Hormonal
Chronic endoplasmic reticulum (ER) stress and the resulting activation of the unfolded protein response (UPR) drive hepatic steatosis and insulin resistance by dysregulating lipid metabolism transcription factors (SREBP-1c, PPARγ) and promoting de novo lipogenesis.
If you are struggling with fatty liver or insulin resistance, reducing the cellular stress on your liver (often caused by high sugar/fat intake) may be more effective than just counting calories. Focus on reducing nutrient overload to allow normal protein folding and lipid regulation.
ER-stress-dependent dysregulation of lipid metabolism may lead to dyslipidemia, insulin resistance, cardiovascular disease, type 2 diabetes, and obesity.
Why this rating
The paper is a review citing multiple animal models and human studies, but lacks direct human intervention trials for the mechanism itself.
Source
Endoplasmic Reticulum Stress and Lipid Metabolism: Mechanisms and Therapeutic Potential
Sana Basseri et al. · Biochemistry Research International · 2011
DOI 10.1155/2012/841362
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