RESUMEN
The purpose of this study was to examine the effects of intermittent versus continuous energy restriction on body composition, resting metabolic rate, and eating behaviors in resistance-trained females. Thirty-eight resistance-trained females (mean ± standard deviation age: 22.3 ± 4.2 years) were randomized to receive either six weeks of a continuous 25% reduction in energy intake (n = 18), or one week of energy balance after every two weeks of 25% energy restriction (eight weeks total; n = 20). Participants were instructed to ingest 1.8 g protein/kilogram bodyweight per day and completed three weekly supervised resistance training sessions throughout the intervention. There were no differences between groups for changes over time in body composition, resting metabolic rate, or seven of the eight measured eating behavior variables (p > 0.05). However, a significant group-by-time interaction for disinhibition (p < 0.01) from the Three-Factor Eating Questionnaire was observed, with values (± standard error) in the continuous group increasing from 4.91 ± 0.73 to 6.17 ± 0.71, while values in the intermittent group decreased from 6.80 ± 0.68 to 6.05 ± 0.68. Thus, diet breaks do not appear to induce improvements in body composition or metabolic rate in comparison with continuous energy restriction over six weeks of dieting, but may be employed for those who desire a short-term break from an energy-restricted diet without fear of fat regain. While diet breaks may reduce the impact of prolonged energy restriction on measures of disinhibition, they also require a longer time period that may be less appealing for some individuals.
RESUMEN
Gene fusions play a critical role in cancer progression. The mechanisms underlying their genesis and cell type specificity are not well understood. About 50% of human prostate cancers display a gene fusion involving the 5' untranslated region of TMPRSS2, an androgen-regulated gene, and the protein-coding sequences of ERG, which encodes an erythroblast transformation-specific (ETS) transcription factor. By studying human prostate cancer cells with fluorescence in situ hybridization, we show that androgen signaling induces proximity of the TMPRSS2 and ERG genomic loci, both located on chromosome 21q22.2. Subsequent exposure of the cells to gamma irradiation, which causes DNA double-strand breaks, facilitates the formation of the TMPRSS2-ERG gene fusion. These results may help explain why TMPRSS2-ERG fusions are restricted to the prostate, which is dependent on androgen signaling.