7 research outputs found

    Attachment Strategies and Neuroendocrine Biomarkers in Obese Children

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    Financial support by FCT, SFRH/SINTD/60115/2009, FSE-UE.Introduction: Quality of the parent-infant relationship influences the mechanisms of development of the child's physiological stress regulation. This study explored associations between attachment strategies and both cortisol and thyroid stimulating hormone, hypothesized to be respectively a potential mediator and a potential intervening variable of the mother-child relationship in obese children. Material and Methods: A sample of 83 obese children (46 boys), aged 10.9 (1.8) years was recruited from a child obesity clinic. Obesity was defined by body mass index percentile adjusted for age and sex. Metabolic biomarkers were measured by routine methods. Attachment strategies were assessed with self and parent-report questionnaires. Family functioning was assessed with parent-reported questionnaires (FACES-III). Multivariate linear regression analyses were performed. Results: Type A, avoidant attachment strategies, had significant positive association with thyroid stimulating hormone levels and negative association with cortisol levels (R-2 = 0.352). Type B, secure attachment strategies, had significant positive associations with both hypothyroidism and body mass index percentile (R-2 = 0.541). ``Insecure attachment'' (types A and C combined) strategies showed some evidence of positive association with thyroid stimulating hormone (R-2 = 0.250). Discussion: These findings suggest that there may be commonalities in the regulation of hypothalamic-pituitary-adrenal and hypothalamic-pituitary-thyroid axes. Processes involved in development of the type A attachment strategy appear to be associated with effects on the regulatory mechanisms of the hypothalamic-pituitary-adrenal axis. Conclusions: In obese children, different attachment strategies are associated with diverse metabolic profiles. How this may contribute to developing differentiated treatment approaches remains to be explored.publishersversionpublishe

    The role of I-FABP as a biomarker of intestinal barrier dysfunction driven by gut microbiota changes in obesity

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    Financial support from Fundacao para Ciencia e Tecnologia (PTDC/AGR-TEC/2227/2012 and SFRH/BD/93073/2013) is gratefully acknowledged.Background: Intestinal fatty-acid binding protein (I-FABP) is expressed in epithelial cells of the mucosal layer of the small intestine tissue. When intestinal mucosal damage occurs, I-FABP is released into the circulation and its plasma concentration increases. In the context of obesity, the gut barrier integrity can be disrupted by dietary fat while intestinal permeability increases. Objective: To investigate whether intestinal fatty acid binding protein (I-FABP) is a suitable plasma marker of intestinal injury and inflammation in obesity. Methods: Twelve male Wistar rats were randomly divided into two groups of six animals each: standard (St) and high-fat (HF) diet fed groups for 12 weeks. Results: HF fed animals developed obesity, insulin resistance and seemed to present increased plasma levels of proinflammatory cytokines (MCP-1 and IL1 beta). The gut microbiota composition of these animals was also altered, with lower number of copies of Bacteroidetes, Prevotella spp. and Lactobacillus spp., in comparison with those from St diet group. Fecal lipopolysaccharide (LPS) concentrations tended to be increased in HF fed animals. Intestinal expression of TLR4 seemed to be also increased in HF fed animals suggesting that HF diet-induced dysbiosis may be behind the systemic inflammation observed. However, in contrast to other intestinal inflammatory diseases, plasma I-FABP levels were decreased in HF fed rats whereas I-FABP expression in jejunum tended to be increased. Conclusions: HF diet-induced obesity is characterized by dysbiosis, insulin resistance and systemic inflammation. In this context, plasmatic I-FABP should not be used as a marker of the intestinal barrier dysfunction and the low-grade chronic inflammatory status.publishersversionpublishe

    Neuroprotective effects of anthocyanins are mediated by gut microbiota

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    The microbes that collectively inhabit the gut, the gut microbiota, constitute the largest and most diverse community in the body. Besides having an important role in the regulation of host energy metabolism, the gut microbiota can also influence neurodevelopment, modulate behavior and contribute to the development of neurological disorders. High-fat (HF) diets are thought to disrupt the profile of the gut microbiota in a manner that may contribute to the neuroinflammation and neurobehavioral changes observed in obesity. Accordingly, we hypothesized that by preventing HF-diet induced dysbiosis it is possible to prevent neuroinflammation and the consequent neurological disorders.info:eu-repo/semantics/publishedVersio

    Can Antioxidative Status Be Involved in Type 1 Diabetes?

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    Background: Type 1 diabetes mellitus (T1DM) is an autoimmune disease with beta-cell destruction, resulting in insulin deficiency. It is now clear that environmental factors also play a role in disease development. The prevalence of type 1 diabetes in children and young people in Portugal is 0.16% between 0 and 19 years of age. The main cause of death in T1DM is cardiovascular disease, and early endothelial dysfunction is its pathophysiologycal precursor. Hyperglycemia is associated with increased production of free radicals and increased oxidative stress. The aim of this study was to analyze the antioxidant status in a pediatric portuguese diabetic population. Methods: The study was conducted to characterize and compare the antioxidant status in children aged 2 - 10 years old, with type 1 diabetes and healthy children. Plasmatic profile of total phenolic content (TPC), ferric reducing antioxidant power (FRAP), Trolox equivalent antioxidant capacity (TEAC) in children with diabetes and controls, pre-pubescent, and with BMI < 85th centile were evaluated. Results: FRAP values were significantly lower in diabetic children compared with healthy controls (P < 0.001). There was not any statistical significant difference in the TPC and the TEAC determinations. Conclusions: Young Portuguese diabetic children have a lower antioxidant status than healthy children.publishersversionpublishe
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