Sleep deprivation has become customary in many societies with the spread of modern educational institutions, and the availability of modern communication gadgets. The hours of sleep have decreased by up to two hours in much of the US. At present, almost 40 percent of young American adults sleep less than seven hours a night, and in middle age, a third of people do not get even six hours of night sleep. This has occurred simultaneously with a significant increase in obesity and diabetes prevalence.
Sleep in humans is usually made up of a single block of 7-9 hours at night, during which feeding is absent. This results in a long overnight period of fasting. For this reason, insulin sensitivity and pancreatic β-cell activity in response to blood sugar levels vary with sleep, maintaining a steady blood glucose level during this fasting period. This is remarkable when compared with the 10-20 mg/dL drop in glucose levels that occurs with the same period of fasting while the person is awake, lying down, and inactive.
Glucose homoeostasis during sleep
The glucose homeostatic mechanisms that operate during sleep therefore include insulin production and sensitivity regulation, the amount of glucose uptake by tissues during sleep, and glucose tolerance in the sleep period. It is important to note that glucose tolerance is at its minimum during the middle part of sleep, and this coincides with a nadir in brain glucose use during slow-wave sleep, and decreased peripheral utilization of glucose. These changes begin to reverse towards morning. They are also associated with sleep in the daytime.
The mechanisms underlying glucose intolerance in sleep-disordered individuals may involve sleep changes. For instance, when human beings are completely deprived of sleep they show increased feeding behavior or reduced glucose tolerance. This is rare, however, with partial loss of sleep being far more common.
This is accompanied by impairment of glucose metabolism over a few days. Leptin levels drop by almost a fifth, and since this is an anorexigenic hormone, feeding is promoted, with sympathetic activation. This has been seen enhanced by an almost 30 percent increase in ghrelin levels, this being a hormone that increases appetite. The desire to eat high-carbohydrate foods correspondingly has been shown to go up by a third. Again, insulin responsiveness was reduced in these subjects.
While the mechanism is debated, the disruption of glucose homeostasis may be caused by sympathetic-mediated inhibition of insulin release. This may be worsened by changes in the appetite-regulating hormones, which in turn elevate levels of growth hormone and cortisol levels in the night. Inflammation is also promoted by loss of sleep even for one night, which may increase the risk of insulin resistance.
Prevention of diabetes by sleep
Many large studies have shown that sleeping for six or less hours, or for nine or more hours, can be predictors of increased risk of glucose intolerance or frank diabetes mellitus, even with adjustment for confounding factors. It is becoming evident that teaching proper sleep habits from childhood on has the potential to be an important intervention in primary prevention of diabetes.
References
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2697035/
- http://jamanetwork.com/journals/jamainternalmedicine/fullarticle/410883
- https://www.ncbi.nlm.nih.gov/pubmed/19627193
- https://www.ncbi.nlm.nih.gov/pubmed/9085517
Further Reading
Exercise shown to curb appetite in diabetes and prediabetes patients