Obesity and Non-Alcoholic Fatty Liver Disease (NAFLD)

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Insulin Resistance: Obesity is often associated with insulin resistance, a condition in which cells have a reduced response to insulin. Insulin resistance can contribute to the accumulation of fat in the liver.

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Increased Lipid Storage: Excess adipose tissue in obesity leads to increased storage of triglycerides in the liver, promoting the development of non-alcoholic fatty liver disease (NAFLD).

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Inflammatory Response: The accumulation of fat in the liver can trigger an inflammatory response, contributing to the progression of NAFLD to more severe stages, such as non-alcoholic steatohepatitis (NASH).

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Hepatic Insulin Resistance: NAFLD is associated with hepatic insulin resistance, where the liver becomes less responsive to the insulin signaling, further promoting fat accumulation.

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Oxidative Stress: Obesity-induced NAFLD is linked to oxidative stress, resulting from an imbalance between the production of reactive oxygen species and the body's ability to neutralize them.

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Release of Pro-Inflammatory Molecules: Adipose tissue in obesity can release pro-inflammatory molecules, such as adipokines, which can contribute to liver inflammation and damage.

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Progression to Fibrosis and Cirrhosis: In some cases, NAFLD can progress to more severe liver conditions, including fibrosis and cirrhosis, which may lead to irreversible liver damage.

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Association with Metabolic Syndrome: NAFLD is often part of a cluster of conditions known as metabolic syndrome, which includes obesity, insulin resistance, high blood pressure, and abnormal lipid levels.

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