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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 mellitus in poor metabolic control. In different catabolic conditions, prostaglandins (PGs) of the E series produced metabolic effects on nitrogen metabolism, decreasing urea formation. In 10 patients with type 2 diabetes in p...

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Bibliographic Details
Published in:Metabolism, clinical and experimental clinical and experimental, 2001-02, Vol.50 (2), p.253-258
Main Authors: Marchesini, Giulio, Zaccheroni, Valeria, Brizi, Mara, Natale, Stefania, Forlani, Gabriele, Bianchi, Giampaolo, Baraldi, Luisa, Melchionda, Nazario
Format: Article
Language:English
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Summary:Amino acid catabolism and urea synthesis are increased in type 2 diabetes mellitus in poor metabolic control. In different catabolic conditions, prostaglandins (PGs) of the E series produced metabolic effects on nitrogen metabolism, decreasing urea formation. In 10 patients with type 2 diabetes in poor metabolic control, urea synthesis and amino acid to urea nitrogen exchange were measured in the basal state and during an alanine load (6 hours) with 2-hour superinfusion of a PGE 1 analog (30 μg/h) or saline in random order. The urea synthesis rate was calculated as the sum of urinary urea excretion and urea accumulation in total body water (TBW); total nitrogen exchange was calculated as the difference between infused amino acid-nitrogen and urea appearance. Plasma α-aminonitrogen (α-amino-N) increased 100% in response to alanine, to a steady-state without differences in relation 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 alanine + saline and to 113.5 ± 34.6 during alanine + PG ( P < .001). Nitrogen exchange was negative at baseline (−25.0 ± 9.0 mmol/h). It became moderately positive during alanine + saline (14.6 ± 25.1) and far more positive 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 hepatic urea-N synthesis in poorly controlled type 2 diabetes. Such metabolic effects have therapeutic implications.
ISSN:0026-0495
1532-8600
DOI:10.1053/meta.2001.19484