Salt Transiently Inhibits Mitochondrial Energetics in Mononuclear Phagocytes.

ABSTRACT:

Background

Dietary high salt (HS) is a leading risk factor for mortality and morbidity. Serum sodium transiently increases postprandially but can also accumulate at sites of inflammation affecting differentiation and function of innate and adaptive immune cells. Here, we focus on how changes in extracellular sodium, mimicking alterations in the circulation and tissues, affect the early metabolic, transcriptional, and functional adaption of human and murine mononuclear phagocytes.

Methods

Using Seahorse technology, pulsed stable isotope-resolved metabolomics, and enzyme activity assays, we characterize the central carbon metabolism and mitochondrial function of human and murine mononuclear phagocytes under HS in vitro. HS as well as pharmacological uncoupling of the electron

SUBMITTER: Geisberger S 

PROVIDER: S-EPMC8270232 | biostudies-literature | 2021 Jul

REPOSITORIES: biostudies-literature