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Metabolic syndrome is a growing health problem worldwide. It is therefore imperative to develop new strategies to treat this pathology. In the past years, the manipulation of NAD⁺ metabolism has emerged as a plausible strategy to ameliorate metabolic syndrome. In particular, an increase in cellular NAD⁺ levels has beneficial effects, likely because of the activation of sirtuins. Previously, we reported that CD38 is the primary NAD⁺ase in mammals. Moreover, CD38 knockout mice have higher NAD⁺ levels and are protected against obesity and metabolic syndrome. Here, we show that CD38 regulates global protein acetylation through changes in NAD⁺ levels and sirtuin activity. In addition, we characterize two CD38 inhibitors: quercetin and apigenin. We show that pharmacological inhibition of CD38 results in higher intracellular NAD⁺ levels and that treatment of cell cultures with apigenin decreases global …