Sleep patterns linked with risk of developing type 2 diabetes

by Barbara Hewitt on December 17, 2013

Six hours of sleep or less a night increases the risk of developing type 2 diabetes while too little or too much is associated with higher rates of obesity, research has found.


Researchers noted that shorter sleep times were associated with greater type 2 diabetes risk

A study of 212,388 adults over the age of 45 found that most, 64.7%, reported normal sleep times of seven or eight hours. But participants that had six hours sleep or less experienced a 30% greater risk of developing insulin resistance and type 2 diabetes.

The study, carried out by researchers at the University of Newcastle in the UK, also showed that having either significantly shorter, under seven hours, or longer, over 10 hours, sleep times was associated with a higher rate of obesity.

The researchers noted with interest that whilst shorter sleep times were associated with greater type 2 diabetes risk, longer sleep times were not. Also of note was that sleep duration was not related to risk of cardiovascular disease.

The research report says that the results are statistically significant and clinically important. In terms of limitations of the study, the research team noted that they were unable to ascertain how much short sleep duration may have been related to presence of a sleep disorder. In addition, the researchers could not be certain of whether type 2 diabetes had existed or not prior to participants reporting their sleep times.

In explanation of the results, the researchers draw attention to the fact that reduced sleep is linked with increases in ghrelin, the hormone which stimulates appetite, and decreases in leptin, the hormone which suppresses appetite.

Meanwhile, research at the Perelman School of Medicine at the University of Pennsylvania in the United States into the effects of sleep deprivation on the brains of older mice has found that it can affect the pancreas.

Nirinjini Naidoo, research associate professor in the Division of Sleep Medicine, found that stress in pancreatic cells due to sleep deprivation may contribute to the loss or dysfunction of these cells important to maintaining proper blood sugar levels, and that these functions may be exacerbated by normal aging.

‘The combined effect of ageing and sleep deprivation resulted in a loss of control of blood sugar reminiscent of pre-diabetes in mice. We hypothesise that older humans might be especially susceptible to the effects of sleep deprivation on the disruption of glucose homeostasis via cell stress,’ said Naidoo.

Older mice fared markedly worse when subjected to sleep deprivation. Pancreas tissue from older mice or from young animals subjected to sleep deprivation exhibited signs of protein misfolding, yet both were able to maintain insulin secretion and control blood sugar levels. Pancreas tissue from acutely sleep deprived aged animals exhibited a marked increase in CHOP, a protein associated with cell death, suggesting a maladaptive response to cellular stress with age that was amplified by sleep deprivation.

Acute sleep deprivation caused increased plasma glucose levels in both young and old animals. However, this change was not overtly related to stress in beta cells, since plasma insulin levels were not lower following acute lack of sleep.

Accordingly, young animals subjected to acute sleep deprivation remained tolerant to a glucose challenge. In a chronic sleep deprivation experiment, young mice were sensitised to insulin and had improved control of their blood sugar, whereas aged animals became hyperglycaemic and failed to maintain appropriate plasma insulin concentrations.


The opinions expressed in this article do not necessarily reflect the views of the Community and should not be interpreted as medical advice. Please see your doctor before making any changes to your diabetes management plan.

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