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Background Diabetic ketoacidosis (DKA) and hyperglycaemia without ketoacidosis are common acute complications of diabetes. Their association with acute kidney injury (AKI) and diabetic kidney disease (DKD) was studied. Methods The study group consisted of 197 children with type 1 diabetes with average diabetes duration of 8.08 ± 2.32 years. The medical history of the patients was retrospectively reviewed. The number of children with severe hyperglycaemia, DKA and AKI was assessed. The association with the risk of chronic kidney disease (CKD) was analysed. Results AKI was found in 14% of cases hospitalised for DKA and 8% of cases hospitalised for hyperglycaemia. Patients with AKI showed a significantly increased corrected sodium (141.23 ± 5.09 mmol/L, p = 0.035). Patients with AKI in DKA showed a significant increase in WBC (20.73 ± 8.71 × 103/µL, p = 0.0009). Follow-up analysis after a minimum of 5 years of diabetes revealed that a single episode of DKA was found in 63 patients and a single episode of AKI in 18 patients. Two or more episodes of DKA were found in 18 patients, and nine cases were complicated by AKI. These patients showed a significant increase in urinary albumin excretion (44.20 ± 64.21 mg/24 h), the highest values of eGFR and the worst glycaemic control. Conclusions Diabetic children can develop AKI in the course of DKA and hyperglycaemia without ketoacidosis, which is associated with volume depletion and reflected by corrected sodium concentration. AKI in DKA seems to be complicated by stress and inflammation activation. AKI and poor glycaemic control with repeated DKA episodes can magnify the risk of progression to DKD. Graphical abstract

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 (

Background. Diabetic ketoacidosis (DKA) is a life- -threatening condition frequently present at type 1 diabetes diagnosis (T1D). Younger children are at greater risk of developing this acute complication. It is alarming due to worldwide rise in T1D incidence with the greatest increase in children aged 28 days) (p = 0.014) and diabetes misdiagnosis (p = 0.001). Autoantibody against zinc transporter 8 was detected significantly more often in children with DKA (p = 0.044). In the group with DKA, glycated hemoglobin level was significantly higher (p = 0.0004), while insulin and C-peptide levels were lower (p = 0.0001 and p = 0.0001, respectively). Conclusions. The prevalence of DKA is high and its se­verity is substantial in children with newly diagnosed T1D from Wielkopolska province. Diabetes misdiag­nosis, symptoms’ duration and age under 4 years are the most common risk factors of DKA development at T1D onset. Autoantibody against zinc transporter 8 is associated with acute T1D onset.

Diabetes mellitus (DM) is due to either defects in not producing enough insulin by the pancreatic -cells, or defects in insulin action on peripheral tissues. Type 1 diabetes (T1D) is the most common type in childhood, resulted from the autoimmunity directed at the pancre-atic -cells. T1D classically presents in lean children with an acute onset of polyuria, polydipsia, weight loss. We describe the case of a 14-year-old girl with acute onset of DM complicated with diabetic ketoacidosis, appendicitis and pancreatitis which was suspected of having T1D. However, regardless a suggestive patient's phenotype at the disease onset tentative diagnosis of T1D was not confirmed. The case report shows that the overlap of the clinical phenotypes of diabetes displays the diversity of diabetes in young population. Then, diagnostic process must be carefully planned to exclude other diabetes forms and accurately ascertain childhood diabetes type.Cukrzyca wynika z defektu produkcji insuliny przez komórki  trzustki lub niewystarczającego jej działania na tkanki obwodowe. Cu-krzyca typu 1 jest najczęstszym typem występującym u dzieci i wynika z autoimmunizacji skierowanej przeciwko komórkom  trzustki. Cukrzyca typu 1 klasycznie występuje u szczupłych osób i charakteryzuje się z ostrym początkiem objawów, takich jak: wielomocz, polidypsja, utrata masy ciała. W pracy opisano przypadek 14-letniej dziewczynki z ostrym początkiem cukrzycy powikłanej cukrzycową kwasicą ketonową, zapaleniem wyrostka robaczkowego oraz zapaleniem trzustki, początkowo podejrzewanej o rozwój cukrzycy typu 1. Jednakże, niezależnie od fenotypu prezentowanego przez dziewczynkę na początku choroby, wstępne rozpoznanie cukrzycy typu 1 nie zostało potwierdzone. Opis przypadku pokazuje, że nakładanie się fenotypów klinicznych cukrzycy wskazuje na różnorodność cukrzy-cy u dzieci. Dlatego proces diagnostyczny powinien być szczegółowo zaplanowany, aby wykluczyć inne rodzaje cukrzycy oraz dokład-nie ustalić jej typ.

Introduction. MicroRNAs (miRNAs) are small noncoding RNA regulating gene expression at the posttranscriptional level. miRNAs have emerged as an important regulators of central and peripheral immune tolerance, therefore study the RNA molecules in the context of type 1 diabetes (T1D) pathogenesis is an important issue. The aim of this study was to investigate miR-652-5p expression level in the new onset T1D and an impact on ADAR and MARCH5, potential target genes. Material and methods. The miR-652-5p expression was investigated in the peripheral blood mononuclear cell of newly diagnosed T1D pediatric patients (n = 28) and age-matched controls (n = 28) by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). miRNA targets were analyzed by luciferase reporter assays. Results. Expression analysis revealed upregulation of miR-652-5p in T1D group compared to non-diabetic controls (p Conclusion. Our study revealed miR-652-5p as potential marker of new onset type 1 diabetes.

Aim Monogenic diabetes (MD) represents 5-7% of antibody-negative diabetes cases and is a heterogeneous group of disorders. Methods We used targeted next-generation sequencing (NGS) on Illumina NextSeq 550 platform involving the SureSelect assay to perform genetic and clinical characteristics of a study group of 684 individuals, including 542 patients referred from 12 Polish Diabetes Centers with suspected MD diagnosed between December 2016 and December 2019 and their 142 family members (FM). Results In 198 probands (36.5%) and 66 FM (46.5%) heterozygous causative variants were confirmed in 11 different MD-related genes, including 31 novel mutations, with the highest number in the GCK gene (206/264), 22/264 in the HNF1A gene and 8/264 in the KCNJ11 gene. Of the 183 probands with MODY1-5 diabetes, 48.6% of them were diagnosed at the pre-diabetes stage and most of them (68.7%) were on diet only at the time of genetic diagnosis, while 31.3% were additionally treated with oral hypoglycaemic drugs and/or insulin. Conclusions In summary, the results obtained confirm the efficacy of targeted NGS method in the molecular diagnosis of patients with suspected MD and broaden the spectrum of new causal variants, while updating our knowledge of the clinical features of patients defined as having MD.

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

Introduction. Obesity and its related disorders, clustered into metabolic syndrome (MetS), are increasingly diagnosed in children and adolescents. Clinical features, which define MetS are also encountered in patients with glucocorticoid excess. Since no evident hypercortisolaemia was detected in obesity and MetS, investigations turned to the local modulators of cortisol action. 11b-hydroxysteroid dehydrogenase type 1, encoded by HSD11B1 gene, controls tissue availability of cortisol by its regeneration from inert cortisone. Changes in HSD11B1 expression and enzyme activity may be influenced by its sequence variants and seem implicated in MetS pathogenesis. Our study was designed to evaluate plausible association of the HSD11B1 polymorphisms with early-onset obesity and features of MetS in Polish children and adolescents. Material and methods. The study comprised of 258 obese children (136 females), aged 12.3 ± 3.6 years, with excessive body mass lasting 7.1 ± 3.8 years. Anthropometric and blood pressure measurements, baseline biochemical analyses and oral glucose tolerance test were performed in all participants. Genotyp­ing of the HSD11B1 variants rs12086634, rs846910, rs4844880, and rs3753519 was conducted in obese youth and compared with 568 lean blood donors. Results. Mean relative body mass index in obese cohort was 164.7 ± 27.1%. Hypertension was detected in 12.4%, impaired fasting glucose in 8.9%, impaired glucose tolerance in 10.8%, diabetes in 2.7%, and dyslipidemia in 31.4% children and adolescents. None of the studied HSD11B1 polymorphisms displayed significant difference in frequency between obese and lean individuals. MetS was diagnosed in 27.6% of 203 patients with obesity aged 10–18 years. Further genotype-stratified analyses of relationship between HSD11B1 variants and particular features of MetS did not confirm increased susceptibility to develop early-onset hyperglycaemia, dyslipidaemia and hypertension in carriers of specific genotypes at rs4844880, rs846910, rs3753519, and rs12086634 (p ≥ 0.05 in all tests). Conclusion. Our study does not support the implication of the HSD11B1 polymorphisms in early-onset obesity and other features of MetS.

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: 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.

Introduction: 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. Material and methods: 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. Results: 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; p < 0.001), 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. Conclusions: 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. (Endokrynol Pol 2014; 65 (5): 342–347)

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.

Monogenic diabetes results from one or more mutations in a single gene. It is a relatively rare genetic condition, therefore, it was frequently unappreciated among clinicians. Consequently, monogenic diabetes is misdiagnosed as type 1 diabetes or type 2 diabetes. Such misclassification leads to an inappropriate treatment, often inconvenient for the patients, such as insulin injections with their permanent glycemic control. The correct diagnosis may completely change previous methods of treatment. Patients diagnosed with GCK mutations may be completely treated with adequate diet. HNF1A/HNF4A affected patients are extremely sensitive to low dose sulphonylureas. Moreover, the exact diagnosis has an impact on patients’ relatives. Mostly, misdiagnosing of monogenic diabetes is caused by its rare occurrence and insufficient training in this area among physicians. According to different studies it may comprise 1–4% of all cases of diabetes. The aim of this article is to emphasize that despite the fact that monogenic diabetes is an uncommon disease, it should always be considered in cases of diabetes with unusual course.

The increasingly obesogenic environment exerts a ponderous impact on the clinical presentation and the course of diabetes. Obesity is strongly linked to T2DM development, yet, the latest observation has shown that more cases of T1DM are diagnosed in youth who had been obese before the onset of the disease. What is more, the presence of autoimmunity is noticed in patients phenotypically classified as T2DM. The overlap of the clinical phenotypes of diabetes has become a new challenge for physicians who formulate a differential diagnosis. There is a question to consider how such patients should be classified. Not to discount the importance of identifying diabetes in an obese child, it is the therapeutic approach to such a complex patient that a physician should mainly focus on. Cases presented herein address the role that childhood obesity plays in making a differential diagnosis of diabetes and even more in choosing the adequate therapy.

Erratum to: Pediatr NephrolDOI 10.1007/s00467-010-1443-zIt has come to our attention that the reported NGAL levelsare 10-fold higher than those reported by other researchers.This is best seen from the normal values reported inTable 1. Inaccurate data is due to a decimal mistake. Allreported serum and urine values for NGAL have to bedivided by 10.

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

Insulin has long been recognized as a key regulator of energy homeostasis via its actions at the level of the brain, but in addition, plays a role in regulating neural control of reproduction. In this review, we consider and compare evidence from animal models demonstrating a role for insulin for physiological control of reproduction by effects on GnRH/LH secretion. We also review the role that insulin plays in prenatal programming of adult reproduction, and consider specific candidate neurons in the adult hypothalamus by which insulin may act to regulate reproductive function. Finally, we review clinical evidence of the role that insulin may play in adult human fertility and reproductive disorders. Overall, while insulin appears to have a significant impact on reproductive neuroendocrine function, there are many unanswered questions regarding its precise sites and mechanisms of action, and their impact on developing and adult reproductive neuroendocrine function.