Nicotinamide adenine dinucleotide (NAD+) is the crucial substrate for NAD+-dependent enzymes, such as sirtuins, that mediate numerous fundamental cellular processes including energy metabolism. NAD+ levels decline with age in both rodents and humans and are reduced in metabolically compromised states such as obesity. To date, various studies have demonstrated positive metabolic effects of replenishing declining NAD+ levels in these conditions through the provision of NAD+ precursors such as nicotinamide mononucleotide (NMN) or nicotinamide riboside (NR). More recently, the reduced forms of these precursors – NMNH and NRH – have demonstrated a greater potency in their ability to increase NAD+ in vitro and in vivo. Thus far, no studies have explored their metabolic impact on the pathogenesis of obesity or diabetes when given long-term. We sought to investigate the metabolic effects of altering NAD+ metabolism with chronic administration of NMNH in a murine model of HFD-induced obesity. We found NMNH acutely raised NAD+ levels more so than any other precursor across multiple tissues. When administered for 12 weeks in HFD-fed mice, weight gain of NMNH-treated mice was attenuated to such an extent that their end weight did not differ from their chow-fed counterparts, whilst vehicle-treated HFD-fed mice gained ~40% body weight (%BW). This attenuation of weight gain was primarily due to a reduction in fat deposition, with 28±2.3 and 3.3±0.5 %BW fat mass gained in vehicle and NMNH-treated HFD-fed mice respectively (n=10; p<0.0001).NMNH-treated mice on both diets demonstrated enhanced endurance capacity, while HFD-NMNH mice showed improved insulin action in comparison to their vehicle-treated counterparts based on an index of insulin sensitivity derived from integration of circulating glucose and insulin levels during a glucose tolerance test. Overall, NMNH shows promising therapeutic potential as an NAD+ precursor to treat major metabolic conditions affecting modern society, such as obesity and type 2 diabetes.