Complex neuroendocrine mechanisms underlie the relationship between sleep
disturbances and an increased risk of obesity and type 2 diabetes. For example, glucose
metabolism is regulated differently depending on the sleep phase (NREM vs. REM), and
an imbalance between them results in impaired glucose tolerance. Sleep deprivation also
triggers a cascade of hormonal changes that are detrimental to body shape and
metabolism. Cortisol levels rise, which is a factor that promotes the development of
insulin resistance, but on the other hand, appetite hormones become deregulated: leptin
(responsible for satiety) levels decrease, and ghrelin (which stimulates hunger) levels
increase. As a result, even short-term sleep deprivation intensifies appetite, especially for
high-calorie foods, which facilitates weight gain. Insufficient sleep acts as a stressor,
activating the HPA axis, which also impairs glucose tolerance. The relationship between
obesity and sleep is bidirectional. Obese individuals report poor sleep quality much
more frequently (79% of subjects) than the control group (36%), and sleep duration of
less than 7 hours has been linked to weight gain. Shift work is a significant risk factor, as
it disrupts circadian rhythms, increasing the risk of obesity and metabolic syndrome.
Keywords: obesity, sleep quality, insulin resistance, glucose metabolism, sleep hygiene
