Horm Metab Res 1992; 24(4): 176-180
DOI: 10.1055/s-2007-1003288
Clinical

© Georg Thieme Verlag, Stuttgart · New York

Effect of the Prostaglandin E1 Analog Enisoproston Glucose and Lipid Metabolism in Patients with Type II Diabetes Mellitus

S. E. Kasim, M. Moran, Sheila Khilnani, Marilyn A. West, K.-L. Catherine Jen
  • Veterans Administration Medical Center, Allen Park, Wayne State University, Detroit, Michigan Clinical Research, G. D. Searle Co., Skokie, Illinois, U. S. A.
Further Information

Publication History

1990

1991

Publication Date:
14 March 2008 (online)

Summary

Short-term studies have suggested that analogs of prostaglandin E may have favorable effects on the carbohydrate and lipid metabolism in patients with type II diabetes mellitus. The present study was undertaken to investigate the long-term effects of a prostaglandin El analog on the regulation of glycemic control and plasma lipids. Twenty patients with type II diabetes received enisoprost, 300 meg/day, for three months. Fasting serum glucose, glycosylated hemoglobin, insulin and C-peptide levels as well as triglyceride, total cholesterol, high density lipoprotein cholesterol and its subfractions, apolipoproteins B and AI and post-heparin lipoprotein lipase and hepatic triglyceride lipase activities were determined. During the first month, enisoprost treatment caused significant decreases in plasma glucose (baseline = 8.72±0.39 mmol/L, 4 week = 7.78±0.5 mmol/L, change = -0.94±0.28 mmol/L, p < 0.01) and total cholesterol (baseline = 5.30±0.23 mmol/L, 4 week = 5.01±0.26 mmol/L, change = -0.28±0.06 mmol/L, p < 0.05). The decrease in cholesterol level was due to a reduction in high density lipoprotein, specifically in high density lipoproten-2 fraction (baseline = 1.29±0.1 mmol/L, 4 week = 1.12±0.08 mmol/L, change = -0.018±0.04 mmol/L, p < 0.05 for the former and baseline = 0.40±0.06 mmol/L, 4 week = 0.27±0.03 mmol/L, change = -0.12±0.03 mmol/L, p < 0.05 for the latter): All of these values returned to the pretreatment levels despite continuation of enisoprost. Glycosylated hemoglobin, insulin, C-peptide, triglyceride, low density lipoprotein-cholesterol, apoprotein B and AI concentrations and post-heparin lipoprotein lipase or hepatic triglyceride activities did not change significantly.

In summary, enisoprost treatment reduced the plasma glucose, cholesterol and high density lipoprotein cholesterol levels in type II diabetic patients. However, these effects were not sustained during long-term treatment. Therefore, further studies are needed to determine the long-term metabolic effects of various prostaglandin analogs.