ABSTRACT Two-thirds of Americans report regularly obtaining an insufficient amount of sleep. Chronic sleep deficiency is associated with a multitude of negative health consequences, including obesity, cardiovascular disease, diabetes, and metabolic syndrome. Habitually sleeping less than the recommended seven hours per night has been linked to increased all-cause mortality and increased risk of mortality associated with metabolic syndrome, and prospective epidemiological studies have found an association between short sleep duration and increased risk of type 2 diabetes. Laboratory studies have shown that sleep restriction to 4-6 hours per night for durations varying from one to 14 days reduces glucose tolerance in otherwise healthy adults. It is now recognized that sleep restriction decreases insulin sensitivity. Multiple additional causative pathways have been explored, including reduced brain glucose utilization, increased sympathetic nervous activity, elevated evening cortisol levels, etc. However, sleep restriction in both free-ranging humans and prior experimental studies is accompanied by longer exposure to Artificial Light At Night (ALAN), an endocrine disruptor which can disrupt circadian rhythmicity. It has recently been recognized that circadian disruption itself can impair glucose metabolism. We hypothesize that endocrine and circadian disruption caused by extended duration ALAN may contribute to the adverse metabolic effects induced by chronic sleep restriction. To test this hypothesis, we will systematically evaluate glucose metabolism in healthy adults in controlled laboratory conditions (light, temperature, diet and activity patterns) using a crossover design consisting of a 7-day baseline, 7-day sleep restriction (to 5h per night) with (Light:Dark 19:5) or without (Light:Dark 14:10) ALAN, 9-day washout, and another 7-day sleep restriction with or without ALAN. Glucose metabolism (using an intravenous glucose tolerance test and a Standardized Mixed Meal Response) and circadian rhythms (using 24-h profiles of plasma melatonin and cortisol) will be assessed before and after each sleep restriction segment. Understanding whether extended duration ALAN is a primary upstream exposure that contributes to the sleep-restriction-induced impairment of glucose metabolism and consequent increase in diabetes risk is important given the widespread prevalence of sleep deficiency. By clarifying a potential modifiable mechanism by which sleep restriction adversely affects whole-body energy homeostasis, our findings will lay the groundwork for the development of novel treatments and countermeasures to mitigate the adverse metabolic effects of chronic sleep restriction.