Glucose and lipid metabolism : the role of sleep, exercise, and adipose tissue
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Habitual sleep restriction (SR) (<7 h/night) is widespread in modern society and may be contributing to the development of type 2 diabetes by inducing insulin resistance (IR) in skeletal muscle (SM) and adipose tissue (AT). A lack of sleep also likely contributes to IR development indirectly by affecting behavior (i.e., physical activity and energy intake). Whether the way sleep is restricted, or prior exercise engagement, impact these outcomes is not fully understood. As SM and AT are particularly susceptible to the ramifications of SR, mechanistically investigating the nuances of their dysfunction in disease states (i.e., obesity and gestational diabetes mellitus) may provide insight into SR-induced metabolic impairments. Given the above, a series of experiments were performed that determined: 1) during modest SR, advancing wake time tends to increase physical activity while delaying sleep time tends to increase energy intake, particularly through high fat and sodium foods; 2) prior evening exercise reduces morning postprandial lipemia in the latter half of a 4-h oral fat tolerance test, but this effect is abolished during SR; 3) gestational diabetes mellitus affects AT in a depot- specific manner, predominantly affecting visceral AT metabolism and inflammation; and 4) in of obese mice, a beta-3 adrenergic receptor agonist has therapeutic effects similar to exercise as it increases lean mass during weight loss, improves glucose tolerance, and alters markers of lipid metabolism in SM. Collectively, these data advance our understanding of the metabolic and behavioral consequences of SR, evaluate the efficacy of therapeutics on these consequences, and mechanistically provide tissue-specific insight into disease states that could hypothetically develop from chronic SR.
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Ph. D.