Hormonal
Hepatic lipid accumulation acts as a primary driver of systemic metabolic dysfunction by serving as ligands for PPARs, which upregulate gluconeogenic, lipogenic, and ketogenic genes, thereby promoting hyperglycemia and hyperlipidemia.
If you have fatty liver, your liver is actively contributing to your metabolic issues (like high blood sugar) by sending chemical signals that tell your body to produce more glucose and store more fat. Treating the fatty liver is not just about removing fat; it is about stopping these active signals that drive systemic disease.
By acting as peroxisome proliferator activated receptor (PPAR) ligands, hepatic non-esterified fatty acids upregulate expression of gluconeogenic, beta-oxidative, lipogenic, and ketogenic genes, promoting hyperglycemia, hyperlipidemia, and ketosis.
Why this rating
The paper is a comprehensive review citing multiple human cohort studies and genetic mouse models, providing strong mechanistic evidence.
Source
Hepatic lipid accumulation: cause and consequence of dysregulated glucoregulatory hormones
Caroline E. Geisler et al. · Journal of Endocrinology · 2017
DOI 10.1530/joe-16-0513
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