Exploring the Potential Impacts of Maternal Early-Life Sleep Deprivation on Metabolic Function of the Offspring( I )

Chronic sleep deprivation (SD) is an extremely common phenomenon with harmful effects on metabolic function in our modern society. Chronic SD during pregnancy would not only increase the risk of gestational problems, but also cause severe and adverse perinatal outcomes. Previous studies have demonstrated that chronic SD during pregnancy would impose significant changes in lipid metabolism, which contributes to the emergency of adiposity and metabolic dysfunction in the offspring. Biochemical reports also revealed that impairments in the epigenetic modifications of adiponectin gene (AdipoQ) during gestational SD may play a central role in the incidence of offspring’s metabolic deficiency. It is indicated that the sensitivity of epigenetic system to environmental factors occurs mainly during the periods of developmental plasticity (i.e. in the gestation or early postnatal life). Alterations in the epigenetic modulation marks offer the plausible explanations of how gestational or early postnatal experience can affect subsequent generation and elicit the detrimental outcomes. Based on this viewpoint, it is reasonable to suggest that the metabolic dysfunction observed in the offspring may result from maternal SD either exposed during the gestation or experienced in their early-life stage. However, as far as can be ascertained, many studies designed to detect the effects of maternal SD on offspring’s metabolic function have only focused on the gestational period. The potential impact of pre-gestational SD on the incidence of offspring’s metabolic dysfunction has never been reported. This study is thus aimed to determine the consequences of chronic SD that experienced during maternal early-life on metabolic function of the offspring, with sequentially focuses on: (1) examining the potential changes of the molecular machinery engaged in adiponectin signaling pathway, and detecting the oxidative / inflammatory responses induced by the modified release of adiponectin [First year] (2) extensively analyzing the functional roles of epigenetic modulation of AdipoQ gene in the incidence of offspring’s metabolic deficiency following maternal early-life SD [Second year] (3) given that orexin could increase the secretion of adiponectin and modulate metabolic function, the present study is therefore aimed to systemically explore the potential effects of orexin on preventing or counteracting the maternal early-life SD-induced cross-generational metabolic deficiency [Third year]. This is an exciting new field of study in which elucidation of the mechanism involved in the cross-generation impact of maternal early-life SD on offspring would not only help us to better understand the potential importance of pre-gestational lifestyle on pre- and postnatal development, but also shed an important light for early intervention of those children born to the mother who has suffered from adverse experience in their early-life stage.