Nmrk1, also known as nicotinamide riboside kinase 1, is an essential enzyme in the utilization of nicotinamide riboside (NR), playing a crucial role in maintaining NAD+ levels [3]. NAD+ is a co-enzyme in redox reactions and a substrate for various enzyme families, and thus Nmrk1 is involved in pathways related to energy metabolism, such as glycolipid metabolism [1,2].

In whole-body and pancreatic β-cell-specific Nrk1 knockout (KO) mice, Nrk1 deficiency led to glucose intolerance and compromised β-cell response to a glucose challenge upon high-fat feeding or aging, indicating its role in maintaining pancreatic β-cell function and glucose tolerance [3]. In liver-specific Nrk1 KO mice, it resulted in decreased gluconeogenic potential, impaired mitochondrial function, and more susceptibility to diet-induced liver DNA damage, suggesting its importance in sustaining hepatic NAD+ levels and hindering diet-induced metabolic damage [4].

In conclusion, Nmrk1 is vital for maintaining NAD+ levels, which is essential for normal function in processes like energy metabolism and glucose homeostasis. Studies using Nrk1 KO mouse models have revealed its significance in pancreatic β-cell function and hepatic metabolism, highlighting its potential as a therapeutic target for metabolic disorders such as type 2 diabetes and hepatic steatosis [1,3,4].