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Both obesity and asthma are increasingly being diagnosed in the childhood population. Obesity is linked to a greater asthma morbidity, and it increases the risk of severity of the disease course. The association between these 2 disorders has not yet been fully elucidated; however, several putative factors have been proposed related to mechanical and inflammatory aspects of obesity. Diet is an important adjustable element in obesity and asthma management. An unhealthy diet based on processed food is likely to promote chronic inflammation in both conditions; hence, appropriate nutrition should be an integral part of the children's therapy. This review discusses dietary models that have a positive impact on patient health.

The prenatal period, during which a fully formed newborn capable of surviving outside its mother’s body is built from a single cell, is critical for human development. It is also the time when the foetus is particularly vulnerable to environmental factors, which may modulate the course of its development. Both epidemiological and animal studies have shown that foetal programming of physiological systems may alter the growth and function of organs and lead to pathology in adulthood. Nutrition is a particularly important environmental factor for the pregnant mother as it affects the condition of offspring. Numerous studies have shown that an unbalanced maternal metabolic status (under- or overnutrition) may cause long-lasting physiological and behavioural alterations, resulting in metabolic disorders, such as obesity and type 2 diabetes (T2DM). Various diets are used in laboratory settings in order to induce maternal obesity and metabolic disorders, and to alter the offspring development. The most popular models are: high-fat, high-sugar, high-fat-high-sugar, and cafeteria diets. Maternal undernutrition models are also used, which results in metabolic problems in offspring. Similarly to animal data, human studies have shown the influence of mothers’ diets on the development of children. There is a strong link between the maternal diet and the birth weight, metabolic state, changes in the cardiovascular and central nervous system of the offspring. The mechanisms linking impaired foetal development and adult diseases remain under discussion. Epigenetic mechanisms are believed to play a major role in prenatal programming. Additionally, sexually dimorphic effects on offspring are observed. Therefore, further research on both sexes is necessary.

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.

Introduction and aim of the study: Considering worldwide epidemic of childhood obesity, its individual progress and complications require early evaluation and prevention. The aim of this study was to assess whether the relatively short-lasting childhood obesity already affects ?-cell function beyond the adaptive hyperinsulinemia. Material and methods: The study comprised 138 overweight and obese patients and 20 healthy controls, aged 13.0?3.3 and 12.4?3.4 years respectively, and classified by their body mass index standard deviation score (BMI-SDS). Patients were also stratified by oral glucose tolerance test (OGTT) as individuals with normal (NGT) or impaired glucose tolerance (IFG/IGT) and as insulin resistant (+IR) or non-resistant (non-IR). Serum insulin levels and indices of insulin resistance/sensitivity were assessed. Children underwent intravenous glucose tolerance test (IVGTT) to evaluate their first phase insulin release (FPIR). Results: Overweight and obese patients demonstrated lower insulin sensitivity indices compared to controls. IVGTT revealed significantly higher FPIR results (mU/l; up to 3 min) in obese vs. control patients (272.9?143.8 vs. 125.4?70.1). The +IR subgroup displayed the highest FPIR values (297.6?156.3). In the observation prolonged up to 10 min, significant differences in insulin secretion between +IR (486.8?213.6), non-IR (393.6?190.6) patients and controls (196.8?82.4) were also found. Moreover, NGT obese patients demonstrated significantly higher insulin (292.1?151.2) levels in FPIR (3min) than control (125.4?70.1) and IFG/IGT (171.5?75.5) group as well. Additionally, the latter group was characterised by the highest insulin resistance and BMI-SDS values. Conclusions: IFG/IGT may present very early in obese children. It reflects failing ?-cell function, which should be recognized as prediabetes and needs urgent intervention to prevent type 2 diabetes.

Epidemia otyłości obejmuje w coraz większym stopniu dzieci i młodzież. Nadmierna masa ciała prowadzi do zaburzeń metabolicznych, cukrzycy typu 2, zaburzeń w układzie sercowo-naczyniowym, układzie oddechowym, układzie szkieletowo-mięśniowym i w sferze psychospołecznej. Otyłość prosta wtórnie wywołuje też zaburzenia hormonalne. W rozwoju powikłań otyłości podstawowe znaczenie ma nasilająca się z czasem trwania choroby insulinooporność i przewlekły stan prozapalny, indukowany przez cytokiny wytwarzane w tkance tłuszczowej. Wiele zaburzeń okazuje się być odwracalnych we wczesnych etapach, jeśli uda się uzyskać chociaż niewielki spadek masy ciała.

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.