Telemedicine screening adolescent metabolic syndrome in Greek schools.

BACKGROUND: Using telemedicine in the school setting in Greece, we screened a representative adolescent sample for MetS (International Diabetes Federation criteria) and explored its associations with anthropometric, sociodemographic and behavioural parameters. MATERIALS AND METHODS: Cross-sectional data were obtained from 12- to 17-year-old high school students. RESULTS: The prevalence of MetS in 1578 adolescents (mean age ± SD 14.4 ± 1.7 years) was 2.6% (3.4% among males; 2.0% among females), highest (4.3%) at age 13 years and lowest (1.3%) at 16 years. Adolescents with MetS had significantly higher mean body mass index (BMI) ± SD than those without MetS (30.2 ± 4.2 vs 21.3 ± 3.2 kg/m2 , respectively; P < 0.001); among participants with obesity, 31.6% had MetS. Abdominal obesity, elevated triglycerides, low HDL-cholesterol, impaired fasting blood glucose (FBG) and elevated blood pressure (BP) were detected in 9.5%, 2.3%, 10.7%, 25.9% and 21.8% of participants, respectively. Additional analysis (modified NCEP:ATPIII youth criteria) demonstrated similar overall prevalence of MetS (2.9%). Statistically significant correlations were found between most anthropometric and MetS characteristics, with the exception of FBG, which was correlated only with systolic BP. BMI was strongly correlated with waist and hip circumferences (r = 0.818, P < 0.001; r = 0.825, P < 0.001, respectively). Single parenthood and older maternal age (>60 years) were risk factors for MetS. Although counterintuitive, body image distortion, body dissatisfaction and bullying about weight were more prevalent in normal weight girls. CONCLUSIONS: The overall prevalence of MetS was low but 12-fold higher when obesity was taken into account. Impaired FBG and elevated BP were the most prevailing features. Telemedicine services were used effectively in Greek schools for screening youth MetS.

Effects of dexamethasone on K(+)-evoked glutamate release from rat hippocampal slices.

Dexamethasone (DEX) at physiologically elevated (stress) concentration (1 microM) decreased K(+)-evoked glutamate release from rat hippocampal slices under superfusion in the presence of Ca2+. On the contrary 10 microM DEX increased this K(+)-evoked glutamate release while 0.1 microM DEX had no effect. The glucocorticoid antagonist for the "classic" receptor, RU 486, completely reversed the effect of 1 microM DEX. Actinomycin D had no effect. Dexamethasone at 1 microM had no effect on the Ca2(+)-independent (10 mM Mg2+ replacing 1 mM Ca2+) K(+)-evoked glutamate release. Dexamethasone at 1 microM or 10 microM had no effect on the phosphate-activated glutaminase--the key enzyme for the biosynthesis of neurotransmitter glutamate. These results suggest that the effect of DEX on K(+)-evoked glutamate release: (i) depends on its concentration; (ii) is exerted on the Ca2(+)-dependent (neurotransmitter release), at least at physiological stress concentrations; and (iii) is exerted via the classical receptor but is nongenomic.