Key result
Genetic obesity increases hepatic apo B RNA editing ~42% in Zucker rats.
Why the study?
The regulation of hepatic apolipoprotein B RNA editing in genetically obese hyperinsulinemic and hypertriglyceridemic Zucker rats was examined to understand molecular differences from lean controls.
May indicate obesity effects on lipoprotein assembly in rats; leaves open human relevance and therapeutic implications.
Hepatic apolipoprotein (apo) B RNA editing was examined in the genetically obese hyperinsulinemic and hypertriglyceridemic Zucker rat. In obese Zucker rats, apo B RNA editing was increased 42% relative to that in lean controls. Correspondingly, the proportion of serum triglyceride-rich lipoprotein containing apo B48 increased 4.7-fold in the obese Zucker rat. Quantification of hepatic total apo B mRNA showed no difference between obese Zucker and lean control rats. In contrast, the hepatic mRNA encoding APOBEC-1, the catalytic subunit of the RNA editing activity, demonstrated an increased abundance of 1.8-fold in obese Zucker rats versus lean controls.
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Phung et al. (1996) studied Genetic obesity, hyperinsulinemia, and hypertriglyceridemia (Zucker rat model). Genetic obesity vs. Lean controls was evaluated on Hepatic apolipoprotein (apo) B RNA editing. Genetically obese Zucker rats demonstrated a 42% increase in hepatic apo B RNA editing and a 4.7-fold increase in the proportion of serum triglyceride-rich lipoprotein containing apo B48 compared to lean controls.
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