Systemic prostaglandin E-1 infusion and hepatic aminonitrogen to urea nitrogen conversion in patients with type 2 diabetes in poor metabolic control

Amino acid catabolism and urea synthesis are increased in type 2 diabetes m ellitus in poor metabolic control. In different catabolic conditions, prost aglandins (PGs) of the E series produced metabolic effects on nitrogen meta bolism, decreasing urea formation. In 10 patients with type 2 diabetes in p oor metabolic control, urea synthesis and amino acid to urea nitrogen excha nge were measured in the basal state and during an alanine load (6 hours) w ith 2-hour superinfusion of a PGE(1) analog (30 mug/h) or saline in random order. The urea synthesis rate was calculated as the sum of urinary urea ex cretion and urea accumulation in total body water (TBW): total nitrogen exc hange was calculated as the difference between infused amino acid-nitrogen and urea appearance. Plasma alpha -aminonitrogen (alpha -amino-N) increased 100% in response to alanine, to a steady-state without differences in rela tion to PG superinfusion. The urea synthesis rate (mean +/- SD) was 34.0 +/ - 11.4 mmol/h in the basal period and increased to 161.2 +/- 37.0 during al anine + saline and to 113.5 +/- 34.6 during alanine + Po (P < .001). Nitrog en exchange was negative at baseline (-25.0 +/- 9.0 mmol/h). It became mode rately positive during alanine + saline (14.6 +/- 25.1) and far more positi ve during alanine + PG (53.5 +/- 21.4), with the difference due to reduced urea formation. The metabolic effects of PG were not related to differences in insulin and glucagon, We conclude that PGE(1) slows the high rate of he patic urea-hi synthesis in poorly controlled type 2 diabetes. Such metaboli c affects have therapeutic implications. Copyright (C) 2001 by W.B. Saunder s Company.