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The INTERACT2 trial demonstrated that intensive BP lowering was associated with improved functional outcomes, although absolute risk reduction was modest

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Here we developed a high-throughput screen to identify compounds that modulate intracellular S

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(181) established a high-iron diet mouse model, demonstrating that iron overload significantly increases iron levels in serum, colonic tissue, and feces, and successfully induces colitis phenotypes and ferroptosis

Insulin resistance impairs insulins ability to suppress adipose tissue lipolysis Increased release of free fatty acids (FFAs) into circulation The liver accumulates fat due to: Excess FFA influx from adipose tissue Increased de novo lipogenesis (SREBP-1c, ChREBP activation) Reduced fatty acid oxidation and impaired autophagy Accumulation of FFAs and lipotoxic intermediates leads to: Mitochondrial dysfunction Oxidative stress (ROS generation) Activation of inflammatory pathways (JNK, NF-B) promotes: Cytokine release (TNF-, IL-6, TGF-) Hepatocyte injury and progression toward NASH Persistent inflammation activates hepatic stellate cells, resulting in: Fibrosis and progressive liver damage Clinical nutrition intervention directly targets key pathological drivers of fatty liver disease: Improving insulin sensitivity through structured medical nutrition therapy Reducing hepatic FFA load by modulating macronutrient quality and timing Limiting de novo lipogenesis via controlled carbohydrate quality and energy balance Supporting mitochondrial function and reducing oxidative stress Addressing gut-liver axis contributors such as endotoxemia Early, individualized dietary intervention can halt or reverse disease progression before irreversible liver damage occurs