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Insulin Polyphagia, Liver Fat, and Choline

Burhz Hoklley

Insulin polyphagia, liver fat accumulation, and choline have gained considerable attention in the field of metabolic research. Insulin polyphagia refers to excessive hunger and increased food consumption resulting from insulin resistance. Non-alcoholic fatty liver disease (NAFLD) is characterized by abnormal fat accumulation in the liver, often associated with insulin resistance. Choline, an essential nutrient, has emerged as a potential modulator of these metabolic processes. This abstract provides a concise overview of the interplay between insulin polyphagia, liver fat, and choline. Insulin polyphagia arises from disrupted insulin signaling and is commonly observed in conditions such as obesity and type 2 diabetes. Hyperinsulinemia, a hallmark of insulin resistance, disturbs the normal feedback loop between insulin and appetite regulation centers in the brain, leading to increased hunger and overeating. NAFLD, closely linked to insulin resistance, encompasses a range of liver conditions characterized by excess fat accumulation. Elevated insulin levels promote fat synthesis and hinder fat oxidation in the liver, resulting in hepatic steatosis. Insulin resistance further exacerbates metabolic disturbances by impairing the suppression of hepatic glucose production.