Aims: To compare the short- and long-term effects of intervention programs on body weight and cardiometabolic risk factors. Methods: 162 obese children (6–11 years) were randomly assigned to three 12-week interventions with a 9-month follow-up period: exercise (E): 90 min moderate exercise 3 days/week (n = 52); diet (D): balanced hypocaloric diet, weekly meetings with dietician (n = 55), and diet + exercise (D+E) (n = 55). Changes in anthropometric variables, cardiometabolic profile and psychological outcome were assessed. Results: At 12 weeks BMI-SDS, cardiometabolic profiles, and psychological score improved in all groups. The decrease in BMI-SDS was greater in D and D+E compared with E (p < 0.001), without a significant difference between the first two groups. Waist circumference and LDL cholesterol decreased more in D+E compared with E (p = 0.026 and p = 0.038, respectively). The increase in adiponectin was greater in D and D+E compared with E (p = 0.004). Anthropometric and cardiometabolic variables regressed without significant differences between groups after 9 months. However, BMI-SDS, body fat percentage and LDL cholesterol were lower compared to baseline. Conclusions: Diet alone or combined with exercise are the most effective short-term interventions for weight loss and improved cardiometabolic profiles, without a difference between them. In the long term, obese children need the long-term support of maintenance approaches.

Caloric imbalance, particularly in critical periods of growth and development, is often the underlying cause of growth abnormalities. Serum levels of leptin are elevated in obesity and are low in malnutrition and malabsorption. The aim of the present study was to determine whether leptin integrates energy levels and growth in vivo, as shown previously in our ex vivo experiments, even in the presence of caloric restriction. In the first part of the study, mice were divided into three groups. Two groups were fed ad libitum and received leptin or vehicle only, and the third group was pair-fed with the group injected with leptin to dissociate leptin's effect on growth from its effect on food consumption. Mice given leptin had a significantly greater tibial length than untreated pair-fed animals and a similar tibial length as control mice fed ad libitum despite their lower weight. In addition, leptin significantly increased the overall size of the epiphyseal growth plate by 11%. On immunohistochemistry and in situ hybridization studies, leptin stimulated both the proliferation and differentiation of tibial growth plate chondrocytes without affecting the overall organization of the plate. There was also a marked increase in the expression and level of IGF-IR. In the second part of the study, two groups of mice were fed only 60% of their normal chow; one was injected with leptin, and the other was injected with vehicle alone. Caloric deprivation by itself reduced serum levels of IGF-I by 70% and the length of the tibia by 5%. Leptin treatment corrected the fasting-induced growth deficiency, but further reduced the level of serum IGF-I. These results indicate that leptin stimulates growth even in the presence of caloric restriction independently of peripheral IGF-I.

Chronic CR-PTSD may be associated with increased circulatory level of neuroactive steroids with inhibitory activity at the GABA(A) receptors. Neurosteroid-induced decreased GABAergic tone may be relevant to the symptomatology and pathophysiology of chronic PTSD, as well as to the frequent co-morbidity of PTSD with depression and anxiety disorders.