The main cause appears as combined inappropriate nutrition and sedentary lifestyles. In the last few decades, the prevalence of obesity has become epidemic through the world and is a major risk factor for type 2 diabetes (T2D) 1. Our findings unveil the time-of-day dependence of NAD +-based therapies and support a chronobiology-based approach. Remarkably, timed NAD + adjusted circadian oscillations of the liver clock until completely inverting its oscillatory phase when increased just before the rest period, resulting in misaligned molecular and behavioral rhythms in male and female mice. However, raising NAD + immediately before the rest phase selectively compromised these responses. Increasing NAD + prior to the active phase in obese male mice ameliorated metabolic markers including body weight, glucose and insulin tolerance, hepatic inflammation and nutrient sensing pathways. Here, we demonstrate that time-of-day determines the efficacy of NAD + treatment for diet-induced metabolic disease in mice. Increasing NAD + is becoming a therapy for metabolic dysfunction however, the impact of daily NAD + fluctuations remains unknown. Misalignment of the clock can cause obesity, which is accompanied by reduced levels of the clock-controlled, rhythmic metabolite NAD +. The circadian clock is an endogenous time-tracking system that anticipates daily environmental changes.
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