Background. Skipping breakfast has been associated with a higher risk of obesity and cardiovascular (CV) risk factors. However, it is not known if skipping breakfast is also correlated with CV risk factors independently from obesity. The mechanisms explaining the role of skipping breakfast on promoting fat accumulation as well as CV risk are not known. Hormones, in particular, insulin-like growth factor-1 (IGF-1), may potentially play a role in the metabolic profile of breakfast skippers. Aim. This cross-sectional study aims to test, in a sample of overweight/obese children, the hypotheses that skipping breakfast is associated with a worse metabolic profile and that IGF-1 levels are associated with this unfavorable metabolic profile. Methods and Results. We enrolled 112 overweight/obese prepubertal children (3–12 years). Anthropometric characteristics (height SDS, weight SDS, and body mass index (BMI) z-score) were measured. Blood samples were collected to evaluate glucose and lipid metabolisms and hormone profile (growth hormone (GH), IGF-1, insulin, and cortisol). The triglycerides/high-density lipoprotein (HDL) cholesterol ratio was calculated as a predictor of cardiovascular risk. Children were divided into two groups according to breakfast habits: consumers (≥5 weekly; N = 76) and skippers (≤4 weekly; N = 36). Glycaemia, total and low-density lipoprotein (LDL) cholesterol, triglycerides (p<0.05), and triglycerides/HDL cholesterol ratio (p<0.001) were higher, while HDL cholesterol was lower (p<0.01) in skippers as compared to consumers. IGF-1 concentrations were inversely correlated with LDL cholesterol (r = −0.279, p=0.013) and directly correlated with HDL cholesterol (r = 0.226, p=0.047). IGF-1 correlated positively with HDL cholesterol (r = 0.266, p=0.045) in consumers and correlated negatively with LDL cholesterol (r = −0.442, p=0.024) in skippers. Breakfast consumption among prepubertal overweight/obese children showed a better lipid profile in comparison with those who skipped breakfast [OR: 0.165 (95% CI: 0.053–0.518), p=0.001]; these latter odds of the increased triglycerides/HDL cholesterol ratio was 6.1-fold higher. Conclusions. Breakfast skippers show a worse lipid profile when compared to breakfast consumers. IGF-1 might play a role as an independent modulator of lipid metabolism.

Objective: Linear growth is impaired in children with type 1 diabetes (T1D) and poor metabolic control. A good metabolic control is a key therapeutic goal to prevent vascular complications and also to ensure appropriate anthropometric development during childhood. In this study, we aimed to identify and characterize the effects of glycemic variability on linear growth in children with T1D. Methods: Data from 144 prepubertal children with T1D were evaluated. Anthropometric measurements (weight, weight-SDS, height, height-SDS, BMI, BMI-SDS) were collected and glycosylated hemoglobin (HbA1c) was measured at admission and every 4 months over a 2-year period. Glycemic variability indexes (glycemic coefficient of variation (CV), glycemic CV percentage (CV%), and the product between HbA1c-mean and HbA1c-SDS/100 (M*SDS-HbA1c/100)) were calculated. According to height-SDS changes after 2 years of follow-up, the study population was divided into three tertile groups and differences across groups were investigated for variables of interest. Results: The three groups were similar in terms of age, gender, and follow-up period. After 2 years, all prepubertal children showed a significant positive trend of anthropometric data. Across the three tertile groups, HbA1c-SDS, CV, CV%, and M*SDS-HbA1c significantly decreased from the first to the third tertile of height-SDS. During follow-up, children with lower Δheight-SDS values reported higher values of HbA1c-SDS, CV, CV%, and M*SDS-HbA1c than subjects with higher linear growth. Conclusions: Glycemic variability correlates with linear growth in children with T1D. Low glycemic variability indexes were reported in higher height-SDS tertiles. Δheight-SDS is inversely correlated with glycemic CV, CV%, and M*SDS-HbA1c.

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Diabetes is considered as a disease with a wide and continuous clinical spectrum, ranging from Type 1 (T1D) and Type 2 Diabetes (T2D) with complex multifactorial causes. In the last years, particular attention has been focused on the predictive value and therapeutic potential of single nucleotide polymorphisms (SNPs). SNPs can alter the seed-sequence in miRNA’s loci and miRNA target sites causing changes in the structure and influencing the binding function. Only few studies have investigated the clinical influence of SNPs, in particular potassium inwardly rectifying channel, subfamily J, member 11 (KCNJ) gene variants in T1D population. The aim of the study is to investigate the occurrence and the possible metabolic significance of KCNJ polymorphism in a group of pediatric patients with T1D. The study was performed in a cohort of 90 Caucasian children and adolescents with T1D and 93 healthy subjects. Rs5210 polymorphism has been analyzed with a prevalence of the GG genotype in the patient group suggesting its association with T1D. Therefore, a relationship was found between GG genotype and body mass index (BMI) at diagnosis and insulin requirement (IR) after 6 months. The study suggested an action for rs5210 in determining the metabolic features of T1D pediatric patients, by showing some clues of insulin resistance in patients carrying that polymorphism.

The HNF1A transcription factor, implicated in the regulation of pancreatic beta cells, as well as in glucose and lipid metabolism, is responsible for type 3 maturity-onset diabetes of the young (MODY3). HNF1A is also involved in increased susceptibility to polygenic forms of diabetes, such as type 2 diabetes (T2D) and gestational diabetes (GD), while its possible role in type 1 diabetes (T1D) is not known. In this study, 277 children and adolescents with T1D and 140 healthy controls were recruited. The following SNPs in HNF1A gene were selected: rs1169286, rs1169288, rs7979478, and rs2259816. Through linear or logistic regression analysis, we analyzed their association with T1D susceptibility and related clinical traits, such as insulin dose-adjusted glycated hemoglobin A1c (IDAA1c) and glycated hemoglobin (HbA1c). We found that rs1169286 was associated with IDAA1c and HbA1c values (p-value = 0.0027 and p-value = 0.0075, respectively), while rs1169288 was associated with IDAA1c (p-value = 0.0081). No association between HNF1A SNPs and T1D development emerged. In conclusion, our findings suggest for the first time that HNF1A variants may be a risk factor for beta cell function and glycaemic control in T1D individuals.

The incidence and prevalence of type 2 diabetes (T2D) are increasing worldwide, affecting both adults and a growing number of children and adolescents. Notably, youth-onset T2D differs in its pathogenesis from later-onset T2D and progresses more rapidly. It is associated with a higher incidence of complications, and these occur earlier. Over the past few decades, numerous therapeutic agents from various drug classes have been approved for use in adults with T2D. In contrast, there is a scarcity of approved treatments for T2D in children. Sodium-glucose cotransporter-2 (SGLT2) inhibitors represent one of the newest classes of oral hypoglycemic agents, which lower blood glucose concentrations by increasing urinary glucose excretion. They have significantly influenced the management of T2D in adults. Promising results have also been reported in the pediatric population. In particular, empagliflozin, a potent and highly selective SGLT2 inhibitor, is an effective and generally well-tolerated anti-hyperglycemic agent widely approved for the treatment of adults with T2D. It has been recently approved for the management of T2D in children aged 10 years and older, in combination with diet and exercise. Here, we report a case of empagliflozin use in a 14-year-old girl with poorly controlled T2D. Furthermore, we review existing data on the use of SGLT2 inhibitors in the pediatric population.