Macro partitioning
CD36 fatty acid translocase drives hepatosteatosis onset and progression to NASH by increasing fatty acid influx into hepatocytes, making it a key driver of NAFLD pathogenesis.
Current research suggests that the protein CD36 plays a significant role in moving fatty acids into liver cells, contributing to fatty liver disease. While there is no specific diet protocol mentioned to target CD36 directly, the findings highlight that managing fatty acid influx is critical. Future treatments may target CD36, but for now, standard NAFLD management focusing on reducing metabolic stress is implied.
CD36 increases FFA uptake and, in the liver, it drives hepatosteatosis onset and might contribute to its progression to NASH.
Why this rating
Supported by clinical studies showing increased CD36 content in patients and animal models, but identified as a review of mechanisms.
Source
Understanding lipotoxicity in NAFLD pathogenesis: is CD36 a key driver?
Patricia Rada et al. · Cell Death and Disease · 2020
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