Nicotinamide adenine dinucleotide (NAD) has been recognised as a critical co-factor in redox reactions for nearly 100 years. In recent times however, NAD has been linked with many other processes (e.g. intermediary metabolism, circadian rhythms, cell differentiation) via its role as a co-substrate for different enzymes, including the sirtuin family of deacylases. NAD levels are reduced in states of metabolic dysfunction (e.g. obesity, old age) and interventions that increase NAD levels, such as the provision of NAD precursors, appear to induce favourable metabolic outcomes. In this seminar I will discuss our recent studies using genetic and pharmacological approaches to investigate how changes in NAD biosynthesis influence metabolic defects that occur during the development of obesity.