Protective Effects Of Sodium Orthovanadate In Rodent Models Of Nafld: A Preclinical Investigation

Abstract

One of the most common metabolic liver diseases is non-alcoholic fatty liver disease (NAFLD). Fatty liver disease, the hepatic expression of a collection of disorders associated with metabolic dysfunction, is commonly observed in patients with diabetes mellitus (DM) and metabolic syndrome (MetS). High-fat meals and environmental toxicity caused by heavy metals like cadmium (Cd) are hallmarks of the contemporary period, which poses major health concerns as a result of improper human activities. Oxidative stress, insulin resistance, inflammation, lipid accumulation, and dietary practices are all linked to the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Chronic liver disease, or NAFLD, is initially associated with fatty liver and hepatic insulin resistance, both of which are strongly impacted by PTP1B.The insulin-mimetic activity of vanadium-based compounds, such as Na3VO4, is drawing interest. In order to increase sugar absorption, sodium orthovanadate (Na3VO4) inhibits PTP1B activity and transports the glucose transporter type 4 (GLUT4) channels to the cell membrane. We speculate that by modifying lipid metabolism, lowering oxidative stress, and decreasing hepatic inflammation, SOV may have therapeutic advantages in NAFLD. In this work, we investigate the impact of SOV in two rodent models of non-alcoholic fatty liver disease (NAFLD): (1) Cadmium-induced liver disease and (2) high-fat diet-induced liver disease. To find out, that SOV can slow the evolution of NAFLD, we measure hepatic lipid accumulation, oxidative stress indicators, inflammatory cytokine profiles, and insulin sensitivity. This work may lead to new pharmacological approaches to treat fatty liver illnesses by revealing the therapeutic potential of SOV.