A randomized-controlled, double-blind study of the impact of selenium supplementation on thyroid autoimmunity and inflammation with focus on the GPx1 genotypes.

PURPOSE: To analyze the impact of selenium supplementation on serum antiTPO levels and thyroid echogenicity in patients with CAT, evaluating the response in subgroups with different GPx1 genotypes. METHODS: CAT patients (n = 55) with positive antiTPO were randomized to selenomethionine (SeMet) 200 µg daily (n = 28) or placebo (n = 27) for 3 months. Assessments included GPx1 genotyping at baseline and serum levels of plasma selenium, erythrocyte GPx1 activity, antiTPO and thyroid echogenicity at baseline, and 3 and 6 months. RESULTS: In the SeMet group, the increase in plasma levels of selenium and erythrocyte GPx1 activity was similar among patients with different GPx1 genotypes. In the overall cohort, patients randomized to SeMet showed a 5 % decrease in antiTPO levels at 3 months (p = non-significant) and 20 % at 6 months (p < 0.001 versus 3 months). In contrast, patients in the placebo group did not show significant changes in antiTPO levels at any time point. Subgroup analysis showed that patients with different GPx1 genotypes presented comparable responses in antiTPO levels and echogenicity index to SeMet. CONCLUSIONS: Selenium supplementation decreased serum antiTPO levels in CAT patients, with similar response among patients with different GPx1 genotypes.

Exercise training associated with diet improves heart rate recovery and cardiac autonomic nervous system activity in obese children.

The purpose of this study was to test the hypotheses that in obese children: 1) hypocaloric diet (D) improves both heart rate recovery at 1 min (Δ HRR1) cfter an exercise test, and cardiac autonomic nervous system activity (CANSA) in obese children; 2) Diet and exercise training (DET) combined leads to greater improvement in both Δ HRR1 after an exercise test and in CANSA, than D alone. Moreover, we examined the relationships among Δ HRR1, CANSA, cardiorespiratory fitness and anthropometric variables (AV) in obese children submitted to D and to DET. 33 obese children (10 ± 0.2 years; body mass index (BMI) >95 (th) percentile) were divided into 2 groups: D (n=15; BMI=31 ± 1 kg/m²)) and DET (n=18; 29 ± 1 kg/m²). All children performed a maximal cardiopulmonary exercise test on a treadmill. The Δ HRR1 or LF/HF ratio (P>0.05). In contrast, the DET group showed increased peak VO2 ( P=0.01) and improved Δ HRR1 (Δ HRR1=37.3 ± 2.6; P=0.01) and LF/HF ratio ( P=0.001). The DET group demonstrated significant relationships among Δ HRR1, peak VO2 and CANSA (P<0.05). In conclusion, DET, in contrast to D, promoted improved ÄΔ HRR1 and CANSA in obese children, suggesting a positive influence of increased levels of cardiorespiratory fitness by exercise training on cardiac autonomic activity.

Weight loss associated with exercise training restores ventilatory efficiency in obese children.

The purpose of this study was to test the hypothesis that in obese children: 1) Ventilatory efficiency (VentE) is decreased during graded exercise; and 2) Weight loss through diet alone (D) improves VentE, and 3) diet associated with exercise training (DET) leads to greater improvement in VentE than by D. Thirty-eight obese children (10+/-0.2 years; BMI >95th percentile) were randomly divided into two study groups: D (n=17; BMI=30+/-1 kg/m (2)) and DET (n=21; 28+/-1 kg/m (2)). Ten lean children were included in a control group (10+/-0.3 years; 17+/-0.5 kg/m (2)). All children performed maximal treadmill testing with respiratory gas analysis (breath-by-breath) to determine the ventilatory anaerobic threshold (VAT) and peak oxygen consumption (VO (2) peak). VentE was determined by the VE/VCO (2) method at VAT. Obese children showed lower VO (2) peak and lower VentE than controls (p<0.05). After interventions, all obese children reduced body weight (p<0.05). D group did not improve in terms of VO (2) peak or VentE (p>0.05). In contrast, the DET group showed increased VO (2) peak (p=0.01) and improved VentE (DeltaVE/VCO (2)=-6.1+/-0.9; p=0.01). VentE is decreased in obese children, where weight loss by means of DET, but not D alone, improves VentE and cardiorespiratory fitness during graded exercise.

Growth hormone receptor messenger ribonucleic acid in normal and pathologic human adrenocortical tissues--an analysis by quantitative polymerase chain reaction technique.

GH receptor (GHR) has been reported to express in both normal rat and human adrenals. However, no study examined GHR expression in diseased human adrenal cortex. We quantitated, with RT-PCR, GHR messenger RNA (mRNA) in both normal and diseased human adrenal cortex with the following results: GHR mRNA levels in four histologically normal, not steroid-stimulated, control adrenal cortices was 1.5-11 x 10(4) molecules/microgram total RNA; in three diffusely hyperplastic adrenals (DH): 6.7-17.7 x 10(4); in two nonfunctioning tumors (NF): 0.84-1.9 x 10(4); in five androgen-producing neoplasms (AP): 4.6-34 x 10(4); and in five glucocorticoid-producing neoplasms (GP): 6.7-87 x 10(4). GHR transcript levels among adrenal cortices, DH, NF, AP, and GP reached statistically significant difference (P < 0.03). The GP group exhibited higher GHR mRNA levels than controls (P < 0.006). NF, as well as GP and AP, tumors had less GHR mRNA than their histologically normal adjacent cortex (P < 0.05). A positive correlation between urinary cortisol and GHR messenger RNA (mRNA) levels from GP and DH was observed (r = 0.93, P < 0.003). Our data suggest that GHR is expressed in both normal and diseased adrenal cortex and that GHR mRNA accumulation is less efficient in adrenocortical neoplasm than their adjacent nonneoplastic cortex. GHR expression in adrenal cortex provides an evidence of direct GH action in this tissue.