No abstract

Taste is involved in food preference and choice, and it is thought that it can modulate appetite and food intake. The present study investigated the effect of savory or sweet taste on satiation, reward, and food intake and according to individual differences in eating behavior traits underlying susceptibility to overeating. In a crossover design, 30 women (BMI = 22.7 ± 2.3; age = 21.9 ± 2.6 y) consumed a fixed energy preload (360 kJ/g) with a savory, sweet, or bland taste before selecting and consuming items from a test meal ad libitum. Sensations of hunger were used to calculate the satiating efficiency of the preloads. A computerized task was used to examine effects on food reward (explicit liking and implicit wanting). The Three Factor Eating Questionnaire was used to compare individual differences in eating behavior traits. Satiation and total food intake did not differ according to preload taste, but there was an effect on explicit liking and food selection. The savory preload reduced liking and intake of high-fat savory foods compared to sweet or bland preloads. The eating behavior trait disinhibition interacted with preload taste to determine test meal intake. Higher scores were associated with increased food intake after the sweet preload compared to the savory preload. Independent of preload taste, disinhibition was associated with lower satiating efficiency of the preloads and enhanced implicit wanting for high-fat sweet food. Savory taste has a stronger modulating effect on food preference than sweet or bland taste and may help to preserve normal appetite regulation in people who are susceptible to overeating.

This research highlights the need for specific messages to help poorly educated families adopt good eating habits.

HepaRG human liver progenitor cells exhibit morphology and functionality of adult hepatocytes. We investigated the susceptibility of HepaRG hepatocytes to in vitro infection with serum-derived hepatitis C virus (HCV) particles (HCVsp) and the potential neutralizing activity of the E1E2-specific monoclonal antibody (mAb) D32.10. The infection was performed using HCVsp when the cells actively divided at day 3 postplating. HCV RNA, E1E2, and core antigens were quantified in HCV particles recovered from culture supernatants of differentiated cells for up to 66 days. The density distributions of particles were analyzed on iodixanol or sucrose gradients. Electron microscopy (EM) and immune-EM studies were performed for ultrastructural analysis of cells and localization of HCV E1E2 proteins in thin sections. HCV infection of HepaRG cells was documented by increasing production of E1E2-core-RNA(1) HCV particles from day 21 to day 63. Infectious particles sedimented between 1.06 and 1.12 g/mL in iodixanol gradients. E1E2 and core antigens were expressed in 50% of HCV-infected cells at day 31. The D32.10 mAb strongly inhibited HCV RNA production in HepaRG culture supernatants. Infected HepaRG cells frozen at day 56 were reseeded at low density. After only 1-3 subcultures and induction of a cell differentiation process the HepaRG cells produced high titer HCV RNA and thus showed to be sustainably infected. Apolipoprotein B-associated empty E1E2 and complete HCV particles were secreted. Characteristic virus-induced intracellular membrane changes and E1E2 protein-association to vesicles were observed. Conclusion: HepaRG progenitor cells permit HCVsp infection. Differentiated HepaRG cells support longterm production of infectious lipoprotein-associated enveloped HCV particles. The E1E2-specific D32.10 mAb neutralizes the infection and this cellular model could be used as a surrogate infection system for the screening of entry inhibitors. (HEPATOLOGY 2011;54:406-417) H epatitis C virus (HCV) infection is a major health problem worldwide because at least 70% of infections persist and cause chronic hepatitis, which may progress to liver cirrhosis and hepatocellular carcinoma. 1 The lack of robust cell culture and small animal models remain stumbling blocks to