Hormonal
Insulin resistance drives hepatic steatosis by disrupting normal insulin signaling, leading to unchecked de novo lipogenesis and increased free fatty acid flux from visceral adipose tissue.
Focus on improving insulin sensitivity through lifestyle changes, as insulin resistance is the primary driver of fat accumulation in the liver. This involves managing energy intake to reduce visceral fat and free fatty acid flux, and potentially reducing carbohydrate load to lower insulin levels, thereby allowing normal lipid metabolism to resume.
IR is a key pathogenic factor for the development of hepatic steatosis... In IR states, the PI3K pathway is eliminated to a certain extent but the up-regulated SREBP-1c leads to a decrease in VLDL synthesis... IR develops after long-term excess energy intake, thus decreasing the inhibitory effects of insulin on peripheral lipolysis and increasing the availability of FFA.
Why this rating
Based on a comprehensive review of multiple human and animal studies cited in the text.
Source
Nonalcoholic fatty liver disease: An overview of current insights in pathogenesis, diagnosis and treatment
T.C.M.A. Schreuder et al. · World Journal of Gastroenterology · 2008
DOI 10.3748/wjg.14.2474
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- Adipose tissue acts as an endocrine organ in obesity, secreting inflammatory cytokines (like TNF-alpha) and adipokines (like RBP4) that induce insulin resistance in the liver and muscle.Good
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