Chronic inorganic nitrate supplementation does not improve metabolic health and worsens disease progression in mice with diet-induced obesity.

Inorganic nitrate (NO) has been proposed to be of therapeutic use as a dietary supplement in obesity and related conditions including the metabolic syndrome (MetS), type II diabetes, and metabolic dysfunction-associated steatotic liver disease (MASLD). Administration of NO to endothelial nitric oxide synthase-deficient mice reversed aspects of MetS; however, the impact of NO supplementation in diet-induced obesity is not well understood. Here we investigated the whole body metabolic phenotype and cardiac and hepatic metabolism in mice fed a high-fat, high-sucrose (HFHS) diet for up to 12 mo of age, supplemented with 1 mM NaNO (or NaCl) in their drinking water.

Bariatric surgery blunts nitrate-mediated improvements in cardiovascular function of overweight women by interfering with gastric S-nitrosothiol formation.

Inorganic nitrate (NO) and nitrate-rich foods have been shown to exert antioxidative effects and lower blood pressure in experimental animal models and human clinical studies. The specific handling of nitrate, including its enterosalivary recirculation, secretion into saliva, oral microbial reduction to nitrite (NO), and the pH-dependent nitrosative capacity in the stomach have all been recognized as being important for nitrate's beneficial effects. Obesity is of major health concern worldwide and associated with increased cardiovascular risk; whether nitrate lowers blood pressure and improves endothelial function in this setting has not been investigated.

Oxidative stress, redox status and surfactant metabolism in mechanically ventilated patients receiving different approaches to oxygen therapy (MecROX): An observational study protocol for mechanistic evaluation.

Background: MecROX is a mechanistic sub-study of the UK-ROX trial which was designed to evaluate the clinical and cost-effectiveness of a conservative approach to oxygen therapy for invasively ventilated adults in intensive care. This is based on the scientific rationale that excess oxygen is harmful. Epithelial cell damage with alveolar surfactant deficiency is characteristic of hyperoxic acute lung injury.