Sleep and obesity

The control of sleep is closely linked to feeding behaviour and energy expenditure. These determine the body weight and in particular the body fat and lean body mass. Body weight and body mass index (weight in kg/height in m squared) [ BMI ] are only indirect indicators of obesity because they do not assess body composition.

Other measures, such as the waist to hip ratio and collar circumference, give an indication of the distribution of body fat and in particular whether it has a central rather than a peripheral location. Central fat deposition is more common in males and post-menopausal females, and peripheral fat is more common in pre-menopausal females.

Control of sleep and obesity
The control of feeding and of exertion involves environmental, social and psychological factors, as well as complex neurological and humoral control systems.

The ventromedial nucleus of the hypothalamus acts as a satiety centre, and inhibits the more lateral feeding centre, which is otherwise tonically active.

Several humoral factors are relevant to the physiological control and abnormalities of sleep.

Leptin is a protein secreted by adipocytes in white fat, which is mainly subcutaneous. Its blood level therefore is an indirect marker of the quantity of energy stored as fat. Its release is increased by insulin, glucocorticoids and sympathetic activity. It inhibits the synthesis of neuropeptide Y, thereby increasing sympathetic activity and energy expenditure.

It also interacts with melanocortin and agouti-related peptide (Agrp) in the arcuate nucleus in the hypothalamus. Leptin also stimulates melanocyte stimulating hormone (MSH) and cocaine and amphetamine regulated transcript (CART), which inhibit appetite. Leptin is a respiratory stimulant, as well as increasing physical activity and energy expenditure and inhibiting appetite.

A genetic failure to produce leptin can lead to obesity of early onset, but in obesity there is usually an increased leptin level due to leptin resistance. Leptin is also increased in obstructive sleep apnoeas due to increased sympathetic activity, but is reduced in narcolepsy, where there is also a loss of the physiological nocturnal increase in leptin secretion.

Chemicals arising from the gut
This is a growth hormone-like peptide, which is released from the stomach in response to gastric distension. Blood levels therefore rise during meals and fall afterwards. Ghrelin not only stimulates growth hormone secretion through its action in the hypothalamus, but also increases appetite and feeding, leading to obesity.

Cholecystokinin (CCK)
This is secreted by the small intestine in response to distension following food intake. It reduces appetite and food intake.

The secretion of this is related to the meal size. It acts on the arcuate nucleus to reduce appetite and increase energy expenditure.

Neuropeptide Y
This is produced in the small intestine and not only delays gastric emptying, which reduces appetite, but also is present in the neurones of the arcuate nucleus that project to the paraventricular nuclei. It decreases food intake.

Glucagon-like peptide 1 (GLPI)
This is produced by the gastro-intestinal tract and also in the brain. It induces a feeling of satiety.

Insulin is secreted by the pancreas in response to a rise in blood sugar after meals. It promotes NREM sleep.

Orexins (hypocretins)
Orexin modifies feeding behaviour to increase food intake. It also inhibits sleep and limits the duration of REM sleep.

These increase appetite.

These lead to satiety.

Pituitary hormones
Growth hormone and cortisol regulate anabolism and catabolism respectively, and both control and are controlled by the state of sleep. Thyroid function also influences obesity and is itself controlled both by circadian rhythms and by sleep.


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