Beata Pyrżak

Relationship Between 25(OH)D and IGF-I in Children and Adolescents with Growth Hormone Deficiency

Recent studies have shown that vitamin D has an impact on the production and secretion of IGF-I in the liver. The aim of our study was to investigate the relationship between the concentrations of 25-hydroxy vitamin D [25(OH)D] and insulin-like growth factor I (IGF-I) in growth hormone deficient children and adolescents before recombinant human growth hormone (rhGH) treatment. The study was retrospective and included 84 children and adolescents aged 4-17. Prior to initiating rhGH therapy, concentrations of 25(OH)D and IGF-I were measured in all patients. IGF-I concentrations were normalized for bone age. The studied group was divided into two subgroups according to serum 25(OH)D levels. Significant positive correlations between 25(OH)D concentration and IGF-I SDS-normalized for bone age were observed in both studied subgroups. The results of our study suggest that vitamin D deficiency could influence IGF-I concentrations in children and adolescents with growth hormone deficiency, and vitamin D deficiency should be normalized before the measurement of IGF-I concentrations to obtain the reliable and unbiased IGF-I values.

Relation of Fat-Mass and Obesity-Associated Gene Polymorphism to Fat Mass Content and Body Mass Index in Obese Children

Fat mass content, fat distribution, and fat-mass and obesity associated (FTO) gene have been reported among a broad spectrum of genetic variation connected with body weight. The aim of our study was to investigate whether the T/A rs9939609 polymorphism of the FTO gene may influence obesity and metabolic indices in children. A 160 children were examined (136 obese and 24 non-obese). The anthropometric measurements and calculations included: height, weight, waist and hip circumference, sum of the thickness of 3 and 10 skin folds, % of fat content, % FAT- BIA , % LBM-BIA. BMI, SDS of BMI, WHR, and WHtR. Fasting plasma total cholesterol (TC), HDL and LDL-cholesterol, triglycerides (TG), oral glucose tolerance test (OGTT), and HOMA-IR were analyzed and the blood pressure were measured. The rs9939609 polymorphism of FTO gene was genotyped by allele-specific real-time polymerase chain- reaction (RT-PCR). We found that the mean concentrations of TC, TG, LDLC, and HOMA-IR were significantly higher, and HDL was lower in the obese than in non-obese children. The presence of TT, but not AA alleles, related to the percentage of fat content, BMI, and z-score of BMI. None of the other anthropometric indices did differ between the children with gene polymorphism and wild homozygous. In conclusion, rs9939609 polymorphism in the fat-mass and obesity-associated gene is associated with BMI and the percent of fat content in children.

Cardiovascular Risk Factors in Obese Children and Adolescents

The aim of the study was to analyze cardiometabolic risk factors andcarotid intima-media thickness (IMT) in obese children. We studied 122 obese children fulfilling the criteria of the International Obesity Task Force and 58 non-obese children. Anthropometric parameters, blood pressure, lipid profile, C-reactive protein, and adiponectin were assessed in all children. Glucose and insulin during the oral glucose tolerance test were assessed in obese children. The IMT was determined using ultrasound B-mode imaging in 81 obese and 32 non-obese children. We found that obese children had significantly higher levels of lipid andother non-lipid atherogenic indicators, but lower levels of adiponectin compared with non-obese children. The difference in the mean carotid IMT was insignificant in the two groups. Taking the combined groups, the level of adiponectin correlated negatively with body mass index and lipid atherogenic indicators. The IMT strongly correlated with systolic blood pressure in obese children. In the children fulfilling the criteria of metabolic syndrome, 17 out of the 84 obese children older than 10 years of age, IMT was greater than in those who did not fulfil these criteria. We conclude that the coexistence of abdominal obesity with abnormal lipid profile and hypertension leads to the early development of atherosclerosis accompanied by increased carotid intima-media thickness. Obesity initiates the atherosclerotic processes in early childhood.

Thyroid dysfunction in obese and overweight children

Obesity and thyroid function are closely related. Thyroid hormones are involved in the regulation of metabolism, thermogenesis, food intake, and fat oxidation. In obese children the most frequent hormonal abnormalities are slight hyperthyrotropinaemia and moderate increases in total T3 and/or fT3 concentrations. Those abnormalities are usually considered a cause of obesity, but according to recent studies, they should actually be considered an adaptation process aimed at increasing resting energy expenditure and total energy expenditure. Those abnormalities do not require any treatment and normalise after substantial weight loss. The mechanisms of those changes are dependent on leptin, thyroid hormone resistance, and mitochondrial dysfunction. The present paper describes the abovementioned mechanisms based on the latest research. We also present a review of some recent original studies evaluating thyroid function in overweight and obese children, including thyroid ultrasound. A thyroid ultrasound scan in obese children frequently shows increased thyroid volume, which correlates with moderately increased TSH levels and a hypoechoic pattern typical of autoimmune thyroiditis, but without antithyroid autoantibodies. Alterations of thyroid function in overweight and obese patients cause an increase in energy expenditure, which facilitates weight loss and prevents further weight gain. Therefore, normalisation of TSH and fT3 after weight loss could explain difficulties in maintaining reduced weight. (Endokrynol Pol 2017; 68 (1): 54-60).

Thyroid Function in Obese Children and Adolescents and Its Association with Anthropometric and Metabolic Parameters

Fat accumulation leads to dysfunction of hypothalamic-pituitary-thyroid axis and to changes in thyroid function. A higher serum level of thyroid stimulating hormone (TSH), with normal levels of thyroid hormones, suggesting subclinical hypothyroidism, is often found in obese individuals. The influence on lipid and glucose metabolism of thyroid dysfunction in obese patients remains unclear. This retrospective study encompassed 110 obese children and 38 healthy non-obese children aged 5-18. Anthropometric measurements, including bioelectrical impedance, were taken in all children. Fasting TSH, fT4, glucose, lipid profile, and a glucose tolerance test in case of the obese individuals, were evaluated. The obese children demonstrated a significantly higher mean concentration of TSH compared with their peers with proper body weight: 2.1 ± 1.0 μIU/ml vs. 1.5 ± 0.6 μIU/ml, p = 0.001. The fT4 was not different between the two groups. In the obese children, TSH correlated with body mass index (BMI) and waist circumference after controlling for age and gender. A multivariate regression analysis showed a relationship of TSH with total cholesterol, LDL cholesterol, triglycerides, and non-HDL after adjusting for BMI. None of these relationships were revealed for fT4. The level of TSH correlated with the degree of abdominal obesity. We conclude that the serum TSH concentration, even remaining within the norm, could adversely affect the lipid profile, irrespective of obesity.

Regulatory T Cells in Obesity

The current concept of the pathogenesis of obesity relates to the inflammation caused by excess of adipose tissue. Regulatory T cells accumulated in visceral adipose tissue (VAT-resident Tregs) are also involved in this pathogenesis. In the present paper the mechanisms responsible for alterations in the number and function of VAT-resident Tregs T in obesity are described. The role of Tregs in inflammation, insulin resistance, atherogenesis, and also the influence on VAT-resident Tregs of adipocytokines and insulin are reviewed.

Metabolic and Immunological Consequences of Vitamin D Deficiency in Obese Children

Numerous studies highlighted the link between vitamin D deficiency and cardiovascular, autoimmune, metabolic diseases, and obesity. However, a clear role of vitamin D in these disorders is still unknown. Vitamin D deficiency in children can be a potential risk factor for developing diseases at a later age. Early prevention and vitamin D supplementation should become a public health priority. This review highlights the clinical implications of vitamin D deficiency in adults and children with obesity.

Association of adiponectin gene G276T polymorphism with atherogenic indicators in obese children.

Adiponectin plays a protective role against atherosclerosis. Genetic investigation has revealed that G276T adiponectin gene polymorphism is related to adiponectin concentration and metabolic disturbances. The aim of the present study was to investigate the association of adiponectin gene G276T polymorphism with indices of atherosclerosis in obese children. We examined 159 children (125 obese and 34 non-obese). G276T of adiponectin gene polymorphism was identified using a PCR-RFLP method. The intima media thickness (IMT) was evaluated in 82 patients. In all children, the anthropometric indices, fasting plasma total cholesterol (TC), HDL and LDL cholesterol, triglycerydes (TG), C-reactive protein (CRP), and adiponectin were measured. Oral glucose tolerance test (OGTT) also was performed. We found that the obese patients presented with higher values of atherogenic indicators than the non-obese patients. The indicators positively correlated with CRP and lipid concentrations. Ninety one percent of obese children presented with elevated IMT which correlated with CRP. The children with GG genotype (GG + GT allele) had lower values of BMI, TC, and TG but higher adiponectin concentrations. The mean level of adiponectin was statistically decreased in the compared with the homozygous TT children. The other anthropometric and atherogenic indicators did not differ between these two sets of obese children. We conclude that adiponectin concentrations were decreased in children with polymorphism G276T in adiponectin gene. The study, however, failed to show significant associations between carotid IMT, lipid markers, blood pressure, or HOMA-IR in obese children.

Influence of Sublingual Immunotherapy on the Expression of Mac-1 Integrin in Neutrophils from Asthmatic Children

Asthma can be effectively treated with sublingual immunotherapy. The influence of -sublingual immunotherapy on the function of granulocytes in asthmatic patients is largely unknown. Mac-1 integrin is a transmembrane protein containing α (CD11b) and β (CD18) chains. High expression of the complex is found on the surface of neutrophils, NK cells, and macrophages. CD11b/CD18 may bind to CD23, ICAM-1, ICAM-2, and ICAM-4. It plays a crucial role in diapedesis of neutrophils. The aim of the present study was to assess Mac-1 expression on neutrophils from asthmatic children before and after sublingual immunotherapy. Twenty five children aged of 8.1 ± 3.1 suffering from atopic asthma and allergic rhinitis, shortlisted for specific immunotherapy, served as the study group. Fifteen healthy individuals, aged 9.8 ± 3.4, served as a control group. The assessment of CD11b and CD18 expression on cells from peripheral blood was performed with a flow cytometer. The tests were performed before and after 12 months of sublingual immunotherapy. In the asthmatic children, 98.08 (90.79-99.12)% of Mac-1 positive neutrophils were detected. The group was divided into two subgroups: of more than 98% and less than 95% of neutrophils with CD11b/CD18 expression in the sample. After immunotherapy, the percentage of Mac-1 positive granulocytes increased to 99.60 (99.29-99.68)%, p = 0.01. In the control group, 90.56 (87.08-88.86)% granulocytes were Mac-1 positive, p = 0.002. We conclude that sublingual immunotherapy strongly influences the function of the immunological system, including Mac-1 expression on neutrophils.

Seasonal Variation in Month of Diagnosis of Polish Children with Type 1 Diabetes - A Multicenter Study

AIM The seasonal variation of incidence of type 1 diabetes (T1D) theory supports the hypothesis that environmental factors play a role in the onset of the disease. The aim of this study is to assess seasonality of month of diagnosis in children with T1D in Poland. MATERIAL AND METHODS the study group consisted of 2174 children from eastern and central Poland diagnosed with T1D between 2010 and 2014. Analysis was performed in different age groups, based on place of residence (rural/urban area) and depending on sex. RESULTS We noted significant seasonality in the incidence of T1D with a peak in diagnosis of diabetes in January and the minimum rate in June. A total of 423 (19%) children were diagnosed in the warmest months (June to August with a mean temperature of 16.8°C) compared to 636 (29%) recognised in the coldest months (December to February with a mean temperature of -1.6°C), OR 0.57 95%CI [0.51-0.67], p<0.0001. We noted a more flat seasonal pattern in children 0-4 years of age compared with subjects 5-17 years old with a week correlation of trend comparison between both groups, r=0.69, p=0.001. Similar seasonal variation in the incidence of T1D was noted in children from urban and rural setting. For girls, seasonal pattern peaks were observed one month earlier as compared to boys. CONCLUSIONS Seasonal variation in incidence of T1D diagnosis of Polish children supports the role of different environmental factors in diabetes onset. The majority of children were diagnosed with diabetes in autumn and winter.