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Body mass index (BMI), serum cytokines and serum obesity markers were evaluated in 33 obese children before, during and after a hypocaloric diet. The cytometric bead array "human inflammatory kit" was used for the evaluation of serum interleukin (IL)-1beta, IL-6, IL-10 and tumor necrosis factor-alpha. On the other hand, the following obesity biomarkers were evaluated by means of a flowcytomix-human obesity 9 plex kit: Soluble Isoform of CD40 Ligand; Soluble Intercellular Adhesion Molecule-1; Leptin; Monocyte Chemoattractant Protein 1; Myeloperoxidase; Osteoprotegerin; Resistin and Soluble TNF-receptors. Actually, throughout the study modifications of BMI were negligible and, therefore, serum cytokines and obesity markers did not show any significant changes in comparison with baseline values. On the other hand, at the different time points considered the majority of obesity markers were higher than normal controls, thus indicating a low grade inflammation in childhood obesity. Therefore, attempts at reducing this inflammatory status in children which predisposes to the metabolic syndrome outcome are discussed.

We examined the relationship between moderate obesity and glucose metabolism, insulin sensitivity and suspected fatty liver in children. We measured body mass index (BMI), z-score BMI, caliper skinfold thickness, waist and hip circumference in 94 participants (mean age 9.7 +/-2.2 years). Fasting blood glucose, insulin, HOMA score, lipid profile and transaminases (ALT, AST) were measured. Fatty liver and skinfold thickness were evaluated by means of ultrasound. The z-score BMI was 2.01 +/-0.39 (mean +/- SD), and the duration of obesity was 4.3+/-3.03 years. A positive correlation was found between caliper and US skinfold thickness for tricipital (r= 0.33; p= 0.003) and sovrailiac skinfold (r= 0.34; p=0.003). Fatty liver was diagnosed in 64% of children and it was positively related to anthropometric measurements. The three sub-groups--group 0 (normal US liver and normal transaminases); group 1 (US fatty liver and normal transaminases); group 2 (US fatty liver and elevated transaminases)--showed a difference concerning z-score BMI, insulin and HOMA parameters (Tukey test: z score BMI group 1 vs group 0 and 2 vs group 0; serum insulin: group 2 vs group 1 and group 2 vs group 0; HOMA IR: group 2 vs group 1 and group 2 vs group 0). Moderately obese children with steatosis exhibited a clear increase of insulin and insulin resistance which represents indices of a future metabolic syndrome. In addition, it is important to perform a liver ultrasound since transaminases seems to be not adequate for the diagnosis of fatty liver.

Obesity represents a chronic inflammatory status and adipocytes release either cytokines or an array of adipokines such as leptin, endowed with immunomodulating and systemic activities. The involvement of cytokines in obesity as well as of the adipokine leptin is supported by the notion that weight reduction normalizes mediators of inflammation. In this framework, we will demonstrate that in obese children, subjected for a period of six months to a hypocaloric diet, reduction of major biochemical and anthropometric parameters correlates with a normalization of immune status. In fact, absolute numbers of CD4+ cells and CD4/CD8 ratio increase, while leptin values fluctuate within normal ranges, being this adipokine involved in the modulation of either innate or adaptive immune responses. In the discussion, the immune abnormalities detected in obesity will be pointed out and emphasis will be placed on the increased frequency of infectious episodes occurring in obese adolescent and adults. Finally, the infectious etiology of obesity will be illustrated in the sense that adipocytes interacting with infectious agents may cause obesity. Taken together, the bulk of available data indicate that childhood obesity should be prevented or reduced to avoid more serious complications in adulthood.