Hormonal
Pharmacological re-activation of AMPK in the liver suppresses hepatic steatosis by inhibiting lipid synthesis and stimulating fatty acid oxidation, whereas genetic loss of AMPK does not cause fatty liver development.
While low AMPK activity is linked to fatty liver, simply having low activity doesn't cause the fat accumulation. However, drugs that activate AMPK (like metformin or specific activators) can help reduce liver fat by blocking fat creation and increasing fat burning. This suggests that targeting AMPK is a valid treatment strategy for fatty liver, even if low AMPK itself isn't the initial cause.
Unexpectedly, we show here that liver-specific AMPK KO mice display normal hepatic lipid homeostasis and are not prone to fatty liver development... In contrast, we found that pharmacological re-activation of downregulated AMPK in fatty liver is sufficient to normalize hepatic lipid content.
Why this rating
High-quality genetic mouse models (liver-specific KO) combined with in vitro human hepatocyte data and pharmacological validation.
Source
AMPK Re-Activation Suppresses Hepatic Steatosis but its Downregulation Does Not Promote Fatty Liver Development
Nadia Boudaba et al. · EBioMedicine · 2018
DOI 10.1016/j.ebiom.2018.01.008
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