This study examined the effect of acute exercise on food motivation, energy intake, and total physical activity in normal-weight and obese women. Participants of both groups were matched (except for Body Mass Index) and conditions (exercise vs. non-exercise) were randomized and counter-balanced. Eighteen normal-weight and 17 obese women completed an exercise and non-exercise day, each performed on the same day of the week. Exercise was performed on a motor-driven treadmill at 3.8 mph and 0% grade for 45 continuous minutes. To test for food motivation, participants were shown a continuous stream of pictures of food and flowers (control) while neural activity was monitored. Data were analyzed using a 2-group x 2-exercise condition x 2-picture type repeated measures analysis of covariance on event-related potential (ERP) amplitude and latency. Dietary records were analyzed using the Food Processor SQL nutrition software. Physical activity was monitored using a GT1M accelerometer. For both groups under both conditions, ERP amplitude was higher and latency was lower for food pictures compared to flower pictures. When normal-weight and obese women were combined, there was a significant condition*picture type interaction for late positive potential (P=0.04) with participants showing less neurological response to food pictures following a 45-minute exercise bout. Exercise did not alter energy intake. However, the exercise condition resulted in significantly more total physical activity, moderate intensity, vigorous intensity, moderate-to-vigorous (MVPA) intensity activity, and less sedentary time than the non-exercise condition. There was a significant group*condition interaction for MVPA (P=0.043) with obese women showing less MVPA than the normal-weight group. The sample of women studied did not show neurological differences in response to pictures of food based upon BMI. However, exercise decreased neurological responses to food, which may indicate lower food motivation. A supervised and planned exercise bout dramatically increased total physical activity in normal-weight and obese women compared to a day without planned exercise. There may be some negative compensation for MVPA in obese women following a 45-minute exercise bout compared to normal-weight women.

Objective: Sleep deprivation has been proposed as a potential correlate of obesity, particularly influencing energy intake. Therefore, the purpose of this study was to compare neural indices of attention related to food motivation and energy intake in normal-weight and obese women under two separate sleep conditions: 1) sleep-restricted (<5 hours) and 2) recommended sleep (~8 hours). This study used a combined cross-over and ex post facto design with condition order counter-balanced. Methods: Twenty-two normal-weight (age=30.9±9.5y, BMI=22.0±1.6 kg/m2) and 18 obese (age=29.7±10.7 y, BMI=36.4±5.3 kg/m2) women completed both sleep conditions. To confirm sleep levels, participants recorded sleep quality and quantity via sleep logs and wore a wrist actigraph. Following each condition, participants reported to the laboratory under the same fed state (energy shake ~10% of total daily needs) to verify they followed the sleep protocol. Subsequently, motivation for food was tested using electroencephalogram (EEG); participants completed a computerized passive-viewing task of food and flowers, while event-related brain potentials (ERPs) were recorded. After EEG testing, participants continued their normal routine but recorded all energy intake using weighed food scales. There were no instructions or limitations on dietary intake. Analyses included P300 and LPP amplitudes in response to picture type, total next day energy intake, and energy intake by several periods of the day. Results: Participants averaged 4.7±0.4 hours of sleep during the sleep-restricted condition and 7.7±0.3 hours during the recommended sleep condition (F=1057.02; P<0.0001). There was no group*condition interaction for next day food motivation (P300: F<2.896, P>0.09; LPP: F<2.967, P>0.093). Next day total energy intake also did not differ by group*condition (F=1.81; P=0.187). When participants were pooled, there was no difference in energy intake by sleep condition (F=0.00; P=0.953). However, when participants’ energy intake was analyzed during the lunch period (following testing to 1:30pm) there was a significant group*condition interaction (F=6.12; P=0.018). The obese women ate significantly more (~300 kcal) during the sleep-deprived condition compared to the recommended condition, whereas the normal-weight women did not. Conclusion: Compared to suggested levels of sleep, sleep restriction and obesity do not influence next day food motivation or total next day energy intake. However, sleep restriction and obesity may influence feeding during certain portions of the day.

Purpose: The purpose of this study was to examine the effects of long-term (24 weeks) physical activity on attention allocated toward food in college freshmen women. Methods: Seventy-nine freshmen college women wore a multi-function pedometer for 24 weeks after being randomly assigned to a daily step level: 10,000; 12,500; or 15,000. After at least 16 weeks of intervention, participants were given a cognitive viewing task (pictures of food and flowers) with the neural response measured using electroencephalogram (EEG) and event-related potentials (ERPs). P300s and LPPs are components of the ERP indicating increased attention to stimuli. Results: There was a significant difference in daily step counts between groups. No interaction between step group and picture condition (food vs. flowers) was found for any of the three ERP (event-related potential) variables (P300 amplitude, P300 latency, LPP amplitude). The 12,500 group showed a significantly elevated response in comparison to the other groups for both food and flowers (F=8.84; P=0.0002). Additionally, subjective rating of hunger was significantly lower in the 15,000 step group (F=4.72; P=0.0030). Conclusion: It appears that long-term increases in physical activity are capable of reducing neural orientation toward hedonic food cues as well as subjective hunger ratings. In addition to increasing energy expenditure, increases in long-term physical activity may also influence the physiological drive to consume food.

L’obésité est un facteur de risque lié à des problèmes physiques, émotionnels et comportementaux. Aujourd’hui, l’alimentation est composée d’un régime typiquement occidental «Western diet» qui est riche en acides gras saturés (AGS) et pauvre en acides gras polyinsaturés (AGPI) tel que les oméga-3 (N-3) et occasionnant un déséquilibre du ratio alimentaire N-6/N-3. Ce déséquilibre est une des causes de la prévalence des maladies mentales y compris celles des troubles de l'humeur et de l’anxiété. L’acide docosahexaénoïque (ADH, 22: 6 n-3) est l’acide gras (AG) le plus abondant dans le cerveau et son accumulation est particulièrement élevée pendant la période périnatale. Il joue un rôle important dans le développement neuronal et d'autres fonctions du cerveau tel l'apprentissage et la mémoire. Des perturbations de l’environnement périnatal peuvent influencer à très long terme l’avenir de la descendance en la rendant plus susceptible de développer des problèmes d’obésité dans un contexte nutritionnel riche. On ignore cependant si le déficit alimentaire chez la mère et particulièrement en ADH aura un impact sur la motivation alimentaire de la progéniture. L’objectif principal de cette thèse est d’étudier le rôle potentiel des N-3 sur la balance énergétique, la motivation alimentaire, la dépression et le niveau d’anxiété des descendants de souris mâles adultes assujetties à une alimentation riche en gras. Nos données ont démontré qu‘un régime maternel déficitaire en ADH durant la période périnatale incitait la descendance à fournir plus d’effort afin d’obtenir un aliment palatable. Ceci entraînerait un dérèglement de l’homéostasie énergétique en augmentant le gain de poids et en diminuant l’activité locomotrice tout en exacerbant le comportement de type anxieux dès que les souris sont exposées à un milieu obésogène. Les acides gras libres (AGL) sont des nutriments essentiels fonctionnant comme des molécules de signalisation dans le cerveau en ayant des récepteurs qui jouent un rôle important dans le contrôle du métabolisme énergétique. Parmi eux, on distingue un récepteur couplé à la protéine G (GPCR), le GPR120. Ce récepteur activé par les AGPI ω-3 intervient dans les mécanismes anti-inflammatoires et insulino-résistants via les N-3. Une mutation dans le gène GPR120 occasionnée par une réduction de l’activité de signalisation du gène est liée à l’obésité humaine. L'objectif premier de cette deuxième étude était d’évaluer l'impact de la stimulation pharmacologique de GPR120 dans le système nerveux central (SNC) sur l'alimentation, les dépenses d'énergie, le comportement de type anxieux et la récompense alimentaire. Nos résultats démontrent qu’une injection centrale aiguë d'agoniste GPR120 III réduit la prise alimentaire ad libitum et la motivation alimentaire pour un aliment riche en gras et en sucre; ainsi que les comportements de type anxieux. L’injection centrale chronique (21 jours) de ce même agoniste GPR120 III transmis par une pompe osmotique a démontré que les souris placées sous diète hypercalorique (HFD n’ont présenté aucune modification lors de la prise alimentaire ni de gain de poids mais qu’il y avait comparativement au groupe de véhicule, une réduction du comportement de type anxieux, que ce soit dans le labyrinthe en croix surélevé (LCS) ou dans le test à champ ouvert (OFT). L’ADH est reconnu pour ses propriétés anorexigènes au niveau central. De plus, la stimulation des récepteurs de GPR120 au niveau du cerveau avec un agoniste synthétique peut produire un effet intense intervenir sur le comportement lié à l'alimentation des rongeurs. Trouver une approche visant à contrôler à la fois la neuroinflammation, la récompense alimentaire et les troubles émotionnels aiderait assurément au traitement de l'obésité et du diabète de type 2. / Obesity is a risk factor for metabolic and mood disorders. The increasing abundance of the "Western diet" that is rich in saturated fatty acids (SFA) and low in polyunsaturated fatty acids (PUFA) omega-3 (N-3) can generate a physiological imbalance in the ratio of N-6/N-3 fatty acids. Such an imbalance has also been implicated in the increased prevalence of mood disorders and metabolic diseases. Docosahexaenoic acid (DHA, 22:6n-3), the most abundant fatty acid (FA) in the brain is accumulated not only during the post-natal period but also during the perinatal period. It plays an important role in neuronal development and other brain functions such as learning and memory. Disturbances of the perinatal environment can influence the sustainable future of the offspring, making it more likely to develop obesity in rich nutritional context. Some data suggest that an inadequate maternal intake of N-3 during pregnancy and the perinatal period may cause an increase in appetite signalling in the offspring as well as an increase rate of neurological and cardio-metabolic disease. It is not known if maternal dietary deficiency in N-3 will have an impact on food motivation of the offspring. The main objective of this thesis was to study the potential effect of dietary deficiency of DHA during the perinatal period on energy balance, food motivation and the anxiety-like behavior of adult male mouse offspring placed on HFD. Our data showed, as expected, that the maternal DHA deficient diet during perinatal period encouraged offspring to work harder to get a palatable food, entailed a dysregulation of energy homeostasis by increasing the body weight and reducing locomotor activity and exacerbated the anxiety-like behavior once they were exposed to an obesogenic environment. Free fatty acids (FFA) are essential nutrients that they also function as signalling molecules in the brain and have receptors that play a significant role in the control of energy metabolism. Among them is GPR120, also known as N-3 FA receptor, a g-protein coupled receptor that is reportedly activated by PUFA and shown to mediate the anti-inflammatory and insulin-sensitizing effects of N-3 FA. A mutation in the GPR120 gene that is associated with reduced GPR120 signalling activity is linked to human obesity. The objective of our second study was to test the impact of pharmacological GPR120 stimulation in the CNS on feeding, energy expenditure, anxiety-like behavior and food reward. Our results showed that an acute central injection GPR120 agonist III: reduced ad libitum food intake and the rewarding effect for high fat, high sugar food; produced a significant decrease in the anxiety-like behavior. While mice with the chronic injection (21 days) of GPR120 III agonist pump on HFD didn’t show any modification in food intake or body weight gain, but show a reduction of anxiety-like behavior in Elevated plus maze (EPM) and open-field test (OFT) compare to the vehicle group. DHA is notifies to have an anorectic action. Furthermore, stimulation of GPR120 receptors with synthetic agonist may cause an acute and profound effect on food related behavior in rodents. To find an approach that aims to control neuroinflammation, food reward and emotional disorders would greatly assist the treatment of obesity and type 2 diabetes.