الفهرس 
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Abstract
IR is closely associated with obesity, hypertension, hyperglycemia, polycystic ovary syndrome and metabolic syndrome.
Diabetes is one of the largest global health emergencies of the 21st century. Each year more and more people live with this condition, which can result in life-changing complications.
Obesity is a fast growing problem that is reaching epidemic proportions worldwide. The association of obesity with type 2 diabetes has been recognized for decades, and the major basis for this link is the ability of obesity to engender insulin resistance.
Inadequate sleep is defined as less than 7 total hours of sleep in young adults, according to National Sleep Foundation guidelines. Experimental studies found that sleep deprivation leads to decrease glucose tolerance and compromise insulin sensitivity.
Concurrent with the increase in obesity prevalence, a decrease in sleep duration has been observed over the past decades. Epidemiologic evidence has shown that short sleep duration is associated with obesity and weight gain.
In this study we aimed to study the effect of sleep disturbance on insulin resistance in obese and type 2 diabetic patients by measuring the fasting insulin and calculate the HOMA-IR. The sleep disturbance was detected by sleep questionnaires.
The study was carried out on 92 subjects classified into four groups: group I: Included 23 patients who were diabetic and obese (BMI ≥ 30), group II: Included 23 patients who were diabetic and nonobese (BMI < 30), group III: Included 23 patients who weren’t diabetic (with normal glucose tolerance test) and obese (BMI ≥ 30) and group IV: Included 23 healthy control subjects who weren’t diabetic (with normal glucose tolerance test) nonobese (BMI < 30).
Anthropometric measurements other than BMI were obtained including WC. Laboratory investigations included routine test as ALT and serum creatinine (to exclude any systemic disease), plasma glucose levels (fasting and 2-hours post prandial) and fasting insulin were done. HOMA-IR was calculated to detect insulin resistance. Sleep questionnaires were introduced to the subjects to detect the sleep disturbance.
The questionnaires were used to evaluate the prevalence of some sleep related parameters and ASP “abnormal sleep patterns” in the studied groups which were ;decrease the total sleep time, snoring, insomnia or sleep difficulty, sleep fragmentation, excessive day time sleepiness and day time dysfunction or impairment of daily activities.
In our study diabetic obese individuals showed significantly higher prevalence of these abnormal sleep patterns than the non diabetic nonobese subjects. Also they showed significantly higher prevalence of sleep deprivation in terms of having significantly less hours of sleep at night on weekdays than the only obese and the non diabetic non obese subjects.
In the whole study group, time to fall asleep or latency period (LP) was significantly associated with FPG, 2HPPG, FI, HOMA-IR, and WC, while number of sleep hours at night were significantly associated with WC and BMI.
It was noticed that not only the quantity of sleep but also the quality and the timing of sleep have an effect on glucose regulation and weight gain.
Although the mechanisms by which sleep duration and diabetes risk are related are not fully understood, it has been suggested that habitually short sleep durations could lead to insulin resistance by increasing sympathetic nervous system activity, raising evening cortisol levels and decreasing cerebral glucose utilization.
In summary, sleep restriction has a deleterious impact on BMI, which may involve multiple biological pathways such as decreased leptin and increased ghrelin level. The imbalance between these hormones, which are part of the orexin system that integrates control of feeding, wakefulness, and energy expenditure, may explain the change in hunger, with increased appetite leading to weight gain.