Background: Ingestion of sweet food is driven by central reward circuits and restrained by endocrine and neurocrine satiety signals. The specific influence of sucrose intake on central affective and reward circuitry and alterations of these mechanisms in the obese are incompletely understood. For this, we hypothesized that (i) similar brain regions are engaged by the stimulation of sweet taste receptors by sucrose and by non-nutrient sweeteners and (ii) during visual food-related cues, obese subjects show greater brain responses to sucrose compared with lean controls.
Methods: In a double-blind, crossover design, 10 obese and 10 lean healthy females received a sucrose or a non-nutrient sweetened beverage prior to viewing food or neutral images. BOLD signal was measured using a 1.5 Tesla MRI scanner.
Key Results: Viewing food images after ingestion of either drink was associated with engagement of similar brain regions (amygdala, hippocampus, thalamus, anterior insula). Obese differed from lean subjects in behavioral and brain responses rating both beverages as less tasteful and satisfying, yet demonstrating greater brain responses. Obese subjects also showed engagement of an additional brain network (including anterior insula, anterior cingulate, hippocampus, and amygdala) only after sucrose ingestion.
Conclusions & Inferences: Obese subjects had a reduced behavioral hedonic response, yet a greater engagement of affective brain networks, particularly after sucrose ingestion, suggesting that in obese subjects, lingual and gut-derived signaling generate less central hedonic effects than food-related memories in response to visual cues, analogous to response patterns implicated in food addiction.
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http://dx.doi.org/10.1111/nmo.12125 | DOI Listing |
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View Article and Find Full Text PDFSci Immunol
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Department of of Toxicology, Faculty of Pharmacy, Istanbul Okan University, Istanbul, Turkey.
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View Article and Find Full Text PDFJ Agric Food Chem
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College of Food Science and Engineering, Northwest A&F University, No. 22 Xinong Road, Yangling, Shaanxi 712100, China.
Quinoa, rich in pharmacologically active ingredients, possesses the potential benefit in preventing cognitive impairments induced by hypoxia. In this study, the efficacy of quinoa ethanol extracts (QEE) consumption (200 and 500 mg/kg/d, respectively) against hypobaric hypoxia (HH)-induced cognitive deficits in mice was investigated. QEE significantly ameliorated hypoxic stress induced by HH, as evidenced by improvements in baseline indices and reductions in hypoxia-inducible factor 1α levels.
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