BACKGROUND: Microvascular dysfunction (MD: impaired performance of blood flow, tissue perfusion, blood pressure, etc.) is one of the earliest stages in the progression of various chronic diseases. OBJECTIVE: The aim of this study was to determine if a difference in microvascular function existed between two metabolically healthy groups that differed in BMI and waist circumference. DESIGN: This study employed a causal comparative design, with two groups: I) normal weight (n =14, BMI 28 kg/m2). METHODS: Microvascular function was assessed by measuring skin blood flow (SkBF) using laser Doppler flowmetry during postocclusive reactive hyperemia (PORH). The area under the SkBF time curve during the 60-second PORH response was used to quantify the magnitude of the microvascular response. RESULTS: Group I (control) had a significantly higher average area under the SkBF time curve (3240 ± 879) than Group II (1948 ± 808) (Z= -3.0094, p = 0.0026). CONCLUSIONS: The overweight/obese subjects exhibited a diminished skin blood flow response to occlusion compared to their normal-weight counterparts. This supports the hypothesis that overweight/obese subjects who are otherwise metabolically healthy exhibit a biological change that is linked to chronic disease.

Adult obesity is associated with increased morbidity and mortality. Increasing success in weight loss maintenance will decrease the prevalence of overweight and obesity, and therefore help control the adverse health effects of excess weight. Much is known about the behavioral characteristics of successful long-term weight loss maintenance, but less is known about the cognitive processes behind weight loss maintenance. The purposes of this study were to (1) identify differences in visual attention to high-energy dense foods between individuals who are normal weight, weight loss maintainers, and overweight/obese in a high-risk (food-buffet) situation; (2) to evaluate differences in food choices from a food buffet between weight status groups; (3) to analyze correlations between food attention and food choice across weight status groups. No significant differences were found between groups with respect to food attention or food choice. Overall, findings from this study may have been limited by methodology, technology, and sample size. Future research is needed to better understand the interaction of cognitive processes and weight loss maintenance.

PURPOSE: To compare the effects of after-school sedentary versus active play on activation in the reward and cognitive control regions of the brain to pictures of high- and low-calorie foods. METHODS: 32 children (12 girls, 20 boys; age 8.7 ± 0.5 years; height 137.9 ± 6.9 cm; weight 32.4 ± 6.2 kg) participated in a randomized crossover study with counterbalanced treatment conditions. Conditions took place on separate days after school and included three hours of active or sedentary play. After each condition, neural activation in reward and cognitive control regions of the brain were assessed using functional magnetic resonance imaging (fMRI) while participants completed a go/no-go task involving pictures of high- and low-calorie foods. General response inhibition was measured by the Stroop task. Hunger was measured upon arrival to the testing facility and just prior to fMRI scans. Mixed effects models were used to evaluate main and interaction effects. RESULTS: Significant stimulus by condition interactions were found in the right superior parietal cortex, right postcentral gyrus and accumbens area (p <<> 0.05). High- versus low-calorie pictures of food elicited significantly different activation bilaterally in the orbitofrontal cortex (p <<> 0.01). Stroop task performance diminished significantly following the sedentary condition compared to the active condition (F = 6.79, p <<> 0.01). Subjective feelings of hunger were not different between conditions at any point. CONCLUSION: Sedentary behavior significantly decreased response inhibition and brain activation to pictures of high-calorie foods in areas of the brain important to the modulation of food intake. Decreased attention, reward, and response inhibition, following sedentary behavior, may contribute to disinhibited eating that can lead to overweight and obesity.

The accumulation of adipose tissue increases the risk of several diseases. The fruits-intake, containing phytochemicals, is inversely correlated with their development. This study evaluated the effects of anthocyanin-rich tart cherries in diet-induced obese (DIO) rats. DIO rats were exposed to a high-fat diet with the supplementation of tart cherry seeds powder (DS) and seed powder plus juice (DJS). After 17 weeks, the DIO rats showed an increase of body weight, glycaemia, insulin, and systolic blood pressure. In the DS and DJS groups, there was a decrease of systolic blood pressure, glycaemia, triglycerides, and thiobarbituric reactive substances in the serum. In the DJS rats, computed tomography revealed a decrease in the spleen-to-liver attenuation ratio. Indeed, sections of the DIO rats presented hepatic injury characterized by steatosis, which was lower in the supplemented groups. In the liver of the DIO compared with rats fed with a standard diet (CHOW), a down-regulation of the GRP94 protein expression and a reduction of LC3- II/LC3-I ratio were found, indicating endoplasmic reticulum stress and impaired autophagy flux. Interestingly, tart cherry supplementation enhanced both unfolded protein response (UPR) and autophagy. This study suggests that tart cherry supplementation, although it did not reduce body weight in the DIO rats, prevented its related risk factors and liver steatosis.

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For nearly three decades, public health officials have been telling Americans that being overweight or obese is extremely dangerous for their health and well-being through public services announcements, popular health news articles, and scientific studies – all decrying the “obesity epidemic” plaguing the United States. In this same period, mean Body Mass Indexes and rates of overweight and obesity in the US have either increased or remained steady, but have seen no wide-spread reversal in direction. Thus, despite public health officials’ diligent efforts, Americans do not seem to be responding to these messages. Any number of causal mechanisms could explain this; however, we should consider the possibility that Americans simply do not believe that being “fat,” “heavy,” or “overweight” is bad for their health. In this dissertation, we ask the question “do you think that being overweight is bad for your health?” by analyzing data from the National Health and Nutrition Examination Survey from 1999 to 2012 – an era in which the frequency of publication on the obesity epidemic reached a record high. Ultimately, we find that Americans are more likely to associate their own status as overweight individuals with lower self-reported health when this status is defined through multiple avenues at once: being clinically overweight, perceiving themselves as overweight persons, and having clinicians tell them directly that they are overweight. Saying “being overweight or obese is unhealthy” is not enough. If Americans do not believe that they are overweight, and if they do not receive personal counsel from medical professionals about their weight status, then they are unlikely to change their opinion of their overall personal health status in light of their status as overweight or obese individuals. Anti-obesity and weight-awareness advocacy has established the mantra: being fat is bad for you. The challenge for public health officials now is to raise awareness about what overweight and obesity truly mean, and to convince clinicians to become much more determined in upholding clinical weight guidelines and informing their patients of their weight statuses. / Sociology

La cellule NK fait partie du système immunitaire inné et participe à l’immunosurveillance anti-tumorale. La compréhension des facteurs affectant leur biologie, telle que la génétique, est donc cruciale. Dans un premier temps, nous avons évalué le rôle de la sous-unité d’intégrine CD11d, sur le phénotype et l'expression d’autres sous-unités (CD11a, CD11b, CD11c, CD18) de diverses cellules immunitaires entre un modèle murin CD11d-KO et une souris C57BL/6 (B6). Nous avons remarqué que l'effet de la délétion de CD11d sur l'expression des autres sous-unités d'intégrine est spécifique à chaque type de cellule immunitaire. La différence la plus notable dans l'expression de CD11b et CD11c a été observée dans les cellules NK. La perte de CD11d dans les cellules NK a entraîné une diminution de l'expression de CD107a après leur activation, ce qui suggère une altération de la dégranulation des cellules NK. Ensuite, malgré une croissance de mélanome similaire, une plus grande proportion de cellules NK issues de CD11d-KO se sont accumulées dans les lits tumoraux par rapport à leur homologue B6. Dans un deuxième temps, nous avons exploité le modèle murin NOD, connu d’avoir des défauts immunitaires importants. L’acquisition des fonctions cytotoxiques des cellules NK se fait par un processus appelé maturation fonctionnelle où une cellule NK est d’abord CD27-CD11b-, suivi du stade CD27+CD11b-, puis CD27+CD11b+ et finalement CD27-CD11b+, soit le stade le plus mature et cytotoxique. Nous avons démontré que les cellules NK de la souris NOD produisent nettement moins d’IFN-γ, de TNFα et de Granzyme B et échouent à réguler l’expression du récepteur d’activation NKG2D pour chaque stade de maturation fonctionnelle. Finalement, nous avons traité des souris immunodéficientes porteuses de tumeurs avec des cellules NK de NOD et B6. Nous avons démontré que, tout comme pour les cellules NK de B6, ce sont surtout des cellules NK CD27+ de NOD qui s’accumulent dans les tumeurs. Par contre, les souris injectées avec des cellules de NOD montraient une croissance tumorale significativement plus importante. De manière générale, ces études sont les premières à élucider les impacts de l’absence de CD11d sur le phénotype et la fonction des cellules NK ainsi que leurs défauts fonctionnels dans la souris NOD au courant de leur maturation fonctionnelle. / NK cells are part of the innate immune system and participate in anti-tumor immunosurveillance. Understanding the factors affecting their biology, such as genetics, is therefore crucial. First, we evaluated the role of the integrin subunit CD11d on the phenotype and expression of other subunits (CD11a, CD11b, CD11c, CD18) of various immune cells between a CD11d-KO mouse model and a C57BL/6 (B6) mouse. We noted that the effect of CD11d deletion on the expression of other integrin subunits is specific to each immune cell type. The most notable difference in CD11b and CD11c expression was observed in NK cells. Loss of CD11d in NK cells resulted in decreased CD107a expression after their activation, suggesting impaired NK cell degranulation. Second, despite similar melanoma growth, a greater proportion of CD11d-KO-derived NK cells accumulated in tumor beds compared to their B6 counterpart. We then exploited the NOD mouse model, known to have significant immune defects. The acquisition of cytotoxic functions of NK cells occurs through a process called functional maturation where an NK cell is first CD27-CD11b-, followed by the CD27+CD11b- stage, then CD27+CD11b+ and finally CD27-CD11b+, the most mature and cytotoxic stage. We demonstrated that NK cells from NOD mice produce significantly less IFN-γ, TNFα, and Granzyme B and fail to regulate the expression of the activation receptor NKG2D for each stage of functional maturation. Finally, we treated immunodeficient tumor-bearing mice with NOD and B6 NK cells. We demonstrated that, as with B6 NK cells, NOD CD27+ NK cells predominantly accumulated in tumors. However, mice injected with NOD NK cells showed significantly greater tumor growth. Overall, these studies are the first to elucidate the impact of the absence of CD11d on the phenotype and function of NK cells as well as their functional defects in NOD mice during their functional maturation.