1. Introduction

The number of patients with diabetes mellitus (DM) is increasing due to changes in people's lifestyles worldwide.

Polyuria is one of the most common complaints among patients with DM. There are two clinical manifestations of diabetes, which are associated with acute or chronic insulin deficiency. This deficiency can be either absolute or relative.

Acute insulin deficiency leads to decompensation of carbohydrate and other types of metabolism, which clinically may result in hyperglycemia, glucosuria, polyuria, polydipsia, hyperphagia, ketoacidosis, and even diabetic coma. The mechanism behind the development of clinical manifestations of acute insulin deficiency includes hyperglycemia, hyperaminoacidemia, hyperlipidemia, and ketoacidosis, caused by disruptions in carbohydrate, protein, and fat metabolism.

Insulin deficiency stimulates gluconeogenesis and lipolysis and inhibits glycogenesis in the liver. Dietary carbohydrates (glucose) are metabolized to a lesser extent in the liver and insulin-dependent tissues than in healthy individuals. Glucagon-stimulated gluconeogenesis for glucose synthesis in the liver (in the context of insulin deficiency) requires the use of amino acids such as alanine. Degrading tissue serves as a source of amino acids.

Since the amino acid alanine is used in gluconeogenesis, the concentration of branched-chain amino acids (valine, leucine, isoleucine) in the blood increases, and their utilization by muscle tissue for protein synthesis decreases. As a result, patients experience hyperkalemia and aminoacidemia. The increase in tissue proteins and amino acids is accompanied by a negative nitrogen balance and is one of the causes of weight loss in patients. This leads to significant hyperglycemia, glucosuria, and polyuria (osmotic diuresis). Fluid loss through urine can reach 3–6 liters per day, resulting in intracellular dehydration and polydipsia [1].

The increase in the number of diabetes patients naturally leads to a rise in deaths caused by complications of the disease.

According to the World Health Organization, 3.8 million people die annually from diabetes-related complications.

DM (diabetes mellitus) can cause various types of nerve fiber damage, but the most common complication negatively impacting patients' quality of life is diabetic distal polyneuropathy [2,3,4,5].

Diabetic neuropathy is a well-established process of nerve structure damage.

It may be asymptomatic or symptomatic and can develop with any type of diabetes. Among the neurological complications of diabetes mellitus, distal polyneuropathy accounts for 70%. According to various studies, this complication occurs in 7.5–10% of patients with type 2 diabetes [4,6].

The first diagnostic symptom of diabetes may be damage to the nervous system.

The development of distal polyneuropathy may indicate a severe course of the underlying disease. The presence of prolonged, uncontrolled hyperglycemia points to a worsening prognosis for the patient. Damage to the peripheral nervous system in the form of mono- and polyneuropathies can lead to balance loss. This increases the risk of trauma and may cause trophic disorders of the limbs and the development of "diabetic foot" syndrome, ultimately leading to additional treatment costs, including surgical intervention, and possibly loss of working ability.

At the same time, physiotherapeutic and non-pharmacological correction methods are expanding every year, including a number of approaches that can be combined [3,7,8].

In patients with diabetes complicated by diabetic polyneuropathy, neuropathy symptoms (pain, tingling, burning or freezing sensations) usually worsen in the evening. Some patients are even forced to take painkillers. Naturally, this disrupts the process of falling asleep and affects sleep quality.

2. Main Part

Diabetes is a widespread disease associated with rapid social and cultural changes such as population aging, urbanization, changes in diet, reduced physical activity, and unhealthy lifestyles. It affects patients' quality of life and leads to a reduced life expectancy [9,10].

Sleep is a period of physical and mental rest. As one of the most essential human needs, sleep is necessary for good health and quality of life [11]. However, sleep disorders, environmental disturbances, and mood disorders negatively impact sleep quality [12,13].

The National Sleep Foundation (2015) recommends that adults aged 26 to 64 sleep an average of 7 to 9 hours per night. However, the recommended sleep duration decreases with age [14,15,16].

Results from three separate studies indicate that sleeping five or fewer hours per day may increase the risk of death by 15% [17].

In addition, short sleep duration (<6 hours per day) is associated with impaired glucose tolerance, increased insulin resistance [17,18,19,20], and a higher incidence of diabetes [21,22,23]. Furthermore, long sleep duration (≥9 hours per day) also increases the risk of developing diabetes [24].

In recent years, it has been found that ineffective sleep duration leads to adverse health outcomes such as obesity, diabetes, hypertension, cardiovascular disease (CVD), and increased mortality [25,26].

Leptin hypersecretion during insomnia leads to increased food intake, especially carbohydrates, which may predispose individuals to obesity or worsen existing obesity. It should be noted that obese patients are prone to chronic degenerative diseases such as diabetes [27].

Additionally, it is known that insomnia suppresses insulin production by increasing cortisol levels. In the long term, this can lead to prediabetes or even full-blown diabetes mellitus [28].

In healthy individuals, the body maintains a balance between insulin secretion and glucose consumption during sleep, preventing blood glucose levels from rising or falling. However, in diabetes patients, this balance is disrupted due to low glucose levels in the blood [28].

It has been proven that sleep deprivation increases blood glucose levels due to reduced glucose metabolism and elevated cortisol levels. In addition to worsening diabetes by raising glucose levels, this can also increase the risk of developing diabetes [29].

The inability of diabetic patients to maintain a normal sleep routine may not only result in daytime fatigue, but also impair metabolic control, glucocorticoid production, and blood glucose regulation, thereby contributing to insulin resistance.

Studies have identified both internal (sleep apnea, insomnia, periodic limb movements) and external (circadian rhythm disruption, poor sleep hygiene, use of psychoactive substances) sleep disorders in diabetic patients. The most common manifestation among these patients was sleep apnea [19,30].

People with sleep apnea exhibit higher leptin levels, which are associated with resistance to leptin’s effects. This condition is worsened in obese patients and increases susceptibility to other diseases, including diabetes [27,13].

Leptin not only regulates appetite but also affects chemoreceptors that detect changes in oxygen and carbon dioxide levels. The pathogenesis of respiratory dysfunction in diabetes patients is also linked to changes in the chemoreceptors involved in central respiratory function [31].

Sleep deprivation is also associated with eye problems in diabetes patients.

Retinopathy may be triggered or worsened by hypoxia during dark hours of sleep. Healthy individuals have sufficient retinal blood flow during sleep. However, in patients with diabetes complicated by retinopathy, the retina does not receive adequate oxygen when ambient light is reduced during nighttime sleep [31].

It is important to note that sleep fragmentation due to poor nighttime sleep quality, and even frequent nocturnal urination, may be a reflexive sign of poor blood glucose control [32].

In addition to high blood glucose levels affecting sleep quality in type 2 diabetes, low nighttime glucose levels—commonly seen in insulin-dependent type 1 or type 2 diabetes—occur in 29–56% of patients. These episodes may be unnoticed or masked by other diabetes symptoms, and they also negatively affect sleep quality.

Psychophysiological insomnia, defined as difficulty falling or staying asleep, is another common internal sleep disorder in patients with diabetes.

Restless legs syndrome—another internal sleep disorder—is characterized by uncomfortable sensations that occur primarily during sleep. The development of this syndrome is associated with aging, uremia, polyneuropathy, rheumatoid arthritis, anemia, and metabolic disorders, including diabetes [33].

External sleep disturbances, particularly activities such as noise, listening to music, reading, watching TV, physical labor, environmental factors, and excessive consumption of food and drinks before bedtime, contribute to delayed sleep onset.

Both internal and external sleep disturbances negatively affect quality of life, and more specifically, sleep quality in patients with diabetes mellitus.

3. Conclusions

1. In patients with diabetes mellitus, polyuria and nocturia—common symptoms of the disease—cause individuals to wake up several times during the night, thereby reducing sleep quality.

2. In diabetic patients with diabetic polyneuropathy, symptoms such as pain typically intensify in the evening, leading to difficulty falling asleep and poorer sleep quality.

3. Leptin secretion increases at night in patients suffering from insomnia, which leads to overeating. In individuals with diabetes, this condition negatively affects glycemic control.

4. In sleep-deprived patients, cortisol production increases the following day, which in turn raises insulin resistance, potentially worsening diabetes mellitus.

ACKNOWLEDGEMENTS

The heading of the Acknowledgment section and the References section must not be numbered.

SAP Productions wishes to acknowledge all the contributors for developing and maintaining this template.