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Brondel L.,Center Europeen des science du Gout | Brondel L.,Ufr Of Medecine Of Luniversite Of Bourgogne | Romer M.A.,Center Europeen des science du Gout | Nougues P.M.,Center Europeen des science du Gout | And 2 more authors.
American Journal of Clinical Nutrition

Background: Acute partial sleep deprivation increases plasma concentrations of ghrelin and decreases those of leptin. Objective: The objective was to observe modifications in energy intake and physical activity after acute partial sleep deprivation in healthy men. Design: Twelve men [age: 22 ± 3 y; body mass index (in kg/m2): 22.30 ± 1.83] completed a randomized 2-condition crossover study. During the first night of each 48-h session, subjects had either ≈8 h (from midnight to 0800) or ≈4 h (from 0200 to 0600) of sleep. All foods consumed subsequently (jam on buttered toast for breakfast, buffet for lunch, and a free menu for dinner) were eaten ad libitum. Physical activity was recorded by an actimeter. Feelings of hunger, perceived pleasantness of the foods, desire to eat some foods, and sensation of sleepiness were also evaluated. Results: In comparison with the 8-h sleep session, subjects consumed 559 ± 617 kcal (ie, 22%) more energy on the day after sleep restriction (P < 0.01), and preprandial hunger was higher before breakfast (P < 0.001) and dinner (P < 0.05). No change in the perceived pleasantness of the foods or in the desire to eat the foods was observed. Physical activity from 1215 to 2015 was higher after sleep restriction than after 8 h of sleep (P < 0.01), even though the sensation of sleepiness was more marked (P < 0.01). Conclusions: One night of reduced sleep subsequently increased food intake and, to a lesser extent, estimated physical activity-related energy expenditure in healthy men. These experimental results, if confirmed by long-term energy balance measurements, suggest that sleep restriction could be a factor that promotes obesity. This trial was registered at clinicaltrials.gov as NCT00986492. © 2010 American Society for Nutrition. Source

Faure F.,Head and Neck Surgery | Da Silva S.V.,Center Europeen des science du Gout | Jakob I.,Center Europeen des science du Gout | Pasquis B.,French National Institute for Agricultural Research | Sicard G.,Center Europeen des science du Gout

Objectives/Hypothesis: Clinical studies have documented that cytotoxic chemotherapy is often associated with body weight loss and decreased enjoyment of food. Besides taste, olfaction plays a role in food intake. We assessed whether systemic chemotherapeutic cancer treatment compromises olfactory function in rats and mice treated with docetaxel (Taxotere; Sanofi-Aventis, Paris, France). Study Design: Randomized, controlled trials on mice and rats. Methods: Male mice received a single and male rats either a single, two, or three docetaxel administrations. Olfactory function was tested by means of electroolfactograms (EOGs) from the chemosensory epithelium of the nasal septum and the endoturbinates. We evaluated and compared the magnitude of EOG responses evoked by different odorants recorded at different time points after treatment. Results: In both animal species, docetaxel administration reduced body weight gain, thus evidencing the general toxic effect of the drug. In both animal species, the olfactory mucosa remained responsive to stimulation of odorants during the whole course of experiment, but treatment revealed regional differences of docetaxel susceptibility and induced marked transitory electrophysiological changes. In mice and rats a significant transitory decrease in EOG response magnitude occurred after a single administration. Unexpectedly, in rats we also observed an increase of the olfactory response following the second administration of the drug. Conclusions: Docetaxel exerts a neurotoxic effect on olfactory epithelia of rodents at doses similar to human doses, thus inducing transitory functional alterations. Although moderate, they are consistent with the hypothesis of a dysfunction of olfactory function. Further experiments are needed to elucidate the origin of the electrophysiological effects and their impact on the olfactory perception. © 2010 The American Laryngological, Rhinological and Otological Society, Inc. Source

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