Key result
Transient hepatic IGF2 overexpression induces fatty liver driven by increased cholesterol and lipid droplet accumulation.
Why the study?
A causal role of IGF2 in the development of hepatic steatosis remains elusive despite its reported overexpression in steatosis and steatohepatitis.
Comparison
Transient hepatic overexpression of Igf2 plasmid vs control Luc plasmid
Design
Preclinical study using hydrodynamic gene delivery
Authors
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Igf2 overexpression fails to induce steatosis in mice; leaves open its causal role in human steatohepatitis.
Transient hepatic overexpression of IGF2 in mice induces free cholesterol and lipid droplet formation, suggesting a causal role for IGF2 in hepatic lipid accumulation and steatosis.
Kessler et al. (2016) studied Hepatic steatosis (n=21). Igf2 plasmid (transient IGF2 overexpression) vs. Luciferase control plasmid was evaluated on Hepatic lipid accumulation (total lipids, cholesterol, phospholipids, and lipid droplets). Transient hepatic overexpression of IGF2 induced a fatty liver characterized by increased cholesterol and phospholipids leading to accumulation of lipid droplets.
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