73 research outputs found

    Emotional eating in youngsters : the role of rejection and emotion regulation

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    Over selectieve eters: een strijd aan tafel

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    The daily relation between parental rejection and emotional eating in youngsters : a diary study

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    KEY POINTS Cross-sectional survey studies have demonstrated significant associations between parental rejection and peer rejection on the one hand and disturbed eating in youngsters, like emotional eating, on the other hand. In this study, we wanted to expand our knowledge on these relationships by investigating the daily fluctuations in these variables. Youngsters completed a 7-day diary to assess daily parental rejection, peer rejection and emotional eating. Using multilevel analyses, our results showed that daily variations in parental rejection were related to daily variations in emotional eating of the youngsters. This highlights the importance of addressing the parent-child relationship in interventions for emotional eating in youngsters.Background: This study investigated the daily relation between parental rejection and peer rejection on the one hand and emotional eating in youngsters on the other hand.Methods: Participants (N = 55) between the ages of 11 and 15 years completed a 7-day diary. A multilevel design was used to examine day-to-day within-person relationships between parental and peer rejection (measured by CHS) and emotional eating (measured by DEBQ-C) of youngsters.Results: The results showed that daily variations in parental rejection were related to daily variations in emotional eating of the youngsters. Daily peer rejection was only marginally significantly related to the emotional eating of the youngsters.Conclusions: These results indicate that especially parental rejection, and to a lesser extent peer rejection, are associated with the emotional eating of youngsters. The findings highlight the importance of addressing the parent-child relationship in interventions for emotional eating in youngsters

    Efficient gene delivery and silencing of mouse and human pancreatic islets

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    <p>Abstract</p> <p>Background</p> <p>In view of the importance of beta cells in glucose homeostasis and the profound repercussions of beta cell pathology on human health, the acquisition of tools to study pancreatic islet function is essential for the design of alternative novel therapies for diabetes. One promising approach toward this goal involves the modification of gene expression profile of beta cells.</p> <p>Results</p> <p>This study describes a new method of gene and siRNA delivery into human pancreatic islets by microporation technology. We demonstrated that mild islet distention with accutase greatly enhanced the transfection efficiency without compromising in vitro function (secretion, apoptosis and viability). As an example, the recently identified gene involved in type 2 diabetes, ZnT8, can be over-expressed or silenced by RNA interference using this technology. Microporation can also be used on rodent islets.</p> <p>Conclusions</p> <p>Taken together, our results demonstrate that microporation technology can be used to modify gene expression in whole rodent and human islets without altering their in vitro function and will be key to the elucidation of the factors responsible for proper islet function.</p

    In vivo expression and functional characterization of the zinc transporter ZnT8 in glucose-induced insulin secretion.

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    International audienceInsulin-secreting pancreatic beta cells are exceptionally rich in zinc. In these cells, zinc is required for zinc-insulin crystallization within secretory vesicles. Secreted zinc has also been proposed to be a paracrine and autocrine modulator of glucagon and insulin secretion in pancreatic alpha and beta cells, respectively. However, little is known about the molecular mechanisms underlying zinc accumulation in insulin-containing vesicles. We previously identified a pancreas-specific zinc transporter, ZnT-8, which colocalized with insulin in cultured beta cells. In this paper we studied its localization in human pancreatic islet cells, and its effect on cellular zinc content and insulin secretion. In human pancreatic islet cells, ZnT-8 was exclusively expressed in insulin-producing beta cells, and colocalized with insulin in these cells. ZnT-8 overexpression stimulated zinc accumulation and increased total intracellular zinc in insulin-secreting INS-1E cells. Furthermore, ZnT-8-overexpressing cells display enhanced glucose-stimulated insulin secretion compared with control cells, only for a high glucose challenge, i.e. >10 mM glucose. Altogether, these data strongly suggest that the zinc transporter ZnT-8 is a key protein for both zinc accumulation and regulation of insulin secretion in pancreatic beta cells

    Variability of sleep stage scoring in late midlife and early old age

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    peer reviewedSleep stage scoring can lead to important inter-expert variability. Although likely, whether this issue is amplified in older populations, which show alterations of sleep electrophysiology, has not been thoroughly assessed. Algorithms for automatic sleep stage scoring may appear ideal to eliminate inter-expert variability. Yet, variability between human experts and algorithm sleep stage scoring in healthy older individuals has not been investigated. Here, we aimed to compare stage scoring of older individuals and hypothesized that variability, whether between experts or considering the algorithm, would be higher than usually reported in the literature. Twenty cognitively normal and healthy late midlife individuals’ (61 ± 5 years; 10 women) night-time sleep recordings were scored by two experts from different research centres and one algorithm. We computed agreements for the entire night (percentage and Cohen's κ) and each sleep stage. Whole-night pairwise agreements were relatively low and ranged from 67% to 78% (κ, 0.54–0.67). Sensitivity across pairs of scorers proved lowest for stages N1 (8.2%–63.4%) and N3 (44.8%–99.3%). Significant differences between experts and/or algorithm were found for total sleep time, sleep efficiency, time spent in N1/N2/N3 and wake after sleep onset (p ≤ 0.005), but not for sleep onset latency, rapid eye movement (REM) and slow-wave sleep (SWS) duration (N2 + N3). Our results confirm high inter-expert variability in healthy aging. Consensus appears good for REM and SWS, considered as a whole. It seems more difficult for N3, potentially because human raters adapt their interpretation according to overall changes in sleep characteristics. Although the algorithm does not substantially reduce variability, it would favour time-efficient standardization

    Plasticity in the Sensitivity to Light in Aging: Decreased Non-visual Impact of Light on Cognitive Brain Activity in Older Individuals but No Impact of Lens Replacement

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    Beyond its essential visual role, light, and particularly blue light, has numerous non-visual effects, including stimulating cognitive functions and alertness. Non-visual effects of light may decrease with aging and contribute to cognitive and sleepiness complaints in aging. However, both the brain and the eye profoundly change in aging. Whether the stimulating effects light on cognitive brain functions varies in aging and how ocular changes may be involved is not established. We compared the impact of blue and orange lights on non-visual cognitive brain activity in younger (23.6 ± 2.5 years), and older individuals with their natural lenses (NL; 66.7 ± 5.1 years) or with intraocular lens (IOL) replacement following cataract surgery (69.6 ± 4.9 years). Analyses reveal that blue light modulates executive brain responses in both young and older individuals. Light effects were, however, stronger in young individuals including in the hippocampus and frontal and cingular cortices. Light effects did not significantly differ between older-IOL and older-NL while regression analyses indicated that differential brain engagement was not underlying age-related differences in light effects. These findings show that, although its impact decreases, light can stimulate cognitive brain activity in aging. Since lens replacement did not affect light impact, the brain seems to adapt to the progressive decrease in retinal light exposure in aging
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