Sleep Patterns, Diet Quality and Energy Balance.

Healthy Active Living and Obesity Research Group, Children's Hospital of Eastern Ontario Research Institute, 401 Smyth Road, Ottawa, Ontario, , K1H 8L1Canada. Electronic address: .
Physiology & Behavior (Impact Factor: 3.16). 09/2013; DOI: 10.1016/j.physbeh.2013.09.006
Source: PubMed

ABSTRACT There is increasing evidence showing that sleep has an influence on eating behaviors. Short sleep duration, poor sleep quality, and later bedtimes are all associated with increased food intake, poor diet quality, and excess body weight. Insufficient sleep seems to facilitate the ingestion of calories when exposed to the modern obesogenic environment of readily accessible food. Lack of sleep has been shown to increase snacking, the number of meals consumed per day, and the preference for energy-rich foods. Proposed mechanisms by which insufficient sleep may increase caloric consumption include: (1) more time and opportunities for eating, (2) psychological distress, (3) greater sensitivity to food reward, (4) disinhibited eating, (5) more energy needed to sustain extended wakefulness, and (6) changes in appetite hormones. Globally, excess energy intake associated with not getting adequate sleep seems to be preferentially driven by hedonic rather than homeostatic factors. Moreover, the consumption of certain types of foods which impact the availability of tryptophan as well as the synthesis of serotonin and melatonin may aid in promoting sleep. In summary, multiple connections exist between sleep patterns, eating behavior and energy balance. Sleep should not be overlooked in obesity research and should be included as part of the lifestyle package that traditionally has focused on diet and physical activity.

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    Frontiers in Endocrinology 01/2014; 5:116.
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    ABSTRACT: Abstract Background: Three-month-old neuron-specific lipoprotein lipase (LPL)-depleted mice (NEXLP(-/-)) mice are preobese and have normal body weight before developing obesity by 4.5 months. This series of experiments investigated responses to novel environment stimuli and acute sleep deprivation in preobese NEXLPL(-/-)) mice to test the hypothesis that neuron-specific LPL deletion alters normal adaptive metabolic responses to environmental challenges. Methods: Three-month-old, age- and weight-matched, male NEXLPL(-/-)) (n=10) and wild-type (WT) (n=10) mice were housed in individual metabolic chambers with a 12-hr dark cycle. Food and water intake, locomotor activity, and calorimetry data were recorded in 12-min intervals. Novel environmental responses were elicited by first-time introduction to chambers at dark onset, followed by acclimation, baseline recording, and 6-hr of sleep deprivation on subsequent experimental days. Results: NEXLPL(-/-)) mice displayed a 1.5-fold greater increase in activity in response to a novel environment than seen in WT controls (P=0.0308), and a two-fold greater increase in food intake following acute sleep deprivation (P=0.0117). NEXLPL(-/-)) mice averaged a 27% higher metabolic rate than WT mice throughout the experiments (P<0.0001). Body weight, composition, and temperature did not differ between murine groups throughout the experiments. Levels of free fatty acid, insulin, glucose, and triglycerides were similar between groups at the terminus. Conclusions: A deficiency in neuronal LPL signaling disrupts normal responses to novel environmental exposure and acute sleep deprivation, a maladaptive response that may contribute to weight gain in genetically predisposed mice, and perhaps humans.
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