Both acute and chronic sleep deprivation impair glucose tolerance during wakefulness. Sleep deprivation alters glucose uptake in the cell membrane and cytoplasm. It also reduces the initial insulin response to glucose, probably because of increased sympathetic activity which regulates pancreatic beta cell function and insulin release. There may also be effects on the later increase in plasma insulin because of impaired synthesis of insulin in response to a raised blood glucose level.
Impaired glucose tolerance is also due to other endocrine responses to sleep deprivation. First the hypothalamic pituitary adrenal axis is activated with a rise in Cortisol secretion early in the night, as is seen in depression and with ageing. There is a reduction in prolactin secretion and a loss of the circadian rhythm and quantity secreted of TSH. Sleep fragmentation reduces growth hormone secretion during the initial NREM sleep cycle, although there is some compensatory increase in secretion during wakefulness. This effect on growth hormone and the autonomic abnormalities both reduce lipolysis.
The peak level of leptin, which is produced by fat cells, is normally seen at around 9.00 pm. In sleep deprivation less leptin is secreted. There is a smaller diurnal amplitude in its secretion, particularly in those who are obese and have a high initial leptin level. The findings are similar to those seen in the elderly. Ghrelin, released by the stomach, has opposite effects to leptin, and its secretion increases by around 25% in sleep deprivation.
The lack of leptin and increase in ghrelin reduce the sensation of satiety and increase hunger and appetite, with an increase particularly for carbohydrate and fatty foods. Sleep deprivation in effect leads to an internal misperception of body fat and other energy stores, leading to increased energy intake coupled with an impaired ability to utilize the absorbed carbohydrates and fats. The insulin resistance due to sleep deprivation further increases the risk of diabetes and is associated with an increased triglyceride level and reduced high-density lipoproteins (HDL). These features, together with hypertension, constitute the 'metabolic syndrome'.
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