Protective effects of nitric oxide on hepatic steatosis induced by total parenteral nutrition in rats.
Abstract
AIM: To investigate the effects of nitric oxide (NO) on hepatic steatosis induced
by total parenteral nutrition (TPN) in rats.
METHODS: Thirty normal Wistar rats were randomly divided into five groups: group
A, free access to food and water; group B, TPN; group C, TPN plus arginine; group
D, TPN plus NG-nitro-L-arginine methyl ester (L-NAME, NO synthase inhibitor);
group E, TPN plus arginine and L-NAME. At the seventh day, liver function tests
were examined, lipid content, nitric oxide level, and nitric oxide synthase (NOS)
activity were measured, and histology was examined.
RESULTS: The hepatic lipid content [triglyceride (mmol/g tissue), cholesterol
(mmol/g tissue)] in group B was increased compared with group A (39.3+/-2.4 and
13.1+/-1.1 vs 6.9+/-0.8 and 5.6+/-0.6) (P<0.05). It was higher in group D (50+/-6
and 14.1+/-1.7) than in group B (P<0.05), whereas lower in group C (18+/-4 and
7+/-3) than in group B (P<0.05). The activity and distribution of NOS in the
liver were associated with the content and distribution of hepatic lipid.
CONCLUSION: These results suggest that nitric oxide produced by the liver may
protect hepatic steatosis induced by total parenteral nutrition in rats.
Keywords:
by total parenteral nutrition (TPN) in rats.
METHODS: Thirty normal Wistar rats were randomly divided into five groups: group
A, free access to food and water; group B, TPN; group C, TPN plus arginine; group
D, TPN plus NG-nitro-L-arginine methyl ester (L-NAME, NO synthase inhibitor);
group E, TPN plus arginine and L-NAME. At the seventh day, liver function tests
were examined, lipid content, nitric oxide level, and nitric oxide synthase (NOS)
activity were measured, and histology was examined.
RESULTS: The hepatic lipid content [triglyceride (mmol/g tissue), cholesterol
(mmol/g tissue)] in group B was increased compared with group A (39.3+/-2.4 and
13.1+/-1.1 vs 6.9+/-0.8 and 5.6+/-0.6) (P<0.05). It was higher in group D (50+/-6
and 14.1+/-1.7) than in group B (P<0.05), whereas lower in group C (18+/-4 and
7+/-3) than in group B (P<0.05). The activity and distribution of NOS in the
liver were associated with the content and distribution of hepatic lipid.
CONCLUSION: These results suggest that nitric oxide produced by the liver may
protect hepatic steatosis induced by total parenteral nutrition in rats.