Homeostasis and food craving in obesity: a functional MRI study.

OBJECTIVES: Food intake in obesity has been found to be reward-based and less contingent on homeostatic needs. Accordingly, previous studies investigating neural processing of food cues observed aberrant processing in reward- and control-related brain regions in obesity. To further investigate the relation between homeostasis and food intake, this study investigated the influence of glucose metabolism on the neuronal response during the regulation of food craving in participants with obesity. METHODS: Twenty-five normal-weight and 25 women with obesity were examined on two occasions after receiving either water or glucose directly into the stomach using a nasogastric tube. Participants were blinded to the type of infusion and were required to refrain from eating for 16 h before each visit. An event-related fMRI paradigm was used to investigate the effect of intestinal glucose load on the neuronal response during the regulation of food craving. RESULTS: A 2 × 2 mixed-model ANOVA revealed that craving regulation was associated with increased activation in fronto-parietal regions in participants with obesity when compared to healthy controls. However, this effect was observed independently from homeostatic satiety. A regression analysis revealed that the reduction of food craving was related to increased activation in the lingual gyrus in individuals with obesity following the infusion of water. CONCLUSIONS: In participants with obesity, the neuronal response during the regulation of food craving is associated with increased neural cognitive top-down control and increased visual food processing. Since this observation was independent from satiety status, our results indicate a reduced influence of homeostasis on neural processing during food craving in obesity. This study was registered on clinicaltrials.org: NCT03075371.

[Follow-up of a cohort of patients after substitution of phenytoin for phenytoin sodium in an epilepsy center]. / Suivi d'une cohorte de patients après substitution de la phénytoïne pour de la phénytoïne sodique dans un centre de lutte contre l'épilepsie.

In March 2012, the French Health Products Safety Agency interrupted the commercialization of di-hydan (phenytoin). It was replaced by diphantoïne (phenytoin sodium) and prescribers were informed that posology was equivalent for both products. We conducted a retrospective study of phenytoinemia and clinical effects comparatively for these two drugs in a population of adult patients with epilepsy admitted in La TEPPE. Forty-four patients were included. Mean age was 47.6 years. Phenytoinemia significantly decreased after substitution (17.14mg/L with di-hydan versus 12.17mg/L with diphantoïne, P<8 10(-6)). Moreover an increase in post substitution posology of diphantoïne was noticed (264.77mg/L with di-hydan versus 274.73mg/L with diphantoïne), although not significant (P=0.11). Increase of seizures was non-significant (P = 0.09). The decrease of phenytoinemia was probably due to the difference of composition between the drugs: a 100mg di-hydan tablet contains 100mg of phenytoin whereas a 100mg diphantoïne tablet contains 92mg. The specific non-linear kinetics of phenytoin reinforces this difference. A prospective study could better evaluate the risk of substituting di-hydan with diphantoïne.