivity might be implicated in pathogenesis of obesity and its adverse outcomes. FKBP5 gene encodes a chaperon protein in the GC receptor (GR) complex, which modulates steroid action upon target genes. Its functional variant, rs1360780, may enhance FKBP5 gene transcription, affect GR signalling and thereby influence the hypothalamo–pituitary–adrenal axis. We investigated the association of rs1360780 with obesity and metabolic characteristics in 250 obese children and adolescents (mean age 12.3±3.6years, BMI ≥95th percentile). Methods Anthropometric measurements, body composition, biochemical and hormonal results were analysed. Genotyping of rs1360780 was compared with 568 lean controls. Results Impaired fasting glucose was present in 8.8%, glucose intolerance in 10.4%, diabetes in 2.8% and dyslipidemia in 28.8% obese individuals. Hypertension was diagnosed in 34 out of 143 patients. No difference was found in FKBP5 polymorphism distribution between subjects with obesity and controls ( p >0.05). Stratification by rs1360780 revealed no differences in body mass and composition. However, carriers of the minor allele displayed enhanced insulin resistance ( p =0.009) and elevated serum triglyceride ( p =0.006), whereas cholesterol, HbA1c, and oral glucose challenge results were similar for all genotypes. Morning ACTH and cortisol did not differ but evening cortisol was higher in minor allele carriers ( p =0.039), although this association was lost in logistic regression analysis. Conclusion This study does not support the association of FKBP5 with obesity but demonstrates plausible implication of its variant in susceptibility to obesity-related insulin resistance and hypertriglyceridemia.

Insulin is one of the major factors regulating adipose tissue function. On the other hand, adipocytes secrete adipocytokines that may influence insulin synthesis and action, and are involved in blood glucose regulation. In type 1 diabetes mellitus (t1DM), beta cells function is replaced with exogenous insulin therapy. This raises a question concerning the impact of t1DM on adipose tissue secretory function. The aim of this study was to evaluate one of the adipocytokines, resistin, serum concentrations in relation to body fat mass in children with t1DM.The study comprised 75 children with t1DM and a control group of 20 healthy coevals. All children had estimated serum resistin concentrations, glycated haemoglobin levels, growth and body weight measurements, and bioelectrical impedance analysis in order to establish body composition.Resistin serum concentrations were significantly lower in children with t1DM vs. controls (median values: 343 vs. 590 pg/mL; mean values ± SD: 577 ± 561 vs. 861 ± 628 pg/mL; p0.001), and they negatively correlated with body fat mass (p = 0.022) and age (p = 0.022) in the t1DM group, but not in the control group. Disease duration, glycated haemoglobin levels and insulin dosage revealed no direct statistical relation to resistin levels.Diminished serum resistin concentrations and a negative correlation between resistin levels and body fat mass in children with type 1 diabetes seem to result from broken physiological adipo-insular regulations, independent of disease duration, its metabolic control and insulin supply.

The aim of this study was to evaluate serum levels and urinary excretion of neutrophil-gelatinase associated lipocalin (respectively sNGAL and uNGAL) and urinary excretion of Cathepsin L (uCathL) in children with type 1 diabetes mellitus (DM1) who presented normoalbuminuria and the estimated glomerular filtration rate (eGFR) above 90 mL/min/1.73 m2.The study group consisted of 63 children with a diabetes duration of 5.16 ± 3.39 years. The degree of albuminuria was based on urine albumin-to-creatinine ratio (ACR), while eGFR was based on serum cystatin C. Glomerular hyperfiltration (GH) was defined as an eGFR value above 135 mL/min/1.73 m2.Children with DM1 showed significantly higher concentrations of uNGAL, and lower sNGAL and uCathL. Significant changes of uNGAL and uCathL levels were even found in children without GH and with optimal glycaemic control (HbA1c7.5%). Positive correlations between uNGAL, ACR and eGFR were shown, as well as between uCathL and eGFR.Significant changes in the concentration of markers of early kidney injury: sNGAL, uNGAL, and uCathL, can occur in children with DM1 and normoalbuminuria. The changes of uNGAL and uCathL can be even found in children without GH and with optimal glycaemic control. The earliest signs of diabetic kidney dysfunction seem to result from tubular damage.

In recent years researchers have become increasingly interested in the particular relation between the function of the thyroid gland and the body mass in the population of obese children. Numerous studies have been conducted and the literature on the related issues has been abounding. Several thereof have strived at pinpointing a significant link between the function of the thyroid axis and the body mass. Yet, it still remains to be clarified whether these subtle changes in the level of thyroid hormones and TSH observed in childhood obesity are responsible for the increased body mass or rather they represent a secondary phenomenon. The mechanism most often put forward by the researchers that links obesity to thyroid function is the increased level of leptin, which affects neurones in the hypothalamus and the thyroid axis causing TRH and TSH secretion. The body mass is positively correlated with serum leptin and elevated level of leptin is connected with an increase in TSH level. However, there is still controversy whether these inconspicuous differences observed in thyroid axis merit the treatment with thyroxine since these changes seem to constitute a consequence rather than a cause of obesity. Therefore, as most authors postulate, primary importance should be placed on lifestyle changes and body weight reduction leaving substitutive treatment as a supplementary option. The purpose of this review is to present the most current issues on child obesity and the related malfunction of the thyroid axis through an overview of international publications from the years 1996-2011.

A clinical criterion of the Wolfram syndrome is the coexistence of diabetes and optic atrophy recognized before the age of 15. Diabetes present in Wolfram syndrome is a result of the selective β cell loss and failed insulin secretion which is probably associated with non-autoimmune pathogenesis.The aim of the study was an evaluation of HLA subtypes and presence of β-cell autoantibodies in patients with molecularly confirmed Wolfram syndrome.9 patients with Wolfram syndrome aged 10-24 years were examined. We also studied 218 patients with type 1 diabetes as a reference group. A control group of 176 healthy individuals was included in the study. Besides the clinical assessment the HLA typing by PCR-SSO was performed. Islet cell antibodies (ICA), antibodies to glutamic acid decarboxylase (GADA), thyrosine phosphatase antibodies (IA2A) and insulin antibodies (IAA) were also detected.In all nine patients the coexistence of diabetes with optic atrophy was observed and in 8/9 individuals additional symptoms were recognized. In patients with Wolfram syndrome a significantly lower age of diagnosis of diabetes (Me=5.0 years) than in type 1 diabetic children (Me=10.4; p=0.002) was observed. Studies of HLA subtypes demonstrated an increased prevalence of HLA-DQw1, DRB1⋅03 and/or 04 and DR2. A comparison of the frequency of the HLA alleles in patients with Wolfram syndrome with type 1 diabetic children showed a more frequent presence of the DRB1⋅1501 (p=0.03; OR=13.28 (2.44-72.12)) and DQB1⋅06 (p=0.016; OR=10.15 (2.49-41.35)) alleles in patients with Wolfram syndrome.Polish patients with Wolfram syndrome have a different profile of the HLA antigens with the presence of DR2, DQw1 and DRB3/4 allele and are negative for diabetes-related autoantibodies, which may confirm non-autoimmune β-cell destruction in this syndrome.

Clinically detectable diabetic nephropathy (DN) begins with the development of microalbuminuria (MA). However, early renal dysfunction may be overlooked despite using that method. On the other hand, the gold standard in DN detection-that is, renal biopsy-is highly invasive. The aim of this study was to evaluate the level of neutrophil-gelatinase-associated lipocalin (NGAL) and interleukin (IL)-18 and their relations to albumin excretion rate (AER) in children with normal-range albuminuria, e.g. in those considered as not presenting diabetic nephropathy. The study group consisted of 22 children (age 12.7 +/- 3.5 years) with type 1 diabetes mellitus (T1DM). Long-term glycemic control was assessed on hemoglobin A1c (HbA1c) levels (8.52 +/- 1.78%). All patients presented normal estimated glomerular filtration rate (eGFR) (141 +/- 23 ml/min/1.73 m(2)) and normal urinary albumin excretion (13.09 +/- 7.63 mg/24 h). Fourteen healthy children served as a control group. Children with T1DM showed increased NGAL values with respect to controls-interestingly, both in serum (sNGAL) (867.43 +/- 341.98 vs. 655.29 +/- 196.17 ng/ml; p = 0.04) and in urine (uNGAL) (420.04 +/- 374.16 vs. 156.53 +/- 185.18 ng/ml, p = 0.04). IL-18 levels were not different in both groups both in serum (58.52 +/- 20.11 vs. 69.79 +/- 58.76 ng/ml; NS) and in urine (14.53 +/- 12.74 vs. 14.60 +/- 10.92 ng/ml; NS). Despite the relatively small study group, the positive correlation between sNGAL and AER was found [AER (mg/24 h) = 3.1893 + 0.01141 x sNGAL (ng/ml); r = 0.51; p = 0.014] as well as between uNGAL and AER [AER (mg/24 h) = 8.7538 + 0.01032 x uNGAL (ng/ml); r = 0.51; p = 0.016]. No relationship between sNGAL and uNGAL, and GFR and HbA1c were found. Normal-range albuminuria does not exclude diabetic nephropathy defined as increased sNGAL and uNGAL concentration. NGAL measurement can be more sensitive than MA and may become a useful tool for evaluating renal involvement in diabetic children.

The epidemic of obesity concerns also children and adolescents. Excess weight increases the risk of metabolic complications, diabetes type 2, hypertension, cardiovascular disease, pulmonary and musculoskeletal disorders, psychosocial problems. Simple obesity leads to secondary endocrine disturbances. Long lasting insulin resistance and proinflammatory state induced by cytokines, which are produced in adipose tissue, play the main role in the development of obesity associated complications. Many disturbances can be reversed at the early stage, if even small weight loss is achieved.

The predisposing role to human obesity of the MC3R gene polymorphism is controversial. In this report we present the first study focused on the search for the MC3R polymorphism in the Polish population. Altogether 257 obese children and adolescents (RBMI>120) and 94 adults, who were never obese or overweight (BMIIle) and two rare mutations (257Arg>Ser and 335Ile>Ser) were identified. The common polymorphism was widely distributed in the obese and control cohorts, while the mutations were identified in four obese subjects only. In case of the 335Ile>Ser substitution a three-generation family, consisting of 20 members, was also analyzed. It was found that all carriers of the 335Ser mutation were obese, but among non-carriers obese subjects also were found. Our study suggests that the predisposing effect to obesity of the 81Ile polymorphic variant is rather unlikely. With regard to the studied rare mutations we suggest that the 335Ser allele may have a small predisposing effect. Electronic supplementary material The online version of this article (doi:10.1007/s11033-013-2808-8) contains supplementary material, which is available to authorized users.

Genes encoding adipokines are considered as candidates for human obesity. In this study we analyzed the expression of leptin (LEP) and adiponectin (ADIPOQ) genes in relation to common 5′-flanking or 5′UTR variants: -2548G>A (LEP), 19A>G (LEP) and -11377C>G (ADIPOQ) in Polish obese children and adolescents. Relative transcription levels in the subcutaneous adipose tissue (real time RT–PCR) and serum protein concentrations (RIA) were measured in 48 obese subjects with known genotypes at three polymorphic sites and in five non-obese controls. None of the studied polymorphisms altered significantly the expression. Significantly elevated relative transcription levels of the LEP gene (P