Effect of the prostaglandin E1 analog enisoprost on glucose and lipid metabolism in patients with type II diabetes mellitus

Siddika E Karakas, M. Moran, S. Khilnani, M. A. West, K. L C Jen

Research output: Contribution to journalArticle

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Abstract

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 E1 analog on the regulation of glycemic control and plasma lipids. Twenty patients with type II diabetes received enisoprost, 300 mcg/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 lipoprotein2 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.

Original languageEnglish (US)
Pages (from-to)176-180
Number of pages5
JournalHormone and Metabolic Research
Volume24
Issue number4
StatePublished - 1992
Externally publishedYes

Fingerprint

Synthetic Prostaglandins
Lipoprotein Lipase
Alprostadil
Medical problems
Lipid Metabolism
Type 2 Diabetes Mellitus
Cholesterol
Glucose
Triglycerides
C-Peptide
Glycosylated Hemoglobin A
Apolipoproteins B
Plasmas
HDL Cholesterol
Heparin
Synthetic Prostaglandins E
Insulin
Liver
Apolipoprotein A-I
Carbohydrate Metabolism

Keywords

  • hepatic lipase
  • lipids
  • lipoprotein lipase
  • prostaglandin E1
  • type II diabetes mellitus

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

Cite this

Effect of the prostaglandin E1 analog enisoprost on glucose and lipid metabolism in patients with type II diabetes mellitus. / Karakas, Siddika E; Moran, M.; Khilnani, S.; West, M. A.; Jen, K. L C.

In: Hormone and Metabolic Research, Vol. 24, No. 4, 1992, p. 176-180.

Research output: Contribution to journalArticle

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abstract = "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 E1 analog on the regulation of glycemic control and plasma lipids. Twenty patients with type II diabetes received enisoprost, 300 mcg/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 lipoprotein2 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.",
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AU - Karakas, Siddika E

AU - Moran, M.

AU - Khilnani, S.

AU - West, M. A.

AU - Jen, K. L C

PY - 1992

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N2 - 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 E1 analog on the regulation of glycemic control and plasma lipids. Twenty patients with type II diabetes received enisoprost, 300 mcg/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 lipoprotein2 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.

AB - 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 E1 analog on the regulation of glycemic control and plasma lipids. Twenty patients with type II diabetes received enisoprost, 300 mcg/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 lipoprotein2 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.

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