🍽️ methionine-choline-deficient diet {methionine-choline deprivation" diet}

Liver Injury: The MCD diet is designed to induce liver injury, characterized by the accumulation of fat in the liver (hepatic steatosis), inflammation (steatohepatitis), and eventually fibrosis and cirrhosis. By depriving the liver of methionine and choline, the MCD diet disrupts lipid metabolism, leading to the development of NAFLD-like symptoms in animal models.

Non-Alcoholic Fatty Liver Disease (NAFLD) Research: The MCD diet is commonly used in preclinical research to model NAFLD, a condition characterized by the accumulation of fat in the liver in the absence of significant alcohol consumption. NAFLD is a prevalent liver disorder associated with obesity, insulin resistance, and metabolic syndrome.

Liver Fibrosis and Cirrhosis: Prolonged exposure to the MCD diet can lead to the progression of liver injury to more advanced stages, including fibrosis and cirrhosis. These conditions involve the excessive deposition of scar tissue in the liver, impairing liver function and potentially leading to liver failure and hepatocellular carcinoma (liver cancer).

Oxidative Stress and Inflammation: The MCD diet-induced liver injury is associated with increased oxidative stress and inflammation within the liver. The depletion of methionine and choline disrupts antioxidant defenses and promotes the production of reactive oxygen species (ROS) and pro-inflammatory cytokines, contributing to tissue damage and disease progression.

Metabolic Dysfunction: Methionine and choline are essential nutrients involved in various metabolic pathways, including lipid metabolism, one-carbon metabolism, and the synthesis of phospholipids and neurotransmitters. Deprivation of these nutrients on the MCD diet can disrupt metabolic homeostasis and contribute to systemic metabolic dysfunction.

Experimental Tool for Liver Disease Research: Despite its limitations and relevance primarily to animal models, the MCD diet serves as a valuable experimental tool for studying the pathogenesis of NAFLD and liver fibrosis and evaluating potential therapeutic interventions for these conditions.