Liver lipid content is reduced in rat given 7-day administration of angiotensin II.

Activation of the renin-angiotensin system may be involved in the development of hepatic steatosis, a condition that is associated with insulin resistance. We showed that in rats, angiotensin II induced accumulation of triglycerides in the renal tubular and cardiac cells, although it significantly reduced the weight of the rats. Here we investigated the liver lipid content of rats given long-term angiotensin II administration. Angiotensin II (0.7 mg/kg/day) was infused into the rats for 7 days via an osmotic minipump. Some rats also received hydralazine or losartan concomitantly. It was shown that angiotensin II reduced oil red O-stainable lipid droplets (6% of the control value) and liver triglyceride content (angiotensin II: 4.6 ± 0.8 µg/mg, control: 11.7 ± 1.1 µg/mg). Both of these phenomena were blocked by losartan, but not by hydralazine. Angiotensin II infusion reduced the expression and activity of AMP-activated protein kinase. In addition, angiotensin II decreased the mRNA expression of peroxisome proliferator-activated receptor-α and genes related to β-oxidation, although mRNA expression of genes related to lipogenesis were not affected. Angiotensin II reduced triglyceride content in the liver, unlike in the kidney or heart, via an AT1 receptor-dependent mechanism.