Association between sleep disturbance and metabolic dysfunctions in adipose tissue: Insights into melatonin's role

Abstract

The increased prevalence of sleep disturbances in modern society is frequently linked to various metabolic disorders, including insulin resistance, obesity, hypertension, fatty liver disease, and cardiometabolic complications. Melatonin, a pineal gland-secreted neurohormone, plays a pivotal role in maintaining the circadian rhythm. It is involved in regulating adipose tissue development, lipid accumulation, browning of white adipose tissue, and activation of brown adipose tissue. The adipose tissue is a dynamic endocrine organ that secretes hormones and cytokines. Recent research has highlighted the significant role of melatonin in the modulation of lipid metabolism, adipogenesis, and thermogenesis in adipose tissues. Circadian rhythms are important in synchronizing metabolic functions with environmental cues, such as light and dark, feeding-fasting states, etc. Irregular sleep patterns, shift work, and exposure to artificial light at night disrupt these rhythms, affecting circadian regulation and compromising metabolic health. Melatonin imbalance due to sleep disturbances results in metabolic dysfunction, increased fat storage, and adipose tissue inflammation. As circadian rhythm and melatonin are both related, a change in circadian rhythm affects the physiology of adipose tissues thereby precipitating metabolic complications through melatonin signaling. This study attempted to understand the mechanisms by which melatonin influences adipose tissue activity, highlighting the role of circadian rhythms in this process. This will enable the development of melatonin-based therapies to mitigate the adverse effects of chronobiological disturbances on the physiology of adipose tissue. Understanding these interactions will provide novel insights for combating obesity and related metabolic conditions.

Keywords: Adipose tissues; Circadian rhythm; Melatonin; Metabolic homeostasis; Sleep disturbances.