Increased urinary prostaglandin excretion in galactose-fed rats

Metabolism. 1989 Jul;38(7):603-5. doi: 10.1016/0026-0495(89)90094-2.

Abstract

Increased renal production of prostaglandins (PG) may contribute to the hyperfiltration that accompanies early diabetes. It was postulated that a putative metabolic abnormality of diabetes, ie, increased flux through the polyol pathway, stimulates renal PG production and that this phenomenon can be prevented by aldose-reductase inhibition. To test this hypothesis, the effects of polyol accumulation on urinary excretion rates (UER) of PGE2 and 6-keto-PGF1 alpha were studied, using the galactose-fed rat model. UER of PGE2 and 6-keto-PGF1 alpha were measured in three groups of weanling Wistar male rats. Group 1 was maintained on normal chow (n = 6), group 2 was fed chow supplemented with 30% galactose (n = 6), and group 3 received chow supplemented with 30% galactose and 0.7% sorbinil (n = 6). Ten 24-hour urine samples were obtained from each group between 151 and 240 days on the respective diets. UER of PGE2 (P less than .001) and 6-keto-PGF1 alpha (P less than .01) were higher in group 2 than in group 1. UER of PGE2 (NS) and 6-keto-PGF1 alpha (NS), respectively, were similar in groups 1 and 3. These data indicate that flux through the polyol pathway modulates the UER of PGE2 and 6-keto-PGF1 alpha. This phenomenon may contribute to the glomerular hyperfiltration of early diabetes.

MeSH terms

  • 6-Ketoprostaglandin F1 alpha / urine*
  • Aldehyde Reductase / antagonists & inhibitors
  • Animals
  • Dietary Carbohydrates / pharmacology
  • Dinoprostone / urine*
  • Galactose / pharmacology*
  • Imidazoles / pharmacology
  • Imidazolidines*
  • Male
  • Radioimmunoassay
  • Rats
  • Rats, Inbred Strains
  • Reference Values

Substances

  • Dietary Carbohydrates
  • Imidazoles
  • Imidazolidines
  • 6-Ketoprostaglandin F1 alpha
  • Aldehyde Reductase
  • sorbinil
  • Dinoprostone
  • Galactose