Nitric oxide required for transition to slower hepatic protein synthesis rates during long-term caloric restriction.

ABSTRACT: Calorie restriction (CR) extends maximal lifespan and maintains cellular homeostasis in various animal models. We have previously shown that CR induces a global reduction of protein fractional synthesis rates (FSRs) across the hepatic proteome in mice, but the timing and regulatory mechanisms remain unclear. Nitric oxide (NO), a bioactive molecule upregulated during CR, is a potential regulator of protein synthesis. To explore the role of NO in hepatic proteome fluxes during CR, we used in vivo deuterium labeling from heavy water and liquid chromatography/mass spectrometry-based (LC/MS-based) flux proteomics in WT and NO-deficient (NO-) mice. We observed a transition to reduced global protein FSRs that occurred rapidly between days 25 and 30 of CR. NO deficiency, whether genetic or pharmac

SUBMITTER: Palacios HH 

PROVIDER: S-EPMC12721896 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature