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Objective. To analyse the association between overweight and obesity and foot structure in children older than 9 years of age, whose longitudinal medial arch (MLA) should be practically established. Design, setting and subject. A cross-sectional study of 245 children (age: 13.22±1.8 years) from four randomly selected schools (Zaragoza, Spain). Body mass index (BMI) was calculated and normal-weight, overweight and obese groups were defined. Footprints for both feet were collected. Measurements. Foot angle (FA) and Chippaux-Smirak index (CSI) were calculated from the footprints. Height and body mass were measured to calculate the BMI. Results. Mean values of FA and CSI in the normal-weight group indicated the presence of a normal MLA; however, in the overweight they indicated an intermediary MLA and in the obese group, a low MLA. Comparison among the groups showed a decrease of FA (p<0.01) and an increase of CSI (p<0.01) with increasing weight associated with a lower MLA. A low but significant correlation (p<0.0001) was found between the z-score BMI and footprint parameters. Conclusions. In children aged 9 to 16.5 years, the increase of body mass is related to a lower MLA. The MLA is lower in these obese children than in the younger ones studied in previous works probably due to the continuous bearing of excessive mass from childhood. A lower MLA could cause health problems. An assessment of foot structure in these children is recommended as the classification of the foot arch type can help decide if treatment to avoid these problems is necessary. [ABSTRACT FROM AUTHOR]

Mitochondria play an important role in the homeostasis of intracellular Ca2+ and regulate its availability for exocytosis. Inhibitors of mitochondria Ca2+ uptake such as protonophore CCCP potentiate the secretory response to a depolarizing pulse of K+. Exposure of cells to agents that directly (cytochalasin D, latrunculin B) or indirectly (PMA) disrupt cortical F-actin networks also potentiate the secretory response to high K+. The effects of cytochalasin D and CCCP on secretion were additive whereas those of PMA and CCCP were not; this suggests different mechanisms for cytochalasin D and CCCP and a similar mechanism for PMA and CCCP. Mitochondria were the site of action of CCCP, because the potentiation of secretion by CCCP was observed even after depletion of Ca2+ from the endoplasmic reticulum. CCCP induced a small increase in the cytosolic Ca2+ concentration ([Ca2+]c) that was not modified by the protein kinase C (PKC) inhibitor chelerythrine. Both CCCP and PMA induced cortical F-actin disassembly, an effect abolished by chelerythrine. In addition, rotenone and oligomycin A, two other mitochondrial inhibitors, also evoked cortical F-actin disassembly and potentiated secretion; again, these effects were blocked by chelerythrine. CCCP also enhanced the phosphorylation of PKC and myristoylated alanine-rich C kinase substance (MARCKS), and these were also inhibited by chelerythrine. The results suggest that the rapid sequestration of Ca2+ by mitochondria would protect the cell from an enhanced PKC activation and cortical F-actin disassembly, thereby limiting the magnitude of the secretory response. [ABSTRACT FROM AUTHOR]