biostudies-literatureUnknown66Cercillieux A<h4>Objective</h4>Disturbances in NAD⁺ metabolism have been described as a hallmark for multiple metabolic and age-related diseases, including type 2 diabetes. While alterations in pancreatic β-cell function are critical determinants of whole-body glucose homeostasis, the role of NAD⁺ metabolism in the endocrine pancreas remains poorly explored. Here, we aimed to evaluate the role of nicotinamide riboside (NR) metabolism in maintaining NAD⁺ levels and pancreatic β-cell function in pathophysiological conditions.<h4>Methods</h4>Whole body and pancreatic β-cell-specific NRK1 knockout (KO) mice were metabolically phenotyped in situations of high-fat feeding and aging. We also analyzed pancreatic β-cell function, β-cell mass and gene expression.<h4>Results</h4>WMolecular metabolism101605https://www.ebi.ac.uk/biostudies/studies/S-EPMC9557729biostudies-literatureNicotinamide riboside kinase 1 protects against diet and age-induced pancreatic β-cell failure.PMC9557729Joffraud MZollinger AJacot GCanto CMetairon SCiarlo ERatajczak JGiroud-Gerbetant JCercillieux AValera-Alberni MSambeat ARumpler MSanchez-Garcia JLfalseNicotinamide riboside kinase 1 protects against diet and age-induced pancreatic β-cell failure.<h4>Objective</h4>Disturbances in NAD⁺ metabolism have been described as a hallmark for multiple metabolic and age-related diseases, including type 2 diabetes. While alterations in pancreatic β-cell function are critical determinants of whole-body glucose homeostasis, the role of NAD⁺ metabolism in the endocrine pancreas remains poorly explored. Here, we aimed to evaluate the role of nicotinamide riboside (NR) metabolism in maintaining NAD⁺ levels and pancreatic β-cell function in pathophysiological conditions.<h4>Methods</h4>Whole body and pancreatic β-cell-specific NRK1 knockout (KO) mice were metabolically phenotyped in situations of high-fat feeding and aging. We also analyzed pancreatic β-cell function, β-cell mass and gene expression.<h4>Results</h4>W2022-01-01T00:00:00Z2022 Sep2025-04-22T02:14:12.654Z2025-04-05T20:21:08.597ZS-EPMC95577293616581110.1016/j.molmet.2022.101605