Nocturnal Lipolysis is the physiological process of breaking down stored triglycerides within adipose tissue into glycerol and non-esterified fatty acids (NEFAs) during the fasting state of sleep. This catabolic process provides the primary energy substrate for the body’s metabolic needs overnight, particularly for organs like the brain and muscle tissue. The process is tightly regulated by the nocturnal hormonal milieu, which shifts away from the fed state’s storage-promoting signals to fasting-state mobilization signals.
Origin
This phenomenon is a fundamental concept in human metabolism and endocrinology, intrinsically linked to the circadian rhythm and the alternating states of feeding and fasting. The term nocturnal emphasizes the timing, reflecting the peak activity of fat breakdown that occurs during the overnight fast. Scientific understanding of its regulation grew significantly with studies defining the pulsatile secretion patterns of Growth Hormone and its impact on substrate utilization during sleep.
Mechanism
The primary hormonal mechanism is driven by the relative scarcity of insulin and the nocturnal surge of Growth Hormone (GH) and catecholamines. Low insulin levels release the inhibitory brake on Hormone-Sensitive Lipase (HSL), the enzyme responsible for cleaving triglycerides. Simultaneously, the large, pulsatile bursts of GH, which occur predominantly during deep sleep, directly stimulate HSL activity in the adipocyte. This synergistic hormonal environment mobilizes stored fat, ensuring a continuous supply of energy for the maintenance of basal metabolic rate throughout the night.
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