Increase in diet-induced thermogenesis at the start of refeeding in severely malnourished anorexia nervosa patients.

Many reports describe the difficulty for anorexia nervosa patients to gain weight during refeeding. To assess whether an increase in diet-induced thermogenesis (DIT) participates to this resistance, we studied DIT by indirect calorimetry in 11 severely malnourished anorexia nervosa patients [body mass index (BMI; in kg/m2) = 13] to accomplish two purposes: 1) to compare DIT in a strict semistarvation state with that obtained after 1 wk refeeding, when metabolism is shifted to a dynamic trend toward regaining weight, without significant change in body composition; 2) to study the effect on DIT of two energetic loads representing each one-third of the energy intake during semistarvation and refeeding, respectively: 1.25 and 2.92 MJ. To avoid bias, the two liquid loads were infused intragastrically in a random double-blind fashion. A significant increase in DIT during refeeding was observed for the two loads (204 +/- 23 kJ for the 1.25-MJ liquid meal and 482 +/- 78 kJ for the 2.92-MJ one, P < 0.02). The higher the load, the larger the increase with refeeding (P < 0.001). This increment in DIT exceeded the increase in active lean body mass and was poorly correlated with lean body mass. These results provide clear evidence of a strong cellular "waste" mechanism in anorexia nervosa patients during the early phase of refeeding, which enhances the adaptative resistance to overfeeding that we have already shown for resting energy expenditure.

Refeeding improves muscle performance without normalization of muscle mass and oxygen consumption in anorexia nervosa patients.

The effect of starvation-related malnutrition on muscle performance and on the energy cost of exercise remains unknown, as does the timing of improvement by refeeding. Indeed, in most diseases that induce malnutrition, muscle dysfunction is worsened by an inflammatory process. Thus, physical performance and the energy cost of exercise were studied in 15 semistarvated malnourished anorexia nervosa (AN) patients during exercise on an ergometric bicycle (3-min steps of 30 W) before and after 8, 30, and 45 d of refeeding. Results were compared with those of 15 normal-weight healthy subjects matched for age, sex, and physical activity. Before refeeding, the workload reached during the exercise was 49% lower in AN patients than in control subjects (P < 0.01). It was correlated with body weight, fat-free mass, and leg muscle circumference (P < 0.002). The performance improved dramatically during refeeding (P < 0.03), reaching normal values after 45 d of refeeding, despite fat-free mass and leg muscle circumference values that were still 20% lower in AN patients than in control subjects (P < 0.01). At this time, the exercise-related VO2 remained unchanged, being approximately 25% lower than that of the control subjects when corrected for muscle mass differences (P < 0.03). In conclusion, in AN patients muscle performance was restored by refeeding long before the patients achieved normal nutritional status. The economic cost of physical activity for these malnourished patients allows them to maintain a relatively high level of physical activity. This relative overactivity has two goals in AN: it reinforces anorexia and contributes to the excess of energy expenditure needed for weight loss.

Effects of cations, polyamines and other aminoglycosides on gentamicin C2. Binding to ribosomes from sensitive and resistant Escherichia coli strains.

Gentamicin C2 interacts cooperatively with ribosomes from a sensitive Escherichia coli strain in a multiphasic way with several classes of sites. It is shown that this binding is highly-dependent on Mg++ and natural endogenous polyamine concentrations. The differences observed between ribosomes from sensitive and resistant strains may be explained by the absence of specific cooperative gentamicin interactions with resistant ribosomes. The effects of other aminoglycoside antibiotics are discussed in terms of structure-activity relationships.

Identification of a short amino acid sequence essential for efficient nuclear targeting of the Epstein-Barr virus nuclear antigen 3A.

The Epstein-Barr virus nuclear antigen 3A is expressed in the nuclei of cells latently infected by the Epstein-Barr virus. We have previously shown that a fragment of 265 amino acids was essential for the proper subcellular localization of the Epstein-Barr virus nuclear antigen 3A. As described in this paper, we have used deletion analysis to identify a decapeptide, RDRRRNPASR, which is essential for nuclear localization of this protein. Furthermore, this decapeptide is a functional nuclear localization signal as demonstrated by its ability to target expression of beta-galactosidase in the nuclei of transfected cells.