What Do People Know about Food, Nutrition and Health?-General Nutrition Knowledge in the Austrian Population.

BACKGROUND: Only limited information is available on the nutrition knowledge of the general Austrian population and how this relates to the nutrition knowledge of health professionals (medical doctors, pharmacists, nutritionist, dieticians) and school teachers. METHODS: Adolescents and adults at the age of 14-75 years (n = 1000), medical doctors (n = 307), pharmacists (n = 295), nutritionists (n = 124), dieticians (n = 160) and school teachers (n = 873) completed an online survey using a German version of the General Nutrition Knowledge Questionnaire-Revised (GNKQ-R) including self-reported data on sex, age, BMI, and health status. Adolescent and adult participants were recruited by a research agency to be representative for the Austrian population for age, sex, and education. A convenience sample was used for health professionals (medical doctors, pharmacists, nutritionist, dieticians) and school teachers. All participants completed a computer-assisted web-based interviewing (CAWI) survey. RESULTS: Total scores for nutrition knowledge of the general population (61.4%) were significantly lower than scores from all other groups (medical doctors 81.3%, pharmacists 83.0%, dieticians 87.5%, nutritionists 85.6%, school teachers 74.5%). The main drivers for better nutritional knowledge were female sex, higher age, and higher level of education, while BMI classification and self-reported health status had no impact. In regard to single questions, the most striking result was the misclassification of sugar as the nutrient with the most calories by 41.4% of the general population while only 29.0% correctly identified fat to be the nutrient with the most calories. CONCLUSIONS: The nutritional knowledge of the general population should be significantly improved in order to lay a basis for better dietary behavior. In view of the relatively low scores of teachers, their nutrition education should be improved in order to enable transfer of sound education in schools.

Inhibition of Lipid Accumulation in Skeletal Muscle and Liver Cells: A Protective Mechanism of Bilirubin Against Diabetes Mellitus Type 2.

Ectopic lipid accumulation in skeletal muscle and liver drives the pathogenesis of diabetes mellitus type 2 (DMT2). Mild hyperbilirubinaemia has been repeatedly suggested to play a role in the prevention of DMT2 and is known for its capacity to shape an improved lipid phenotype in humans and in animals. To date, the effect of bilirubin on lipid accumulation in tissues that are prone to ectopic lipid deposition is unclear. Therefore, we analyzed the effect of bilirubin on lipid accumulation in skeletal muscle and liver cell lines. C2C12 skeletal mouse muscle and HepG2 human liver cells were treated with physiological concentrations of free fatty acids (FFA) (0.5 mM and 1 mM) and unconjugated bilirubin (UCB) (17.1 and 55 µM). The intracellular presence of UCB upon exogenous UCB administration was confirmed by HPLC and the lipid accumulation was assessed by using Nile red. Exposure of both cell lines to UCB significantly reduced lipid accumulation by up to 23% (p ≤ 0.001) in HepG2 and by up to 17% (p ≤ 0.01) in C2C12 cells at 0.5 and 5 h under hypoglycaemic conditions. Simultaneously, UCB slightly increased FFA uptake in HepG2 cells after 0.5 and 5 h and in C2C12 cells after 12 h as confirmed by gas chromatographic analyses of the remaining FFA content in the incubation media. The effects of UCB on lipid accumulation and uptake were abolished in the presence of higher glucose concentrations. Monitoring the uptake of a radiolabeled glucose analogue [18F]FDG: (2-deoxy-2-[18F]fluoro-D-glucose) into both cell types further indicated higher glucose consumption in the presence of UCB. In conclusion, our findings show that UCB considerably decreases lipid accumulation in skeletal muscle and liver cells within a short incubation time of max. 5 h which suggests that mildly elevated bilirubin levels could lower ectopic lipid deposition, a major key element in the pathogenesis of DMT2.