Hepatic and pancreatic effects of polyenoylphosphatidylcholine in rats with alloxan-induced diabetes

Cell Biochem Funct. 1996 Jun;14(2):131-7. doi: 10.1002/cbf.657.

Abstract

Polyenoylphosphatidylcholine (PPC: 100 or 300 mg kg-1 b.w., by gastric intubation for 30 days) produced a clearcut protection of the liver of rats treated with alloxan (150 mg kg-1 b.w., i.p.). The liver of rats treated with alloxan was characterized by hydropic dystrophy and lymphocytic infiltrations. Treatment with alloxan increased serum gamma-GT and ALAT activities. The liver structure of rats treated with PPC did not differ from the liver of control animals. PPC normalized the biochemical abnormalities caused by the diabetes. The number of pancreatic islets and beta/alpha cell ratio decreased in the diabetic rats. A number of beta-cells in this group did not contain granules. PPC prevented the decrease in the number of islets and the beta/alpha cell ratio in the pancreas of the diabetic rats. The intensity of staining of beta-cell granules in the pancreas of PPC-treated rats had a position intermediate between the control and diabetic groups. Alloxan increased the blood glucose content where treatment with PPC decreased this. The results suggest that PPC acts as a cytoprotector in the liver and pancreas of rats with experimental diabetes induced by alloxan.

MeSH terms

  • Alloxan / adverse effects
  • Animals
  • Blood Glucose / analysis
  • Diabetes Mellitus, Experimental / chemically induced
  • Diabetes Mellitus, Experimental / physiopathology*
  • Fat Emulsions, Intravenous
  • Lipids / blood
  • Liver / drug effects*
  • Liver / enzymology
  • Liver / pathology
  • Male
  • Pancreas / drug effects*
  • Pancreas / pathology
  • Phosphatidylcholines / pharmacology*
  • Rats
  • Rats, Inbred Strains
  • Transferases / blood

Substances

  • Blood Glucose
  • Fat Emulsions, Intravenous
  • Lipids
  • Phosphatidylcholines
  • lipostabil
  • Alloxan
  • Transferases