SIRT1 and Glucose intolerance: NR treatment inhibited high-fat DIO by stimulating Sirt1 activity and increasing NAD+ levels.NMN in diabetes mouse model enhanced glucose intolerance, and increased hepatic insulin sensitivity or through restoring NAD+ levels.NR/NMN in a high-fat diet fed mice increased the use of lipids as substrates, improved insulin sensitivity, and increased energy expenditure.