Autophagy proteins are modulated in the liver and hypothalamus of the offspring of mice with diet-induced obesity.

Nutritional excess during pregnancy and lactation has a negative impact on offspring phenotype. In adulthood, obesity and lipid overload represent factors that compromise autophagy, a process of lysosomal degradation. Despite knowledge of the impact of obesity on autophagy, changes in offspring of obese dams have yet to be investigated. In this study, we tested the hypothesis that maternal obesity induced by a high fat diet (HFD) modulates autophagy proteins in the hypothalamus and liver of the offspring of mice. At birth (d0), offspring of obese dams (HFD-O) showed an increase in p62 protein and a decrease in LC3-II, but only in the liver. After weaning (d18), the offspring of HFD-O animals showed impairment of autophagy markers in both tissues compared to control offspring (SC-O). Between day 18 and day 42, both groups received a control diet and we observed that the protein content of p62 remained increased in the livers of the HFD-O offspring. However, after 82days, we did not find any modulation in offspring autophagy proteins. On the other hand, when the offspring of obese dams that received an HFD from day 42 until day 82 (OH-H) were compared with the offspring from the controls that only received an HFD in adulthood (OC-H), we saw impairment in autophagy proteins in both tissues. In conclusion, this study describes that HFD-O offspring showed early impairment of autophagy proteins. Although the molecular mechanisms have not been explored, it is possible that changes in autophagy markers could be associated with metabolic disturbances of offspring.

Disordered eating among adolescent female swimmers: dietary, biochemical, and body composition factors.

OBJECTIVE: To verify associations among body composition, biochemical parameters, and food intake in adolescent female swimmers with and without disordered eating (DE). METHODS: Seventy-seven athletes 11 to 19 y old from clubs in Rio de Janeiro, Brazil were studied. DE was assessed through three questionnaires (Eating Attitudes Test-26; Bulimic Investigatory Test, Edinburgh; and Body Shape Questionnaire), body composition by dual-energy x-ray absorptiometry, and food intake by a 3-d diet record. Biochemical parameters related to iron, folic acid, and vitamin B12 were analyzed. The Fisher exact test, Mann-Whitney test, and the Spearman coefficient were calculated. RESULTS: DE was found in 44.2% of the sample. DE-positive compared with DE-negative athletes presented greater body fat percentage (11-14 y: 27.5% versus 23.4%, P = 0.023; 15-19 y: 30.2% versus 24.1%, P = 0.006) and fat mass (11-14 y: 13.8 versus 10.3 kg, P = 0.010; 15-19 y: 17.0 versus 13.2 kg, P = 0.027). In relation to food intake, DE-positive athletes presented lower protein consumption in the 11- to 14-y-old group and lower calcium intake adequacy in the 15- to 19-y-old group. Most other dietary parameters showed a low adequacy of consumption, with no difference between athletes with and without DE. Four DE-positive athletes presented anemia or iron deficiency. CONCLUSION: DE-positive compared with DE-negative athletes presented a higher percentage of body fat and fat mass, lower protein consumption in the 11- to 14-y-old group, and lower calcium intake adequacy in the 15- to 19-y-old group. Greater attention should be given to the nutritional state of these athletes, considering the number of adolescents with anemia and an inadequate dietary intake.